Speech perception in individuals with auditory neuropathy

Chapter 10 covers hearing and the auditory cortex.  I wanted to do some research on the hearing disorder known as auditory neuropathy.  According to the article "Speech perception in individuals with auditory neuropathy", one of the main characteristics of this disorder is disrupted auditory nerve activity with normal or almost normal cochlear amplification function.  There is also an impaired capacity for temporal processing, as well as difficulty understanding speech.  There are many probable causes of auditory neuropathy, such as drug agents, infections, hereditary neuropathies, etc.  Researchers believe that clear speech is easier for those with auditory neuropathy to understand as opposed to normal conversational speech.  There is higher intelligibility in clear speech than conversational speech.  In this study, researchers wanted to compare clear speech versus conversational speech in participants with this hearing disorder.  They also wanted to see if cochlear implants would make a difference in hearing.  The researchers used a sample of 13 participants who had been diagnosed with AN.  7 received cochlear implants.  Speech sentences recorded in clear and conversational speech styles were used.  The participants were asked to copy the sentences they heard by typing them on a computer.  After testing the participants, researchers found that participants heard the sentences much better when the clear speech style was used.  They also found that those with the cochlear implants had a greater hearing advantage.  These findings suggest that cochlear implants could be an effective method of treatment for this disorder.  The researchers also suggested innovative hearing aids that incorporate temporal envelope enhancement, low-frequency filtering, and high-frequency transposition as another method of treatment.

Zeng, F., & Liu, S. (2006). Speech perception in individuals with auditory neuropathy. Journal Of Speech, Language & Hearing Research, 49(2), 367-380. Retrieved from EBSCOhost.

Obese children show hyperactivation to food pictures in brain networks linked to motivation, reward, and cognitive control

Obesity has been a growing epidemic over the past 20 years. To the knowledge of the researchers, there has only been three previous studies have examined food motivation in healthy weight (HW) youths. Although studies have examined brain activation differences between HW and obese adults have been done, there are no published studies examining the differences in brain activation between HW and obese children.

Students included 10 obese but otherwise healthy children and 10 HW children. The participants viewed pictures of food, animals, and Gaussian-blurred control images during two scanning sessions; one after fasting for 4 hours, and one immediately after eating a uniform meal. The order of meals was counterbalanced. Functional scans involved three repetitions of each block of each stimulus type, alternated between blocks of blurred images.

After eating, the obese group showed greater activation and the HW group to food vs. non-food pictures in the orbitofrontal cortex. Obese subjects also showed significant reduction in brain activation between pre and post-meal conditions only in the superior and medial frontal gyri and thalamus. No changes were observed in the a priori limibic and paralimbic brain regions.

Food images in the study produced significant brain activations in the limbic and paralimbic regions for both obeses and HW groups. The obeses group showed greater activation to food pictures than the HW group in the frontal and paralimbic cortex under both pre- and post-meal conditions.

International Journal of Obesity (2010) 34, 1494-1500
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Cortical activation during cocaine use and extinction in rhesus monkeys

            Acute re-exposure to cocaine or drug cues associated with cocaine use can elicit drug cravings and relapse. Acute cocaine administration increased cerebral blood flow mainly in the frontal and parietal regions. FMRI studies have shown patterns of brain activation following cocaine administration. Regions including cingulated and lateral prefrontal cortex showed short duration activations that were correlated with ratings of “rush”. Nucleus accumbens showed sustained activation associated with ratings of “craving”.

            This study was the first one to use nonhuman primates in measuring acute cocaine use changes in brain activity. First, cocaine was administered noncontingently. Secondly, the same subjects were trained to self administer cocaine under a fixed ratio. Thirdly, the nonhuman primates were taught to self administer cocaine under a complex , second order schedule.

            Drug administration was not contingent on a behavioral response by the subjects. Cocaine induced a significant increase in whole brain blood flow. Self administration behavior remained robust even in the absence of cocaine delivery. All subjects also learned to self administer under the complex, two step delivery system.

            The areas of major activation included the anterior cingulated cortex, a region associated with the extended limbic system. Self administered cocaine led to greater increases in extracellular dopamine in the nucleus accumbens.

Psychopharmacology (2010) 208: 191-199
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Effects of alcoholism severity and smoking on executive neurocognitive function

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Glass, J., Buu, A., Adams, K., Nigg, J., Puttler, L., Jester, J., & Zucker, R. (2009). Effects of alcoholism severity and smoking on executive neurocognitive function. Addiction, 104(1), 38-48. doi:10.1111/j.1360-0443.2008.02415.x. Retrieved from EBSCO.

In Chapter 15 we discuss in more depth the concepts, components, and principles in cognition, beyond that of learning and memory. We also discuss in more detail the biological and neurophysiological processes that underlie cognition. Also of importance to take away from this chapter are not only points about how our brain thinks, but events, drugs, deficits, and other things that inhibits how we think. For instance, we learned in chapter 8 that psychotic drugs can definitely affect how we perceive, think, and move. As we also know, chronic use of a specific drug produces neurological and biological changes that are often detrimental to our health and lifestyle if the behavior is not reversed. One example in particular is that of alcohol. Previous studies, as cited in this article, have shown that alcoholics have deficits in cognition. These impairments range from memory, processing visual sensations, to higher cognitive functions such as problem solving and making judgments. Cigarettes serve as another example of drug that can cause neurological impairments. The researchers chose to study the combination of both chronic alcohol abuse and cigarette smoking for two reasons: 1) cigarette smoking occurs at higher rates in alcoholism, and 2) the literature has ignored the combined effects of these. The study was a longitudinal design that compared alcoholic men to nonalcoholic men across 12 years. The used various neuropsychological measures consisting of tests of cognitive ability. They also measured reaction-time. They used the collective measurements to define their variable of executive functioning. As expected, both of these habits had an inverse relationship with the overall executive functioning scores; this relationship was effective in using alcohol and smoking habits to predict executive functioning in regression analysis. Interestingly enough, though, researchers found that IQ played an interaction with the effect of alcoholism on cognitive abilities, but IQ did not interact with smoking habits to affect reaction speeds. Alcoholism was also found to have a negative relationship with education, IQ. Alcohol was also related to ADHD and depressive symptoms, while smoking was not. This study shows that future research should also consider the robust findings in smoking when dealing with the cognitive function in alcoholics, in that the cognitive effects of smoking seem to be more localized than those of alcohol use. Another new and exciting finding in this study is a variation of something that many of us have been taught in drug-prevention lessons; alcohol and other drug use is likely to diminish your inhibitions. This study found neurological evidence and showed an actual relationship between alcoholism and the performance on a task requiring participants to stop or inhibit a response. Poor performance on this measure may indicate, say the researchers, that impulsive behaviors may make matters worse both in cognition and treatment in alcoholism patients.

Medial temporal lobe structures participate differentially in consolidation of safe and aversive taste memories

De la Cruz, V., Rodriguez-Ortiz, C. J., Balderas, I., & Bermudez-Rattoni, F. (2008). Medial temporal lobe structures participate differentially in consolidation of safe and aversive taste memories. European Journal of Neuroscience, 28(7), 1377-1381. doi:10.1111/j.1460-9568.2008.06432.x. Retrived from EBSCO.

