Chronic restraint stress affects serotonin transporter uptake kinetics but not binding sites in the rat hippocampus

Abstract

Disturbances in serotonergic neurotransmission and stressful life events have been implicated in depressive disorders (Anisman et al., 2008). The serotonin (5-HT) transporter (SERT) plays a key role in serotonergic neurotransmission by controlling synaptic 5-HT availability through the reuptake of 5-HT into presynaptic neurons (Murphy et al., 2004). While a number of animal experiments have shown increased synthesis and release of 5-HT after various stressful stimuli (Anisman et al., 2008), only a few studies have addressed the effects of acute stress on SERT function, and the impact of chronic stress on SERT activity has not previously been reported. Chronic stress paradigms in animals recapitulate many of the core behavioral characteristics of clinical depression and are fundamental for delineating stress-induced neurochemical and molecular processes implicated in depressive disorders (Willner, 2005). To increase the understanding of how chronic stress affects serotonergic signaling we examined the effects of chronic restraint stress (CRS; 1/2h/21 days and 6h/21 days) on [H]5-HT uptake kinetics and binding of [H]-S-citalopram in the rat hippocampus and prefrontal cortex; two brain regions receiving dense serotonergic innervations and of critical importance for the brain’s response to stress.