5-HT1B mRNA expression after chronic social stress

Chronic stress contributes to vulnerability for depression and drug addiction. The function of the serotonergic system has been found to be modified by chronic stress and these changes may play an important role in stress-related relapses to drug craving. The 5-HT1B receptor is expressed in nucleus accumbens (NAc) projection neurons and modulates drug reward mechanisms and there is evidence suggesting that stress alters the regulation and function of these receptors. To examine the role of these receptors in integrating the effects of stress on reward mechanisms, we examined whether chronic or acute social defeat stress (SDS) regulates 5-HT1B mRNA in dorsal and ventral striatum, regions that are critical for integrating the effects of environmental stressors on reward motivated behavior. In addition, 5-HT1B mRNA regulation in response to another acute stressor, inescapable tailshock, was measured. Our results indicate that intermittent and daily SDS procedures attenuated body weight gain, induced adrenal hypertrophy, and reduced the preference for saccharin, a sweet solution preferred by normal rats. There was a trend for daily, but not intermittent SDS to increase 5-HT1B receptor mRNA levels in nucleus accumbens. Therefore, in the next experiment, we examined daily SDS in greater detail and found that it increased 5-HT1B receptor mRNA expression in rostral nucleus accumbens shell, an area especially associated with reward functions. Neither acute SDS, nor acute tailshock stress had a significant impact on 5-HT1B mRNA expression in the striatum. Since increased 5-HT1B receptor expression in nucleus accumbens shell neurons can facilitate cocaine and alcohol reward mechanisms, this adaptation in endogenous 5-HT1B mRNA may be involved in the SDS-associated increase in vulnerability for developing addiction.

► Chronic social defeat induces hedonic deficits. ► Chronic social defeat upregulates 5-HT1B receptor mRNA expression in the NAcSh. ► 5-HT1B mRNA is regulated by stress along a rostral–caudal gradient.