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            In Chapter 14, the specific processes involved in different types of learning and memory are the focus. There are two types of association learning that we discuss: classical (or Pavlovian) conditioning and operant conditioning. Classical conditioning involves the pairing of a neutral stimulus and an unconditioned stimulus to elicit a conditioned response. This type of learning occurs without conscious awareness and is a reflexive behavior.  This type of association learning is so reflexive, in fact, that we do not even realize it has occurred after the fact either – we may react to a conditioned stimulus and be unable to explain why we have done so. We have all had an experience in which a certain food has caused a terrible upset stomach or that awful situation when your digestive system just refuses to accept the food and must get it out somehow (you know what I mean). From that time on, we avoid that food like the black plague, refusing to even try variations of the food in some cases. This learned taste aversion is by the very process that was previously explained: classical conditioning. The question arises, though: what biological processes underlie this type of learning? Evolutionary psychologists point to the importance of learning from taste of objects for survival. Truthfully, learning nor memory can be linked to a localized area in the brain; different types of learning and different types of memory occur in different areas, and most often have interactions from other areas as well. Even though this is the case, researchers attempt to find neurological correlates with classically conditioned behaviors. For example, De la Cruz, Rodriguez-Ortiz, Balderas, & Bermudez-Rattoni (2008) examined medial temporal lobe structures and their role in taste memories. As we learned from Chapter 14, the medial temporal lobe plays a key role in the consolidation of implicit memories, which are precisely the type of memories involved in classical conditioning (due to their reflexive nature). The investigators used a population of rats to study their brain activity. Specifically, they looked into the perirhinal cortex, the dorsal hippocampus, the basolateral nucleus of the amygdala, and the central nucleus of the amygdala. Instead of simply looking at learned taste aversions, they also examined safe taste memories – memories of foods that are safe to eat (from a survival standpoint). They injected the protein synthesis inhibitor anisomycin into the rats to study these areas. They found different specific areas are responsible for the protein synthesis to stabilize taste aversions than those that are responsible in learning which tastes are “safe.” The realized that the central nucleus of the amygdala, is required in taste aversion, but interestingly the basolateral nucleus is not. Contrary to what they expected to see, the perirhinal cortex and the hippocampus where required for safe taste memories. Researchers suggest these differences in locations are dependent upon the consequences associated with tastes (i.e. sickness or no response).

Musical experience shapes human brainstem encoding of linguistic pitch patterns

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Wong, P. M., Skoe, E., Russo, N., Dees, T., & Kraus, N. (2007). Musical experience shapes human brainstem encoding of linguistic pitch patterns. Nature Neuroscience, 10(4), 420-422. doi:10.1038/nn1872

            Chapter 10 has a primary focus on auditory processes in both language and music. It discusses the structures of the ear and the auditory cortex, as well as the neural activity in discerning properties of sound, such as loudness, location, and patterns. One property of sound the authors of our text discuss is pitch, the frequency of sounds waves, which is begun to be coded by hair cells in the cochlea of the ear. Auditory signals such as music and speech have been attributed to the cortical region of the brain. However, this particular research article examines the subcortical regions that are involved in audition. Specifically, researchers recorded the activity in the brainstem during the encoding process of linguistic pitch. To do this, they measured frequency following response, which is assumed to begin in the auditory brainstem, or the inferior colliculus to be exact. The development and learning of language is not entirely innate or biological. In fact, previous research has shown that experiences within a language enhance how we encode linguistic information. For example, Chinese language speakers can easily distinguish between short syllables that sound exactly the same to western listeners, and these sounds actually convey different meanings within their own language. Based on this knowledge, researchers decided to present three syllables with different intonation and measure the frequency following response. With these measures, investigators compared musicians with individuals who were not musicians. As expected, there was a positive linear relationship between musical training and the tracking of a pitch. The results were consistent with their hypothesis; musicians had more robust and faithful encoding in the brainstem than non-musicians. This basically meant that musical ability predicted the ability to perceive the differing sound structures in a foreign language. The interesting implication of this research is that it could provide a neurological explanation for previous research findings that musicians have a stronger ability to learn language. Musicians obviously have more experience in encoding, deciphering, and responding to information regarding pitch from their frequent musical experiences. The interaction between auditory acuity and cognitive demands is suggested by the researchers to be mediated by feedback from the higher cortex areas to the inferior colliculus. This means that information regarding pitch is relayed from subcortical strucutres to the outer cortex, which leads to more successful interpretation of linguistic pitch. The researchers in this study, though, advise caution with interpretation, since correlational relationships could be explained by a third variable, such as genetics.

Permanent deficits in brain functions caused by long-term ketamine treatment in mice

Sun, L. L., Lam, W. P., Wong, Y. W., Lam, L. H., Tang, H. C., Wai, M. S., & ... Yew, D. T. (2011). Permanent deficits in brain functions caused by long-term ketamine treatment in mice. Human & Experimental Toxicology, 30(9), 1287-1296. doi:10.1177/0960327110388958

Drug use is found in the media, in schools, and even in the home. One cannot study a high school student body (or be a part of one) without at least hearing about the waterfall of drugs available to youth nowadays and how many of these youth are using. In high school, I remember the repeated advances of my peers to get me to use pharmaceutical and street drugs, and that is why I wanted to know more on the topic of how recreational drug use can lead to brain damage. I was intrigued when I heard of teenagers using a drug called Ketamine, a drug I’d never heard of before. Ketamine is an anesthetic that is now used as a hallucinogen.

            Mice were used in this survey, and each were split up into three different groups, each group getting a different amount of Ketamine time ( the first received dosages for one month, the second for 3 months, the third for 6 months). In each group, 20 mice were given Ketamine while ten were given a saline solution equal to the amount of Ketamine in their group. Once the dosages were administered, the mice were put through 3 behavioral analyses (one measuring reaction to pain, another being a maze). Over time the mice would excrete the dosages of either Ketamine or saline. After the behavioral analyses, the rats were killed and samples were taken from each rat and placed in a machine called a TUNEL, where cell death and clusters of cell death could be measured.

            What the researchers found was that, even though learning and memory were not affected, body weights and neuromuscular levels were lower for the Ketamine group after six months of usage. Also, in the Ketamine group the ventral tegmental area, important for rewarding eating behavior, was damaged.

Sleep Deprivation impairs hippocampus-mediated contextual learning but not amygdala cued learning in rats.

Ruskin, D. N., Liu, C., Dunn, K. E., Bazan, N. G., & LaHoste, G. J. (2004). Sleep deprivation impairs hippocampus-mediated contextual learning but not amygdala-mediated cued learning in rats. European Journal of Neuroscience, 19(11), 3121-3124. doi:10.1111/j.0953-816X.2004.03426.x

Sleep is the ever vital process that we as humans need in order to make sense of the world around us and to be able to do such things as learn, recall, or cohabitate. Without it, even after one night, effectiveness and efficiency seem to decline. Sleep deprivation has often been studied to see how animals react to a lack of this needed process, and its effects. The reason I chose this particular article was out of desire and interest for specifics, and the fact that, as a college student I all too often suffer from sleep deprivation personally. I knew that sleep deprivation was harmful, but I curious to what degree and to which regions of the brain suffer the most. Contextual learning is one where the specimen of individual learns based on the surroundings (area) and this kind of learning takes place in the hippocampus. Cued learning takes root in the amygdale and is usually paired with a stimuli.  

