Gabaergic Modulation of The Stress Response

MARTIJENA I.D, RODRIGUEZ MANZANARES P, LACERRA C, MOLINA VA

SYNAPSE

WILEY-LISS, DIV JOHN WILEY & SONS INC

Año: 2002 p. 86 - 94

0887-4476

the modulation of the central response to stress. In the present study we evaluate the influence of a brief restraint exposure on GABA-stimulated chloride influx in diverse brain areas presumed to have a major role in the mediation of emotional behaviors following aversive stimulation.Areduced chloride uptake after stress exposure was only observed in frontal cortex and amygdala. Moreover, rats subjected to such stressor performed an anxiogenic behavior when exposed later to the elevated plus-maze. A comparable behavior in the elevated plus-maze was observed between animals that were allowed to chew during the restraint experience and those without any stressful manipulation, suggesting that chewing served as an efficient coping behavioral strategy during such threatening situations. In order to explore if chewing during the restraint experience could suppress the reduction in GABA-stimulated chloride uptake induced by this stressor, rats were allowed or not to chew during restraint and in both cases GABAstimulated chloride influx was assayed in frontal cortex and amygdala. The finding of this experiment showed that restrained rats that have the possibility to chew exhibited a similar GABA-stimulated chloride uptake in cortical tissue to that shown by control, unstressed rats. Moreover, chewing in response to restraint attenuated the reduction of GABA-stimulated chloride uptake in amygdala, supporting the notion that chewing is an effective coping response to restraint. These experiments suggest that a reduced GABAergic inhibitory control in these areas could be implicated in the emotional sequelae generated by this uncontrollable stressor and that the suppression of this reduction seems to be associated with the occurrence of coping behavioral response to such fear-inducing stimulus. Synapse 45:86–94, 2002. © 2002 Wiley-Liss, Inc.Synapse 45:86–94, 2002. © 2002 Wiley-Liss, Inc.