Glutamatergic basolateral amygdala to anterior insular cortex circuitry maintains rewarding contextual memory
Findings have shown that anterior insular cortex (aIC) lesions disrupt the maintenance of drug addiction, while imaging studies suggest that connections between amygdala and aIC participate in drug seeking. However, the role of the BLA aIC pathway in rewarding contextual memory has not been assessed. Using a cre recombinase under the tyrosine hydroxylase (TH+ promoter mouse model to induce a real time conditioned place preference (rtCPP) we show that photoactivation of TH+ neurons induced electrophysiological responses in VTA neurons, dopamine release and neuronal modulation in the aIC. Conversely, memory retrieval induced a strong release of glutamate, dopamine, and norepinephrine in the aIC. Only intra aIC blockade of the glutamatergic N methyl D aspartate receptor accelerated rtCPP extinction. Finally, photoinhibition of glutamatergic BLA aIC pathway produced disinhibition of local circuits in the aIC, accelerating rtCPP extinction and impairing reinstatement. Thus, activity of the glutamatergic projection from the BLA to the aIC is critical for maintenance of rewarding contextual memory. Gil Lievana et al. show that the basolateral amygdala anterior insular cortex (BLA aIC) pathway is involved in the maintenance of rewarding contextual memory. They use pharmacological, behavioral and electrophysiological approaches to demonstrate that this is due to the glutamatergic projection from the BLA to the aIC.
Communications Biology