The set up for this study was that the rats were split up into the control group (those without sleep deprivation) and the experimental group (those with sleep deprivation). The manner in which the rats were sleep deprived were that they were placed on planks that floated on water and whenever the rat was on the point of falling asleep, the plank would tip, waking the rat. This was effective for both REM and nREM. Immediately after to either control or manipulation rats were conditioned. The rats were conditioned for freezing movement but pairing a 2 minute sound with a 30 second shock.

Exactly one day from conditioning, two types of observations occurred: one where the rats were in the same room, the second being the rats were in a new room with the same tone. In both scenerios freezing behavior was watched for.

            The results indicate that for the control, both hippocampus and amygdale brought on healthy responses. The results also show that contextual learning was less effective in the experimental group than the cued learning. The study also found that increased conditioning did not help with hippocampus- mediated learning.   

Comparing the neural basis of decision making in social dilemmas of people with different social value orientations, a fMRI study.

The topic of chapter 12 was motivation and emotion. The article I found was studying correlates of intrinsic motivation versus extrinsic motivation with cooperation comparing participants that differed in personality traits, which was measured by the Social Value Orientation. The researchers used a total of 28 participants, who they asked to play several prisoners dilemma games that were one shot and weak in cooperative incentives. The participants were also asked to play coordination games with an anonymous partner, which in turn offered stronger incentives for cooperation. The activities were carried out while participants were under the MRI scanner. Results showed that participants adjusted their behavior to be more cooperative when there were extrinsic incentives. Data from the MRI gave truth to the researchers’ developed hypothesis. The study aimed to study which brain areas were active when cooperation was given and when cooperation was opposed. The study used proself to describe individuals that were intrinsic and prosocial to describe individuals that were more extrinsically motivated. Researchers discovered increased activation in the precuneus, dorsolateral prefrontal cortex, and posterior superior temporal sulcus (STS). Moral judgment, compliance and social awareness were found in intrinsically motivated prosocials' and increased activation was found in the anterior superior temporal sulcus, lateral orbitofrontal cortex, and inferior parietal lobule.

Emonds, G., Declerck, C. H., Boone, C., Vandervliet, E. J. M., & Parizel, P. M. (2011). Comparing the neural basis of decision making in social dilemmas of people with different social value orientations, a fMRI study. Journal of Neuroscience, Psychology, and Economics, 4(1), 11-24. doi:10.1037/a0020151

Amygdala and insula response to emotional images in patients with generalized social anxiety disorder

Sabin G Shah,  Heide Klumpp,  Mike Angstadt,  Pradeep J Nathan,  K Luan Phan. Amygdala and insula response to emotional images in patients with generalized social anxiety disorder. Journal of Psychiatry & Neuroscience : JPN.  Ottawa:Jul 2009.  Vol. 34,  Iss. 4,  p. 296-302 (7 pp.)

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I chose this article because I thought t was interesting to learn about the parts of the brain that are activated when dealing with emotional processing. The present article deals with people who suffer from generalized social anxiety disorder and looking at their emotional processing. The amygdala is known to serve functions in emotional processing. The study used eleven patents with generalized social anxiety disorder and eleven healthy control subjects. The participants underwent functional magnetic resonance imaging while viewing sets of emotionally specific pictures. The images were positive, negative and neutral. The results found that participants with gSAD displayed enhanced bilateral amygdale and insula reactivity to negative versus neutral images compared to the healthy control participants. The gSAD group the extent of activation in the amygdale activation was correlated with social anxiety severity. Insula activation was correlated with trait anxiety. The researcher’s findings found that the amygdala and insula responses are hyper- reactive to general emotional images with negative emotional content and that these brain regions. The study shows the importance of studying different parts of the brain and how they affect emotional responses to different stimuli .With more studies into this area will help to better understand how certain types of people respond to things they way they do.

Lack of the serotonin transporter in mice reduces locomotor activity and leads to gender-dependent late onset obesity

Lack of the serotonin transporter in mice reduces locomotor activity and leads to gender-dependent late onset obesity. International Journal of Obesity. Retrieved from psychology journals.

Serotonin is one of the molecular mediators regulating hunger.  There are other mediators such as leptin.  In this experiment, a group of mice was examined to see the interrelationships between serotonin, brain derived neurotropic factor (BNDF), and leptin receptors.  The mice remained at constant conditions with a twelve hour night day cycle and average room temperature of 22-24 C.  Exercise was monitored outside by a treadmill outside of the home cage.  The researchers also monitored the food intake and the rats’ weight before and after using the treadmill.  Before any blood analysis, two groups were created: normally fed mice and fasted mice.  Blood samples were analyzed for: leptin, insulin, adiponetcin, and glucose.  Mice were ethically euthanized and their brains were examined.  The liver was collected also for a record of fat storage.  Samples were frozen immediately after being prepared.  RNA was extracted.  Results showed that body weight was not different between younger (less than five months) male and female rats with serotonin deficiency and normal weight rats.  Those male mice with the deficiency who were over five months had significantly higher weight than normal weight mice.  The younger mice with deficiency were less active than the normal weight mice. 

Sexual dysfunction after traumatic brain injury

In Chapter 12 of our textbook we learned about the hypothalamus and how it controls sexual behaviors in both the male and female. People thinking, dreaming, and planning about sex may all include activity in the amygdala, the hypothalamus, and the cortex. But what if you had a brain injury and was having sexual difficulties? This is what the article is about. Sexual dysfunction is characterized by a disturbance in sexual desire and in psychophysiological changes associated with sexual response cycles. Researchers have realized that many people with TBI are experiencing sexual dysfunction and they have begun to examine the frequency of it.  This research studies 322 individuals with TBI(traumatic brain injury) and 264 normal individuals with no TBI. Participants were given a QOL(Quality of Life) survey to fill out which has a detailed  section on many areas of bodily functions. Those relevant to sexual functioning, endocrine disorders, and perceived health are reported in this study. Participants also filled out a Beck Depression Inventory. The quality of life interview was given over the phone or in person. Participants were asked such questions about sexual functions, rating of health, rating of mood, rating of QOL, and endocrine difficulty. Thus this study is completely self report. They found that in individuals with TBI and those without TBI the only significant predictor of sexual functioning was age. While it is known that sexual desires decrease with age anyways, it was found that those with TBI had a decrease in sexual functioning at a younger age than those not disabled. Women reported greater sexual involvement after TBI while men reported less.

Mary R., H., Wayne A., G., Steven, F., Lisa, H., & Ellen, L. (2000). Sexual dysfunction after traumatic brain injury. NeuroRehabilitation, 15(2), 107. Retrieved from EBSCOhost.

