Functional topography of glutamatergic and GABAergic neurotransmissions along the rostrocaudal axis of the posterior insular cortex regulating cardiovascular/autonomic responses to stress in rats.

We investigated the role of glutamatergic and GABAergic neurotransmissions within the rostral-posterior insular cortex (rpIC) and caudal-posterior IC (cpIC) subregions of the posterior IC (pIC) in cardiovascular responses and local neuronal activation evoked by acute restraint stress in male rats. We identified that treatment of the rpIC with a cocktail containing the GABAA receptor antagonist SR95531 and the GABAB receptor antagonist CGP35348 enhanced restraint-evoked tachycardia, whereas the same pharmacological approach in the cpIC decreased this response. Treatment of the rpIC with the nonselective ionotropic glutamate receptors antagonist kynurenic acid decreased the drop in tail skin temperature, and GABA receptor antagonism caused an opposite effect. Restraint increased Fos-positive cells in rpIC and cpIC, and local treatment with the glutamate receptor antagonism decreased this effect in both subregions. These data suggest a site-specific control of stress-evoked tachycardia by GABAergic mechanisms in the pIC. Moreover, sympathetically-mediated cutaneous vasoconstriction is specifically controlled by rpIC through opposite role of glutamatergic (facilitatory) and GABAergic (inhibitory) neurotransmissions.