Abstract
Central amygdala (CeA) neurons expressing protein kinase Cδ (PKCδ+) or somatostatin (Som+) differentially modulate diverse behaviors. The underlying features supporting cell-type-specific function in the CeA, however, remain unknown. Using whole-cell patch-clamp electrophysiology in acute mouse brain slices and biocytin-based neuronal reconstructions, we demonstrate that neuronal morphology and relative excitability are two distinguishing features between Som+ and PKCδ+ neurons in the laterocapsular subdivision of the CeA (CeLC). Som+ neurons, for example, are more excitable, compact, and with more complex dendritic arborizations than PKCδ+ neurons. Cell size, intrinsic membrane properties, and anatomic localization were further shown to correlate with cell-type-specific differences in excitability. Lastly, in the context of neuropathic pain, we show a shift in the excitability equilibrium between PKCδ+ and Som+ neurons, suggesting that imbalances in the relative output of these cells underlie maladaptive changes in behaviors. Together, our results identify fundamentally important distinguishing features of PKCδ+ and Som+ cells that support cell-type-specific function in the CeA.