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Localization of asymmetric brain function in emotion and depression

Herrington, J. D., Heller, W., Mohanty, A., Engels, A. S., Banich, M. T., Webb, A. G., & Miller, G. A. (2010). Localization of asymmetric brain function in emotion and depression. Psychophysiology, 47(3), 442-454. doi:10.1111/j.1469-8986.2009.00958.x

Localization of asymmetric brain function in emotion and depression

           I chose this article because I would like to learn more about how the brain is affected during different emotions and depression cases. I fell that emotions are important to everyday life and depression is most likely to affect someone we know or are close to at some point in our lives. Many previous studies by using EEG have shown that depression is linked to abnormal functioning in the asymmetries of the frontal cortex, these studies have failed to identify the specific location of the brain using fMRI and PET scans. The major goal of this study was to show a location of where the asymmetric abnormal functioning patterns occur in relation to emotion and depression.  This study hypothesized that emotional process are connected to asymmetric patterns of fMRI activity, particularly in the dorsolateral prefrontal cortex (DLPFC). They selected their participants by screening a large group of undergraduate using the Anhedonic Depression and Anxious Arousal scales of the Mood and Anxiety Symptom Questionnaire. By their scores they then divided them into the experimental and control groups. All of the participants scored below the 50^th percentile on the MASQ and the depressed scored in the 80^th percentile or above.  There were 28 participants in this study, 11 depressed individuals and 18 non-depressed control individuals. Then they gave the PSWQ and MASQ again prior to the fMRI the two groups did not vary on the PSWQ and MASQ but they did differ on the predicted direction on the MASQ- Anhedonic Depression scores. They completed the emotion-word Stroop task which included pleasant, unpleasant, and neutral words; there were 256 word stimuli included. The fMRI was a series of 370 images, but there was testing prior to the fMRI. The behavioral performance on the task had three hypotheses. First they hypothesized that both the experimental group, depressed individuals, and the control groups would take longer to respond to the emotional words than to the neutral words, Second they would have greater differentiation for unpleasant words than for pleasant words, and Third the depressed individuals would show a larger Stroop effect for unpleasant words than the control group. The results of their study found both of the groups showed a leftward lateralization for pleasant words in the DLPFC. In another DLPFC area the depressed individuals showed a more right lateralized activation than the control group, which replicated the findings previously by the EEG. The data found in this study confirmed that emotional stimulus processing and trait depression are linked to asymmetric brain functions in the distinct sub regions of the DLPFC. This study was very accurate to prove its hypothesis in finding the location in the frontal cortex most associated with emotion more specifically depression. I feel like this study was very interesting in showing the different regions affected most by emotion and depression. 

http://defd.colorado.edu/research/publications/LocalizationAsymmetricBrain.pdf 

Sleep problems in individuals with spinal cord injury: Frequency and age effects.

Chapter 13 discusses sleep and the parts of the brain that regulate and play a part in sleep. I found this article interesting because it studies the spinal cord and injuries that effect sleep. Difficulty sleeping is a common problem among people. It can be implied that people with injuries would have more problems sleeping than people without injuries. The objectives of the study were to replicate previous studies of severe sleep difficulties in individual with spinal cord injuries as compared to normal samples. The second objective was to examine the association between aging variables and severe sleep difficulties. Researchers used a cross-sectional survey design. There were a total of 620 participants with spinal cord injuries in the study. Participants were given a survey of demographics and one that measured the severity of sleep difficulties called the Medical Outcome Study Sleep scale. Results showed that sleeping problems in individuals that have spinal cord injuries were more common than the normal sample. Older participants had less problems with sleeping problems than younger participants.  Researchers found that age onset and the durations of spinal cord injuries were not associated significantly with sleep difficulties.

Jensen, M. P., Hirsh, A. T., Molton, I. R., & Bamer, A. M. (2009). Sleep problems in individuals with spinal cord injury: Frequency and age effects. Rehabilitation Psychology, 54(3), 323-331. doi:10.1037/a0016345

The Unrested Resting Brain: Sleep Deprivation Alters Activity within the Default-mode Network

Gujar, N., Seung-Schik, Y., Hu, P., & Walker, M. P. (2010). The Unrested Resting Brain: Sleep Deprivation Alters Activity within the Default-mode Network. Journal of Cognitive Neuroscience, 22(8), 1637-1648. Retrieved from EBSCOhost

The Unrested Resting Brain: Sleep Deprivation Alters Activity within the Default-mode Network

          I chose this article because I think that the way our sleep affects us in all aspects of life, and seeing as college students are the leaders of not getting adequate sleep I found this article interesting. It is important to note that sleep deprivation not only affects our brain but all aspects of our functioning life. Many studies have been conducted on the affects of sleep deprivation on cognitive task performance. However little has been said about the affects of sleep deprivation on resting-state modes of brain activation. In this study they hypothesize that the integrity of activity within this default-mode network is dependent on a night of prior sleep. They examine whether a night of sleep of sleep deprivation disrupts the task-induced deactivation, the differences in the deactivations and their relation to on-task trial success, and whether the extent of the alterations relates to the amount of prior sleep or the duration of wakeful time. The participants in this study consisted of 28 health people both male and female. They randomly assigned into two groups, sleep deprived or sleep rested. They went without caffeine or alcohol for 72 hrs prior to study and throughout the entire study and maintained a normal sleep-wake rhythm. The study lasted a full week. The subjects performed incidental memory encoding task while undergoing an event related fMRI scan, completed a surprise recognition test, after having restful sleep. The manipulation occurred before the fMRI scan: sleep rested groupà awake during day 1 and slept on night 1, and the sleep deprived groupà were awake across day and night 1. During the fMRI session they presented 150 images, they had a time of passive visual fixation and then an “on-task” phase where they were asked to respond about the picture. They wore MRI compatible goggles to aid in detection of brain activation. The fMRI’s were analyzed using SPM2 (Statistical Parametric Mapping) and ROC (Receiver Operator Characteristics) methods. They found that task-induced deactivation in both groups within both regions was associated with the amount of prior sleep not the duration of waking consciousness.  They also found that one night of sleep loss cause  a two directional imbalance in the brain structures both anterior and posterior that are connected with the default-mode network. The imbalance occurred most prevalently in the failed task trails. The sleep-deprived brain causes problems with on-task brain activity and off-task resting state modes of brain activity. It is interesting to know that not how long we have been awake but the sleep we had prior to the period of wakefulness is what depicts our brains performance on some tasks.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883887/?tool=pubmed

Altered Brain Activation During Response Inhibition in Obstructive Sleep Apnea

Ayalon, L., Ancoli-Israel, S., & Drummond, S. (2009). Altered brain activation during response inhibition in obstructive sleep apnea. Journal of Sleep Research, 18(2), 204-208. Retrieved from EBSCOhost. doi:10.1111/j.1365-2869.2008.00707.x

Chapter 13 in our textbook describes many sleep disorders, with sleep apnea being one of them.  Sleep apnea is the inability to breathe while sleeping.  People with this sleep disorder have to wake up in order to breathe.  The current study is examining obstructive sleep apnea (OSA), which is having repeated occurrences of upper airway obstruction during sleep.  Several studies have been conducted to research the behavioral effects of OSA, but not many studies have been done on the neural connections underlying these behavioral effects.  The researchers of this study used the “Go-NoGo” task, a response inhibition task, to determine if participants with OSA would show a poorer performance on this task as well as a decrease in cerebral activation in brain regions related to tasks.  Fourteen participants had OSA and 14 participants were in the control group.  The participants were studied using fMRI (functional magnetic resonance imaging).  During the fMRI, participants completed the Go-NoGo task, a short-term memory task, and a sensorimotor task.  For the Go-NoGo task, participants were asked to press a button as fast as they could every time they saw a shape (Go stimuli) and to withhold their responses every time they saw a small pentagon (NoGo stimuli).  This task lasted a little more than six minutes.  After participants completed the Go-NoGo task, they were given the Stanford Sleepiness Scale, Karolinska Sleepiness Scale, and a 10-point Likert scale that assessed these factors: how difficult the task was, their concentration ability, how much effort they put into the task, and also how much motivation they had to perform the task efficiently.  After analyzing the results, the researchers found that those participants with OSA displayed more false positives, or “errors of commission,” during the NoGo trials.  The participants with OSA showed a decrease in brain activation during the NoGo trials in the left postcentral gyrus, cingulate gyrus, inferior parietal lobe, right inferior frontal gyrus and insula, and the right putamen.  These results show that individuals with OSA have impaired cerebral activation during cognitive tasks like the response inhibition task used in this study.  Studies such as this one will help people to better understand that the reason for cognitive deficits in individuals with OSA may be due to the underlying abnormalities in the way their brain functions.

