Social Influences on Depressive-Like Behaivor Following Neuropathic Injury: A Role for Oxytocin and IL-1β
Year: 2009
Type: article
Abstract: The physiological link between neuropathic pain and depression remains unknown despite a high co-morbidity between these two disorders.A mouse model of spared nerve injury (SNI) was employed to test the hypothesis that nerve injury precipitates depression through the induction of inflammation in the brain, and that exposure to chronic social isolation the behavioral and neuroinflammatory consequences of nerve injury.Mice were pair housed or socially isolated for two weeks prior to spared nerve injury, and were subsequently monitored for the development of mechanical allodynia and depressive-like behavior.Brain tissue was then collected and processed for the determination of potential physiological mediators.Measures of allodynia were similar for neuropathic mice regardless of housing on postoperative days 1 and 3, but by day 7 allodynia was significantly greater for mice that were socially isolated than pair housed.Furthermore, depressive-like behavior, determined via the Porsolt forced swim test, developed only among socially isolated mice with nerve injury.Socially isolated mice with nerve injury also were the only experimental group to exhibit increased frontal cortex IL-1β gene expression; IL-1β is a proinflammatory cytokine that has been implicated in depression.Central treatment of socially isolated mice with oxytocin (OT), a neuropeptide associated with social bonding, attenuated the effects of peripheral nerve injury on depressive-like behavior and reduced frontal cortex IL-1β protein levels in socially isolated animals.Conversely, pair housed animals treated with a selective oxytocin receptor antagonist developed depressive-like
Author: Greg J. Norman
Institution: The Ohio State University
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2739652633