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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.<\/jats:p>","DOI":"10.1093\/cercor\/bhaf304","type":"journal-article","created":{"date-parts":[[2025,11,17]],"date-time":"2025-11-17T15:39:29Z","timestamp":1763393969000},"source":"Crossref","is-referenced-by-count":3,"title":["Functional topography of glutamatergic and GABAergic neurotransmissions along the rostrocaudal axis of the posterior insular cortex regulating cardiovascular\/autonomic responses to stress in rats"],"prefix":"10.1093","volume":"35","author":[{"given":"Adrielly","family":"Santos","sequence":"first","affiliation":[{"name":"Laboratory of Pharmacology, S\u00e3o Paulo State University (UNESP), School of Pharmaceutical Sciences , Rodovia Araraquara-Ja\u00fa km 01 s\/n, Araraquara, S\u00e3o Paulo , 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