Cortical excitability changes in patients with sleep-wake disturbances after traumatic brain injury

Raffaele Nardone,  Jürgen Bergmann,  Alexander Kunz,  Francesca Caleri,  Martin Seidl,  Frediano Tezzon,  Franz Gerstenbrand,  Eugen Trinka,  Stefan Golaszewski. Cortical excitability changes in patients with sleep-wake disturbances after traumatic brain injury. Journal of Neurotrauma.  New York:Jul 2011.  Vol. 28,  Iss. 7,  p. 1165-1171

http://proquest.umi.com/pqdweb?did=2400894941&Fmt=6&clientId=3856&RQT=309&VName=PQD

I chose this article because I thought learning about the functioning of the brain during REM sleep would be an interesting topic to learn about. This article focuses on neural patterns in the brain in relation to rapid eye movement sleep phase. The study had seventeen participants that had normal or corrected – to- normal visual acuity, normal eye movements, and free of psychiatric / sleep disorders and medication. The participants had to stay awake night until the beginning of the experiment and they had sleep inside a MR scanner for two nights in a row. The participants who showed distinct REM sleep in the scanner were also selected to participate in a control experiment during which participants made self-paced saccades in total darkness. The results found that the experiment in which subjects made self-paced saccades in total darkness showed no activation in the visual cortex. The REM – related activation in the primary visual cortex without any input from the retina shows evidence for the existence of human potogeniculoccipital waves (PGO waves) . These results help find a link between REM sleep and dreaming. The time-course analysis of blood oxygenation level dependent responses in the study indicated that the activation of the pontine tegmentum, ventrposterior thalamus and primary visual cortex started before the occurrence of REMs. The researcher’s findings displayed that specific parts of the brain are activated during this stage sleep.

A long-term ecstasy-related change in visual perception

Brown, J., Edwards, M., McKone, E., & Ward, J. (2007). A long-term ecstasy-related change in visual perception. Psychopharmacology, 193(3), 437-446.

http://ezproxy.utm.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=45007556&site=ehost-live

I chose this article because I thought it would be interesting to look for drugs effect on the vision centers of the brain. Ecstasy is a popular recreational drug used today however many users do not realize the lasting damage to their brain after long term use. The present article looks at long -term consequences of ecstasy use on the occipital lobe.Ecstacy is known to cause changes to serotonin system in chronic users. Serotonin may be involved lateral inhibition between orientation sensitive neurons in the occipital lobe. The researchers wanted to look at behavioral changes in the occipital lobe using a tilt aftereffect illusion. Thirty ecstasy users and thirty four non drug users were used as controls. Drug use histories were obtained from each participant. The experimenters used a Gabor which is sinusoidal variation of luminance level within a Gaussian window displayed on a screen. The participants were asked to sit with their head on a chin rest, with their eyes level with the center of the monitor. A curved –forehead rest was used to restrict head tilt. A series of lines showed up on the screen and the experiment consisted of three phases. The pre-adaptation test, the adaptation phase and the post- adaptation test were performed. The participants indicated if they perceived that the lines in the Gabor had been sloped to the left or the right using two keys on the keyboard. The results showed that ecstasy users who had not used amphetamines for115 days or more had a larger average tilt aftereffect than non-drug using controls after adaptation to forty degrees stimuli but not after adaptation to 15 degrees stimuli. The results were consistent with the researcher’s idea that long term ecstasy damage to the serotonin system causes behavioral changes on visual perception. The article does prove that there can be harmful effect

Reduced cognitive ability in alcohol dependence: Examining the role of covarying externalizing psychopathology.

The topic of chapter 8 was Alcohol and Drugs from a neural perspective. The article I found was entitled “Reduced cognitive ability in alcohol dependence: Examining the role of covarying externalizing psychopathology.” This study aimed to study alcohol dependence, referred to as AD, and its effects on reducing cognitive ability and other externalizing disorders. There were a total of 477 participants in the study with a varied history of externalizing disorders. Externalizing disorders are defined as conduct, antisocial behavior and substance problems. Researchers looked at short-term memory, conditional associative learning, intelligence, and working memory capacity. The subsample had 285 participants that were diagnosed with AD by the Diagnostic and Statistical Manual of Mental Disorders diagnosis. Data analyses showed that   participants that had both a history of childhood conduct disorder (CCD) and alcohol dependence scored lower on cognitive measures when compared with those who had alcohol dependence and no history of childhood conduct disorder. Models showed that latent externalizing factor predicted reduced cognitive ability. The study also found that alcohol dependent participants had an externalizing factor associated with cognitive ability.  

Finn, P. R., Rickert, M. E., Miller, M. A., Lucas, J., Bogg, T., Bobova, L., & Cantrell, H. (2009). Reduced cognitive ability in alcohol dependence: Examining the role of covarying externalizing psychopathology. Journal of Abnormal Psychology, 118(1), 100-116. doi:10.1037/a0014656

Smoking produces rapid rise of [11C] nicotine in human brain

Berridge, M. S., Apana, S. M., Nagano, K. K., Berridge, C. E., Leisure, G. P., & Boswell, M. V. (2010). Smoking produces rapid rise of [¹¹C]nicotine in human brain. Psychopharmacology, 209(4), 383-394. doi:10.1007/s00213-010-1809-8

Smoking produces rapid rise of [11C] nicotine in human brain  

I chose this article because I feel that smoking and nicotine it a very interesting topic when dealing with the brain. Most think that smoking mainly affects the lungs, teeth, gums and so one but how many times do you hear well I wonder if this cigarette is affecting my brain.  This article looks at the difference of nicotine being smoked and then by being given intravenously and how the rate is showed present rise in the brain. Intravenously was previously researched. There has been research done on how fast drugs enter the brain and their effects on the different parts of the brain. There have been in-depth studies on how nicotine and cocaine rise in the brain have been related to having tolerance and sensitization to the drug. In this case the rate at which the drug affects and enters the brain is important because it affects behavior and psychological thinking. In this experiment they hypothesized the rate of rise on nicotine in the brain after one puff is rapid enough to affect the neuropharmacology and behavioral psychology of smoking. They used 12 healthy subjects both male and female, who were smokers with no restriction on amount they smoked. All of these individuals labeled themselves as “addicted” to smoking. The method they used was preparing a 10 mm length cigarette into a device that only allowed for the participant to smoke one puff. The cigarettes were Carbon-11 labeled nicotine. They then did PET scans on the patients looking at their lungs, brain regions, and arterial and venous blood curves. These patients had brain MRI’s done a week before the study in order to provide a baseline. When they analyzed the MRI and PET scans they found that in the brain and lung regions there was decay-corrected [11C] nicotine activity present. They found in this study that there was a rise on nicotine following a single puff, in just 15 seconds after the puff the nicotine had reached 50% of the maximum brain levels. In accordance to previous research this study proved that a single puff on nicotine reached the brain faster than when it is intravenously inserted. This study is very interesting in that it provides a better understanding of just how quick smoking can affect not only the body but also the brain. 

