Electrical Stimulation Of Insular Cortex Research Articles

Extracellular glucose-dependent IPSC enhancement by leptin in fast-spiking to pyramidal neuron connections via JAK2-PI3K pathway in the rat insular cortex

Leptin is produced in the adipocytes and plays a pivotal role in regulation of energy balance by controlling appetite and metabolism. Leptin receptors are widely distributed in the brain, especially in the hypothalamus, hippocampus, and neocortex. The insular cortex (IC) processes gustatory and visceral information, which functionally correlate to feeding behavior. However, it is still an open issue whether and how leptin modulates IC neural activities. Our paired whole-cell patch-clamp recordings using IC slice preparations demonstrated that unitary inhibitory postsynaptic currents (uIPSCs) but not uEPSCs were potentiated by leptin in the connections between pyramidal (PNs) and fast-spiking neurons (FSNs). The leptin-induced increase in uIPSC amplitude was accompanied by a decrease in paired-pulse ratio. Under application of inhibitors of JAK2-PI3K but not MAPK pathway, leptin did not change uIPSC amplitude. Variance-mean analysis revealed that leptin increased the release probability but not the quantal size and the number of release site. These electrophysiological findings suggest that the leptin-induced uIPSC increase is mediated by activation of JAK2-PI3K pathway in presynaptic FSNs. An in vivo optical imaging revealed that leptin application decreased excitatory propagation in IC induced by electrical stimulation of IC. These leptin-induced effects were not observed under the low energy states: low glucose concentration (2.5 mM) in vitro and one-day-fasting condition in vivo. However, leptin enhanced uIPSCs under application of low glucose with an AMPK inhibitor. These results suggest that leptin suppresses IC excitation by facilitating GABA release in FSN→PN connections, which may not occur under a hunger state.

3H-2-Deoxyglucose uptake after electrical stimulation of cardioactive sites in insular cortex and mediodorsal nucleus of the thalamus in rabbits

The uptake of 3H-2-deoxyglucose ( 3H-2-DG) in selected brain structures was determined subsequent to electrical stimulation of insular cortex (Ins) and the mediodorsal (MD) nucleus of the thalamus in rabbits. Stimulation of Ins elicited parasympathetic-like responding (i.e., bradycardia and depressor responses); whereas MD stimulation produced sympathetic-like responses (bradycardia and pressor responses). Stimulation of Ins also resulted in increased 3H-2-DG activity in ipsilateral MD and the ventromedial/ventroposterior complex as well as the contralateral Ins compared to nonstimulated control subjects. The central nucleus of the amygdala also showed increased activity after Ins stimulation. In 2 animals stimulation of Ins resulted in increased 3H-2-DG activity in the caudate/putamen complex. Stimulation of MD resulted in ipsilateral increases in 3H-2-DG activity in the midline, agranular prefrontal cortex, as well as the ipsilateral Ins, and the caudate nucleus and putamen/globus pallidus complex. Two animals also showed increases in 3H-2-DG activity in ipsilateral substantia nigra. However, no increased activity was observed in the lateral hypothalamus, the parabrachial nuclei, the nucleus tractus solitarius, or the dorsal motor nucleus of the vagus, although it has been shown that efferents from Ins reach these areas. A more significant finding however, was that the reciprocal connections of MD and Ins appear to be activated by stimulation of either structure, even though their relationship to autonomic function appears to be quite different.

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.