Uehara, T., Sumiyoshi, T., Matsuoka, T., Itoh, H., & Kurachi, M. (2006). Role of 5-HT<sub>1A</sub> receptors in the modulation of stress-induced lactate metabolism in the medial prefrontal cortex and basolateral amygdala. Psychopharmacology, 186(2), 218-225. Retrieved from EBSCOhost. doi:10.1007/s00213-006-0370-y
Lactate has been known to reflect neural activity in the brain and also is a major factor in energy metabolism. Researchers previously looked at the effect of benzodiazepines on acute stress-induced energy demand in the basolateral amygdala (BLA) by analyzing the concentrations of extracellular lactate. They found that many stressors, which included foot shock and psychological stress, increased the energy metabolism in the BLA and that some of these changes were actually regulated by benzodiazepines. The purpose of their current study was to see if changes in extracellular lactate in the BLA and the medial prefrontal cortex (mPFC) due to stress from a foot shock are caused by tandospirone or perospirone and also if these specific drugs are blocked by a selective 5-HT1A (serotonin receptors) antagonist. Adult male Wistar rats were used in this study, and a dialysis probe was surgically placed into the left mPFC and BLA. Tandospirone and perospirone were injected 10 minutes before the foot shock stress was applied. The foot shock stress was applied in a communication box that was connected to a shock generator and a timer box that would ultimately deliver the foot shock (0.5 mA for 5 seconds that was administered every 30 seconds for 20 minutes). The researchers found that in the mPFC, tandospirone increased the lactate levels, but that perospirone did not affect the lactate levels. Neither tandospirone nor perospirone had affected the lactate levels in the BLA. However, both in the mPFC and the BLA, there was an increase found in lactate levels due to foot shock stress. This study concluded that in both of these regions, mPFC (cortical) and BLA (limbic), the increase in lactate levels is partially due to the regulation of the 5-HT1A receptors.
No comments:
Post a Comment