Hypothalamus, sexual arousal and psychosexual identity in human males: a functional magnetic resonance imaging study

In chapter 12, we discussed the importance of the hypothalamus. It is involved in many involuntary functions, such as temperature control, biological rhythms, and sexual drive. In this article, researchers look at how the hypothalamus is involved with sexual response in males. The researchers wanted to investigate the correlation between cerebral responses during sexual arousal and the DSI, or deep sexual identity, in males. The DSI of the participants is assessed using a test known as the Franck drawing completion test (FDCT). The test provides accordance/non-accordance between self-reported and psychological sexual identity of the participant. They used a sample of 18 healthy, self-professed heterosexual males. The participants were shown 6 erotic videos, 6 sports video, and 12 neutral videos. Neutral videos were shown in between and only used as a relaxing pause between the 2 main stimuli. Cerebral activity of the participants was monitored by functional magnetic resonance imaging. Sexual arousal was found during all erotic videos and none of the control videos. There was a statistically significant positive correlation between the blood oxygen level-dependent signal in the bilateral hypothalamus and the FDCT during the erotic stimuli. An increase in blood oxygen level-dependent activation positively correlated with a higher DSI profile. These results imply that the psychosexual identity of males is related to the functional features of the bilateral hypothalamus. Also, this correlation was found only in the bilateral hypothalamus, which suggests that the psychosexual identity of males is related strictly to this region of the brain. This part of the hypothalamus is thought to be involved with instinctual drives such as reproduction.

Brunetti, M. M., Babiloni, C. C., Ferretti, A. A., Del Gratta, C. C., Merla, A. A., Olivetti Belardinelli, M. M., & Romani, G. L. (2008). Hypothalamus, sexual arousal and psychosexual identity in human males: a functional magnetic resonance imaging study. European Journal of Neuroscience, 27(11), 2922-2927. Retrieved from EBSCOhost. doi:10.1111/j.1460-9568.2008.06241.x

Relationship of Sleep Quantity and Quality with 24-Hour Urinary Catecholamines and Salivary Awakening Cortisol in Healthy Middle-aged Adults

Zhang J; Ma RCW; Kong APS; So WY; Li AM; Lam SP; Li SX; Yu MWM; Ho CS; Chan MHM; Zhang B; Wing YK. Relationship of sleep quantity and quality with 24-hour urinary catecholamines and salivary awakening cortisol in healthy middle-aged adults. SLEEP 2011; 34(2):225-233.

Short sleep duration is a huge problem affecting modern society. It is associated with cardiovascular problems, metabolic disturbances, hypertension, diabetes, and many other grave illnesses.  Despite all of these and many other associations, the pathophysiologic mechanism in mediating poor sleep and various medical problems remains unclear.

Sleep deprivation is considered to be a form of stress. The hypothalamic-pituitary-adrenal axis (HPA) and locus ceruleus-norepinephrine-autonomic system are two of the brain systems involved in stress-response. Normal sleep decreases the sympathetic nervous system activity (arousing) and increases the parasympathetic nerving system activity (calming).

In this study, researchers aimed to: 1. “explore the level of stability in sleep/wake patterns of middle-aged adults over a three-year follow up period” and 2. “explore the relationship of sleep quantity and quality as measured by actigraphy with 24 hour urinary catecholamines and 3-day salivary awakening cortisol”.

This study was part of a large epidemiologic study that started back in 2003, regarding children and their parents sleep quality. After participants that could not participate in this particular study were ruled out, the sample contained 96 valid subjects with at least one day of actigraphy, 98 subjects with a valid 24-hour urinary catecholamine, and 101 subjects with valid 3-day salivary cortisol results. There was some overlap between these three groups.

The participants filled out detailed questionnaires, a consecutive 2-week sleep log, physical examinations, a 3-day actigraphic assessment, a 3-day morning salivary awakening cortisol, and a 24-hour urinary catecholamine collection. During the physical examination, weight, height, waist circumference, hip circumference, BMI, blood pressure, and a blood sample were measured. Sleep/wake patterns were measured through the consecutive two-week journals. Researchers asked the participants to record the time they went to bed and got up every day for the two-week period. From these records, each participant’s wake up time, bed time, and duration of time in bed was averaged. Researchers utilized an actigraphy wristwatch to measure participants’ time in bed, actual sleep duration, sleep onset latency, wake after sleep onset, and sleep efficiency. Researchers instructed all participants to collect 24 hour urinary samples during the time that they were completing actigraphic assessment so that the researchers could look for an association between objective sleep parameters and cacatecholamine levels. Researchers also had participants collect three saliva samples on three separate days right after they awoke.

Results of statistical analysis showed that there was a high correlation between baseline and follow up measures of various sleep/wake patterns, (r = 0.79 for bedtime, r = 0.64 for wakeup time, and r = 0.60 for time in bed, respectively, p < .001). There were moderate to high correlations in sleep/wake patterns between the participants’ two-week sleep logs and 3-day actigraphy measures, r = 0.43, 0.48, and 0.81 for wake-up time, time spent in bed, and bedtime, respectively, p < .001). Poor sleepers had higher levels of stress hormones in their urine. A lower three-day awakening cortisol level was found in participants that had a lower amount of time in bed than in subjects that had a higher amount of time in bed. Among male and female poor sleepers, males had a higher amount of stress hormones in their urine samples. Among the actigraphic results, sleep onset latency was significantly correlated with higher BMI, waist/hip ratio, systolic blood pressure, and diastolic blood pressure. The urinary hormone levels were positively correlated with waist/hip ratio and diastolic blood pressure.

            The researchers proposed that the level of stability of sleep patterns across the two year time-span could mean that unhealthy sleep patterns could have a persistent effect on a person. The increased hormones in the 24 hour urine samples suggest that the sympathetic nervous system may indeed by stimulated by poor sleep quality and duration.

Overnight Therapy? The Role of Sleep in Emotional Brain Processing.

Chapter 13: Why Do we Sleep and Dream?
Cognitive neuroscience continues to build meaningful connections between affective behavior and human brain function. Within the biological and physiological sciences, a similar focus has taken place. This is the focusing on the role of sleep in various neurocognitive processes and, most recently, on the interaction between sleep and emotional regulation. This peer reviewed article gives a broad array of diverse findings across basic and clinical research domains, resulting in a convergent view of sleep-dependent emotional brain processing. On the basis of the neurobiology of sleep this article describes the overnight modulation of affective neural systems and the reprocessing of recent emotional experiences. Both seem to address the appropriate next-day reactivity of limbic and associated autonomic networks. Furthermore, a rapid eye movement (REM) sleep hypothesis of emotional-memory processing is proposed, the implications of which may provide brain-based insights into the association between sleep abnormalities and the initiation and maintenance of mood disturbances. This basis on REM sleep is quite influenced from the brain. The peribrachial area in the dorsal is part of the brainstem just anterior to the cerebellum. Therefore, these areas of the brain allow us to both sleep and dream in which are reoccurrences of events past, present, and future.

Overnight therapy? The role of sleep in emotional brain processing.

