Loading...

005 | Chronic stress exposure alters signaling pathway that facilitates Gpm6a neuroplastic function

Cellular and Molecular Neurobiology

Author: Sofia Elisa Alzuri | email: sofia.alzuri@gmail.com


Sofia Elisa Alzuri 1°2°, Natasa Hlavacova , Daniela Jezova , Beata  Fuchsova 1°2°

1° Instituto de Investigaciones Biotecnológicas, Universidad Nacional de San Martín (UNSAM) – Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), San Martín, Buenos Aires, Argentina
2° Escuela de Bio y Nanotecnologías (EByN), Universidad Nacional de San Martín, San Martín, Buenos Aires, Argentina
3° Laboratory of Pharmacological Neuroendocrinology, Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.

Gpm6a is a neuronal membrane glycoprotein that functions in different processes of neuronal plasticity and the mechanism of its action involves the actin regulator Coronin-1a (Coro1a) via a signaling pathway that includes the small GTPase Rac1 and its downstream effector the p21-activated kinase 1 (Pak1). Disruptions of neuroplasticity mechanisms in the hippocampus play a significant role in chronic stress response but the intracellular mechanisms underlying these alterations are poorly understood. It has been shown that chronic stress modifies hippocampal expression of Gpm6a in a variety of animal models so we asked whether the signaling pathway that facilitates Gpm6a neuroplastic function is also affected by chronic stress exposure. Here we show that, apart from Gpm6a mRNA level, also Coro1a mRNA level is decreased in the hippocampus of chronically stressed rats. Furthermore, we show that mRNA level of two members of group I Paks predominantly expressed in neurons, Pak1and Pak3, are significantly diminished. No differences were observed for the ubiquitously expressed Pak2. The small Rho GTPases Rac1 and Cdc42 are known to play a central role in the activation of Pak1 and Pak3. Here we observed a significant increase in Rac1 expression while no differences were observed for Cdc42. We suppose that the alterations in the expression of these genes could be directly related to the morphological alterations found in the hippocampus of chronically stressed animals.