GLUTAMATERGIC ROL IN THE LIGHT NEUROFILAMENT DECREASE IN CA3 HIPPOCAMPAL NEURONS OF ANIMALS EXPOSED TO INESCAPABLE STRESS

CLADOUCHOS MARÍA LAURA; FERNÁNDEZ MACEDO GEORGINA V.; SIFONIOS LAURA; WIKINSKI SILVIA

Rosario, Argentina

Congreso; XLI Reunión Anual de la Sociedad Argentina de Farmacología Experimental.; 2009

Sociedad Argentina de Farmacología Experimental

The main goal of this work was to investigate the signal transduction pathway associated with the decrease of the light neurofilament subunit (NFL) in CA3 hippocampal neurons of animals exposed to inescapable stress. Male adult rats were injected with an antagonist of NMDA receptor (MK-801 0.1mg/kg i.p.), an antagonist of AMPA (CNQX 0.75 mg/kg i.p.) receptor or vehicle 30 minutes before exposure to a protocol of inescapable shocks (I) (one session of 60 footshocks lasting 15 sec each during 1 hour). Control group (C) consisted of rats not exposed to stress. One hour or four days later the animals were sacrificed for 1) PKA and PKC activity measurement in hippocampus extracts; 2) immunohistochemistry of NFL in slices of brain. Results: 1) No differences were found in PKA or PKC activity between C and I animals. 2) I-vehicle animals showed a significant decrement compared with C-vehicle animals (p<0.05) in NFL relative area. The antagonist MK-801 prevented this reduction (I-MK-801 vs I-vehicle, p<0.05). Similarly, CNQX prevented NFL diminution in I animals (p<0.001). No differences were found in C-MK-801 or C-CNQX in comparison with C-vehicle (p>0.05). We conclude that glutamate is implicated in the decrease of NFL in CA3 hippocampal neurons of stressed animals. PKA and PKC seem not participate in the above mentioned NFL decrement. Supported by: PICT 31953 and UBACYT M073.