Walker, Matthew P.; van der Helm, Els

Psychological Bulletin, Vol 135(5), Sep 2009, 731-748. doi: 10.1037/a0016570 [Journal Article]

Overnight Therapy? The Role of Sleep in Emotional Brain Processing.

Chapter 13: Why Do we Sleep and Dream?
Cognitive neuroscience continues to build meaningful connections between affective behavior and human brain function. Within the biological and physiological sciences, a similar focus has taken place. This is the focusing on the role of sleep in various neurocognitive processes and, most recently, on the interaction between sleep and emotional regulation. This peer reviewed article gives a broad array of diverse findings across basic and clinical research domains, resulting in a convergent view of sleep-dependent emotional brain processing. On the basis of the neurobiology of sleep this article describes the overnight modulation of affective neural systems and the reprocessing of recent emotional experiences. Both seem to address the appropriate next-day reactivity of limbic and associated autonomic networks. Furthermore, a rapid eye movement (REM) sleep hypothesis of emotional-memory processing is proposed, the implications of which may provide brain-based insights into the association between sleep abnormalities and the initiation and maintenance of mood disturbances. This basis on REM sleep is quite influenced from the brain. The peribrachial area in the dorsal is part of the brainstem just anterior to the cerebellum. Therefore, these areas of the brain allow us to both sleep and dream in which are reoccurrences of events past, present, and future.

Emotion and motivation: The Role of the Amygdala, Ventral Striatum, and Prefrontal Cortex

Chapter12: What Causes Emotional and Motivated Behavior

Emotions are multifaceted, but a key aspect of emotion involves the assessment of the value of environmental stimuli. This peer reviewed article brings many psychological representations, including representations of stimulus value, which are formed in the brain during instrumental conditioning tasks. These representations may be related directly to the many functions of the cortex such as the cortical and sub cortical neural structures.  The basolateral amygdala (BLA) is required for conditioned stimulus to gain access to the current value of the specific unconditioned stimulus that it predicts. The central nucleus of the amygdala acts as a controller of brainstem arousal and response systems, and serves in some forms of stimulus–response for conditioning. The nucleus appears not to be required for knowledge of the contingency between instrumental actions and their outcomes. The prelimbic cortex is required for the detection of instrumental action–outcome contingencies. The orbit frontal cortex, like the BLA, may act as a reinforce value that govern instrumental choice of behavior. Finally, the anterior cingulated cortex, implicated in human disorders of emotion and attention, may have multiple roles in responding to the emotional significance of stimuli and to errors in performance, preventing responding to inappropriate stimuli. In chapter 12 of our text it reviews in more depth the neuroanatomy of motivated behavior.

Neuroscience & Biobehavioral Reviews, Volume 26, Issue 3, May 2002, Pages 321-352
Rudolf N. Cardinal, John A. Parkinson, Jeremy Hall, Barry J. Everitt  

Received 20 February 2002; Accepted 20 February 2002. Available online 10 April 2002.

Strategies and Methods for Research on Sex Differences

Chapter 8: How Do Drugs & Hormones Influence the Brain & Behavior?

Female and male brains differ. A lot of this is due to a combination of genetic and hormonal events and they continue throughout their lifespan. A female’s reproductive status and ovarian cycle have to be taken into account when studying sex differences in health and disease susceptibility, in neuroscience, the pharmacological effects of drugs, and in the study of brain and behavior. It is important to determine that there is a sex difference in the traits of males and females, taking into consideration the reproductive cycle of the female. This article describes methods and procedures to assist scientists new to the field in designing and conducting experiments to investigate sex differences in research involving males and female’s brain and behavior due to drugs. In chapter 8 of the Introduction to Brain and Behavior it goes more in depth about the sex differences as it relates to drugs. As the article states and our book reinstates we must take in account to women’s ovarian cycle. Because of this women are more likely to abuse particular drugs and are more sensitive to drugs than men. This is due women’s body size and their hormonal differences. Basically before we are able to understand how drugs and hormones influence the brain and behavior we have to understand males and females bodily function. Only after this we can then make conclusions. Because of the potential confounding effects of stress on measures of sex differences in brain and behavior, it is highly recommended that studies of sex differences be designed with the possible impact of stress in mind.

Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods

Dimitropoulos, A., & Schultz, R. (2008). Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods. Journal of Autism & Developmental Disorders, 38(9), 1642-1653. Retrieved from EBSCOhost.  doi:10.1007/s10803-008-0546-x

In Chapter 12 of our textbook, there is a discussion on the role that the hypothalamus plays in the control of our eating.  Hyperphagia is a disorder in which one overeats, which leads to significant weight gain.  In class we discussed that the tuberal region of the hypothalamus is the “eating center,” and that within this region is the ventromedial hypothalamus.  When there is damage (lesion) to this specific area in animals, it increases the animal’s appetite and causes it to become obese.  Although this occurred in animals, it has not yet been proven in humans.  I believe Elisabeth talked about in class how her relative had Prader-Willi syndrome (PWS), which is a developmental disorder with characteristics of hyperphagia and the preoccupation with food.  The researchers in the current study discuss that the cause of hyperphagia associated with PWS is unknown, but that it is thought to have some association with an abnormality in hypothalamic circuitry.  The purpose of their study was to examine the food-related neural circuitry using fMRI (functional magnetic resonance imaging) in people with PWS and other matched controls.  Nine participants with PWS were scanned with fMRI.  Ten participants who were developmentally delayed were matched controls with similar BMI as the PWS participants.  The participants performed a perceptual discrimination task, and the changes in blood oxygen level-dependent (BOLD) contrast were measured.  They had to choose whether high-calorie food, low-calorie food, or nonfoods were “similar” or “different” objects.  After this task, the participants had to complete a food preference assessment to evaluate their preferences of high- and low- calorie foods.  Researchers found that the participants with PWS showed hyperactivation in neural circuitry known for mediating hunger and motivation (hypothalamus) to high-calorie foods.  So according to the results, abnormally activated neural circuitry may provoke abnormally strong hunger states.  This study was one of the first fMRI investigations of PWS using visual images of food.  I believe that studies on PWS like this one will help to further understand this disorder and what brain-related causes might be possible.  This could help in the future treatment of individuals with PWS.

Dopamine Activity in the Lateral Anterior Hypothalamus Modulates AAS-Induced Aggression through D2 but not D5 Receptors

Melloni, Richard H., Jr. & Schwartzer, Jared J. (2010). Dopamine activity in the lateral anterior hypothalamus modulates AAS-induced aggression through D2 but not D5 receptors. Behavioral Neuroscience, Vol 124 (5). doi: 10.1037/a0020899

The hypothalamus, as we learn in chapter 12, has a lot to do with generation of behavior. With roles in eating, drinking, sexual behavior, aggression, and many others, it is a small part of the brain that has a very active role.

Researchers in this study were interested in past research that shows the effects of increased aggression in teenagers using synthesized steroids (anabolic androgenic steroids). The anterior hypothalamus is a region with the function of controlling aggression. It connects to other hypothalamic and limbic nuclei. When teenagers take these AAS, the anterior hypothalamus produces more dopamine to combat the increased aggression. This increase in dopamine is localized in the nucleus circularis and the medial supraoptic nucleus. These two nuclei moderate the aggression through the lateral subdivision of the anterior hypothalamus.

