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Cell-Type Specificity of Neuronal Excitability and Morphology in the Central Amygdala

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...

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Detalles Bibliográficos
Autores principales: Adke, Anisha P., Khan, Aleisha, Ahn, Hye-Sook, Becker, Jordan J., Wilson, Torri D., Valdivia, Spring, Sugimura, Yae K., Martinez Gonzalez, Santiago, Carrasquillo, Yarimar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society for Neuroscience 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7877473/
https://www.ncbi.nlm.nih.gov/pubmed/33188006
http://dx.doi.org/10.1523/ENEURO.0402-20.2020
Descripción
Sumario: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.