Tuesday, October 11, 2011

Stress and IL-1β contribute to the development of depressive-like behavior following peripheral nerve injury.


Acute pain helps us survive. Chronic pain, however, can be debilitating and lead to a reduced quality of life. This study sought to target neuropathic pain, pained derived from a lesion or dysfunction of nervous tissue, stress, and depressive-like behavior after nerve injury. The goals of the study were to determine whether peripheral nerve injury precipitates depressive-like behavior in a mouse model of neuropathic pain, and to elucidate the mechanism through which chronic stress impacts behavioral and physiological responses to nerve injury. The researchers hypothesized that chronic stress before a nerve injuty would decrease nocioceptive threshold and increase the development of depressive-like behavior.

The researchers assigned 40 adult male mice to four main groups: sham surgery with no exposure to stress, sham surgery with exposure to chronic stress, surgery with no stress, or surgery with exposure to chronic stress. In the surgery, the tibial and common peroneal nerves were ligated and transected. The stressor consisted of placing a mouse in a 50-mL transparent tube for 2 hours per day for 14 consecutive days.

The results found that stress exacerbates physiological symptoms in response to surgery. The groups that had received the surgery were more likely to float during a forced swim task, suggesting that there was an increase in depressive-like behavior among animals undergoing surgery.
The study established that peripheral nerve injury induces the expression of IL-1β in the brain, which in turn contributes to depressive-like behavior. When animals are stressed, the conditions that result from surgery are worsened; however, when there is no surgery, stress has no effect on pain threshold.

Norman, GJ, Karelina, K, Zhang, N, Walton, JC, Morris, JS, DeVries, AC. Stress and IL-1β contribute to the development of depressive-like behavior following peripheral nerve injury. Molecular Psychiatry(2010) 15, 404-414

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