There are two classifications of dopamine receptors: D1 receptors and D2 receptors. Both receptors are coupled with G-proteins. The two receptors produce opposite responses.  Activation of D2 receptors produces neural inhibition (by decreasing adenylyl cyclase). Activation of D1 receptors produces neural excitation (by increasing adenylyl cyclase).

Research has shown that some drugs have been effective on reducing aggression in mice by blocking D2 receptors, but they have negative side effects such as a decrease in motor control and a decrease in arousal.

Less is known about receptivity of D5 receptors to steroids. Researchers in this study used microinjection techniques to determine whether antagonism of the D2 or D5 receptors in the anterior hypothalamus suppresses adolescent aggression produced by anabolic androgenic steroids.

A sample of 108 male Syrian hamsters was used in the study. The hamsters were given daily subcutaneous injections of a steroid mixture consisting of testosterone cypionate, nandrolone decanoate, and boldenone undecylenate dissolved in sesame oil for 30 consecutive days during the time period of their adolescent development. This daily treatment design was to emulate a chronic use regimen. This type of study has showed increased aggression in 85% of a sample of hamsters. A small sample of hamsters was given an injection of sesame oil alone as a control.

Researchers implanted a cannula device into the hamsters heads, aimed at the anterior hypothalamus. This is what they used to stick the injection needle into the right area. After each injection, the hamsters were placed in their cages for ten minutes before they were tested for aggressive behaviors using the resident-intruder paradigm. During the testing, one hamster was put in a cage with another hamster. A composite aggression score was compiled for each hamster by observing the total number of attacks and bites during the test period (10 minutes). The researchers also measured any changes in motor activity across the ten minute time span.

To examine the D5 receptor expression, the researchers did not cannulate one set of hamsters. One day after that group’s behavioral testing, the animals were killed and their brains were removed, postfixed in a perfusion fixative and paraformaldehyde, and cryoprotected in a sucrose and saline solution overnight. Brain slides of the Lateral anterior hypothalamus were magnified and the cells were counted.

Results indicated that adolescent hamsters exposed to the steroids did show increased aggression. They committed more than five times the aggressive acts than the oil-treated control group. For the aggression control treatment, those hamsters given high doses had significantly less social contact with the “intruder” hamsters as opposed to those given the medium or low dose. Eticlopride, but not SCH-23390, modulated steroid-induced aggression without motor and social side-effects. Treatment with moderate doses of steroids in adolescence resulted in an increase in dopamine and the expression of D2 receptors. Researchers reported that D5 receptors’ function is still difficult to discern. It is not yet known if these receptors are involved in the aggression control, like the D2 receptors.

Brain Serotonin Transporter in Human Methamphetamine Users

Kish, S., Fitzmaurice, P., Boileau, I., Schmunk, G., Ang, L., Furukawa, Y., & ... Tong, J. (2009). Brain serotonin transporter in human methamphetamine users. Psychopharmacology, 202(4), 649-661. Retrieved from EBSCOhost. doi:10.1007/s00213-008-1346-x

Chapter 8 of our textbook discusses amphetamines and how they release dopamine into its synapse and also block the reuptake of dopamine.  Methamphetamine, which is an illegal amphetamine, is easy to make and is very intoxicating.  Due to the fact that it is inexpensive and easy to obtain, this drug can potentially be extremely devastating.  In the current study, the researchers discuss how methamphetamine usage can damage not only dopamine neurons but serotonin neurons as well.  Many previous research studies have suggested that problems in cognition and aggression may be due to the reduction of serotonin levels.  There was not much research conducted on protein levels of the serotonin transporter (SERT) in methamphetamine users, so the purpose of this study was to determine if there was a decrease in protein levels of the serotonin transporter (SERT) in the brains of chronic methamphetamine (MA) users.  Post-mortem brains were used in this study with 24 controls and 16 chronic users of MA.  Blood samples and scalp hair samples were obtained from the majority of the post-mortem brains.  All of the control brains were neurologically normal and tested negative for drugs of abuse.  All of the brains of chronic MA users tested positive for the presence of MA.  SERT immunoreactivity was measured using an immunoblotting procedure in the brains of chronic MA users.  The researchers found that there was a significant decrease in SERT levels in the orbitofrontal and occipital cortices.  There were other areas, such as the caudate, putamen, and thalamus, that showed a decrease in SERT levels, but it was not a significant decrease.  By conducting this study, the researchers found that in chronic MA users, SERT is somewhat decreased in the brain but that there is a much more significant decrease in dopamine levels.

A deficit in the ability to form new human memories without sleep

Seung-Schik, Y., Hu, P. T., Gujar, N., Jolesz, F. A., & Walker, M. P. (2007). A deficit in the ability to form new human memories without sleep. Nature Neuroscience, 10(3), 385-392. Retrieved October 11, 2011, from Academic Search Premier. doi:10.1038/nn1851

This study was conducted using an fMRI design to explore the capability of the brain to create new episodic memories without prior sleep. This study was composed of 28 participants who were randomly assigned to a sleep-deprived or a sleep control group. All participants had a encoding session for episodic memory during fMRI scanning where they viewed picture slide. They returned two days later in order to classify the pictures they saw again as old or new slides. Researchers hypothesized that one night of being sleep deprived would significantly decrease the subjects’ ability to encode memory and that the impairments would be related to neural deficits in the medial temporal lobe memory systems. Past studies have shown that obtaining sleep after learning is important in order for its consolidation into memory.. The question of whether sleep before learning is as important when forming new memories is still open for discussion. The researchers did find that there was a considerable decline in the activity of the hippocampus when episodic memory was encoding which resulted in worse retention. The researchers also found that the prefrontal regions play a major role in predicting the encoding ability of individuals who have been deprived of sleep in contrast to those who have had a normal night’s sleep. From these results it can be gathered that inadequate sleep can compromise an individual’s neural and behavioral ability to commit new occurrences into memory. Sleep is definitely critical when it comes to encoding new memories after learning and it is also just as important before learning when it comes to prepping the brain for memory formation in the upcoming day.

Selective attention to affective value alters how the brain processes taste stimuli

Grabenhorst, F., & Rolls, E. T. (2008). Selective attention to affective value alters how the brain processes taste stimuli. European Journal of Neuroscience, 27(3), 723-729. Retrieved October 11, 2011, from Academic Search Premier. doi:10.1111/j.1460-9568.2008.06033.x

This study was conducted in order to determine how  selective attention to affect influences sensory processing.  Within this study there were six males and six females with ages ranging from 21 to 35. Past studies indicate that the primary taste cortex is located in the anterior insula in humans.  Taste neurons are recorded and found  in the exact insular and opercular cortex and are project forward into the orbitofrontal cortex the site in which humans activations to taste are located. Subjects were told to remember and rate the pleasantness of a taste stimulus which was 0.1 m monosodium glutamate, their activations were higher  in the medial orbitofrontal and pregenual cingulate cortex . Their activations were lower when they were told  to remember and rate the taste intensity level.  However, activations were higher in the insular taste cortex when the participants were told to remember and rate the intensity.  There was significance when the taste process was dissociated, depending upon the relevance of their focus on pleasantness or intensity. This study showed that the brain responds to taste differently depending upon whether affect is significant and also upon the situation in which the subjects are asked to taste. Thus, when focus is given to the affect, the brain engages differently when it is representing the sensory stimulus of taste than when attention is given to the physical characteristics, such as intensity, of a stimulus.