Expression of actin regulator coronin 1a is altered in the hippocampus of chroically stressed rats

BEATA FUCHSOVA; NATASHA HLAVACOVA ; ANABEL ALVAREZ JULIA ; V DANEVOVA ; MONTELEONE, MELISA C; CSANOVA A; BROCCO MARCELA ADRIANA; JEZOVA DANIELA

Conferencia; 57th Czech - Slovak Psychopharmacological Conference; 2015

Disruptions in neuroplasticity mechanisms play a significant role in chronic stress response and in the etiology of depression. The intracellular mechanisms underlying these alterations are poorly understood. The member of the proteolipid protein (PLP/DM20) family,the neuronal membrane glycoprotein M6a (GPM6A), has been shown to act in the processes of neuronal remodeling and plasticity such as neurite outgrowth, filopodia formation and synaptogenesis. In animal models of chronic stress, Gpm6a mRNA level decreases in the hippocampus. This downregulation was shown to be prevented by administration of antidepressants. The neuroplastic function of GPM6A in filopodium formation involves association with the actin regulator coronin 1a (CORO1A). The aim of this study was to test the hypothesis that the hippocampal expression of CORO1A is altered by chronic stress exposure and correlates with neuroendocrine and behavioral parameters. Adult male Sprague Dawley rats were exposed to repeated restraint stress (2 h daily for 18 days) or remained undisturbed (n=10 per treatment group). All rats underwent the forced swim test (FST) and plus maze test to asses depression-like behavior and anxiety. Quantitative PCR was used to evaluate gene expression changes in the hippocampus. Levels of aldosterone and corticosterone were measured by RIA. Exposure to restraint stress resulted in a statistically significant decrease in mRNA levels of coro1a as well as Gpm6a and Bdnf in the hippocampus of stressed animals. These rats also demonstrated significantly increased levels of corticosterone and decreased ratio of aldosterone/corticosterone with a tendency towards significance (p=0.0859, Mann-Whitney test, two tailed). Furthermore, we observed a correlation of aldosterone levels with anxiety behaviour in stressed group. No correlation between the gene expression and either hormonal levels or behavioral parameters was found.           The present study demonstrates that the pathway involved in filopodium formation by GPM6A and CORO1A is altered in the hippocampus of stressed rats. The reductions in the expression of these genes could be directly related to the morphological alterations found in the brain of chronically stressed animals.