Abstract
In adulthood, chronic exposure to stressful experiences disrupts synaptic plasticity and cognitive function. Previous studies have shown that perirhinal cortex-dependent object recognition memory is impaired by chronic stress. However, the stress effects on molecular expression and structural plasticity in the perirhinal cortex remain unclear. In this study, we applied the chronic social defeat stress (CSDS) paradigm and measured the mRNA levels of nectin-1, nectin-3 and neurexin-1, three synaptic cell adhesion molecules (CAMs) implicated in the adverse stress effects, in the perirhinal cortex of wild-type (WT) and conditional forebrain corticotropin-releasing hormone receptor 1 conditional knockout (CRHR1-CKO) mice. Chronic stress reduced perirhinal nectin-1 mRNA levels in WT but not CRHR1-CKO mice. In conditional forebrain corticotropin-releasing hormone conditional overexpression (CRH-COE) mice, perirhinal nectin-1 mRNA levels were also reduced, indicating that chronic stress modulates nectin-1 expression through the CRH-CRHR1 system. Moreover, chronic stress altered dendritic spine morphology in the main apical dendrites and reduced spine density in the oblique apical dendrites of perirhinal layer V pyramidal neurons. Our data suggest that chronic stress disrupts cell adhesion and dendritic spine plasticity in perirhinal neurons, which may contribute to stress-induced impairments of perirhinal cortex-dependent memory.
Highlights
Repeated exposure to severe stress during adulthood impairs memory and increases the risk for psychiatric disorders in susceptible individuals (de Kloet et al, 2005; Lupien et al, 2009; Chattarji et al, 2015; Duman et al, 2016)
We investigated the effects of chronic social defeat stress (CSDS) on the mRNA levels of nectin-1, nectin-3 and neurexin-1 in the mouse perirhinal cortex, and examined the involvement of the corticotropin-releasing hormone (CRH)-CRH receptor 1 (CRHR1) system in the stress effects
We further found that perirhinal nectin-1 partially colocalized with rat pyramidal cell (RPC), glutamic acid decarboxylase 67 (GAD67), and calbindin, indicating that nectin-1 is expressed by both excitatory pyramidal neurons and inhibitory interneurons
Summary
Repeated exposure to severe stress during adulthood impairs memory and increases the risk for psychiatric disorders in susceptible individuals (de Kloet et al, 2005; Lupien et al, 2009; Chattarji et al, 2015; Duman et al, 2016). Chronic adult stress or early-life stress reduces hippocampal levels of nectin-3 and neurexin-1 in a CRH receptor 1 (CRHR1)-dependent manner (Wang et al, 2011a,b; Liao et al, 2014). Suppression of hippocampal nectin-3 levels reduces dendritic spine density and impairs long-term spatial memory, while overexpression of hippocampal nectin-3 attenuates stress-induced spine loss and memory deficits (Wang et al, 2013; van der Kooij et al, 2014). It remains unknown whether nectins and neurexins in the perirhinal cortex are influenced by chronic stress. Chronic stress might evoke dendritic spine remodeling in perirhinal layer V pyramidal neurons
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