Electrical stimulation of insular cortex elicits cardiac inhibition but insular lesions do not abolish conditioned bradycardia in rabbits.

Conscious rabbits received electrical stimulation of insular and more posterior perirhinal cortex through chronically implanted electrodes. Active sites for cardiovascular responses were found in both anterior and posterior insular cortex as well as more posterior perirhinal regions. Although differential response topographies occurred related to anterior versus posterior insular cortex, all heart rate responses consisted of bradycardia. Pharmacological manipulations revealed that this bradycardia was due to a combination of vagal and sympatho-inhibitory mechanisms. Some posterior sites yielded pressor responses, and bradycardia which was sensitive to phentolamine, suggesting that the bradycardia in these instances was due to activation of the baroreceptor reflex. All other blood pressure changes were depressor responses. In a second experiment two different groups of rabbits with lesions of either anterior or posterior agranular insular cortex were compared with a third group of animals with sham lesions in a differential Pavlovian conditioning experiment. No lesion completely abolished the classically conditioned bradycardia associated with tone/shock contingencies. However, anterior insular lesions attenuated the magnitude of the conditioned bradycardia compared to the posterior and sham lesions. Control experiments suggested that this attenuation was due to the lesion's effects on the conditioned stimulus/unconditioned stimulus association and not to its effects on unconditioned responding to the conditioned stimulus or unconditioned stimulus alone.