α2δ-2 is required for depolarization-induced suppression of excitation in Purkinje cells.

ABSTRACT: α2δ proteins (CACNA2D1-4) are required for normal neurological function and contribute to membrane trafficking of voltage-gated calcium channels, through which calcium entry initiates numerous physiological processes. However, it remains unclear how α2δ proteins influence calcium-mediated signalling to control neuronal output. Using whole-cell recordings of mouse Purkinje cells, we show that α2δ-2 is required for functional coupling of postsynaptic voltage-dependent calcium entry with calcium-dependent effector mechanisms controlling two different outputs, depolarization-induced suppression of excitation and spike afterhyperpolarization. Our findings indicate an important role for α2δ-2 proteins in regulating functional postsynaptic calcium channel coupling in neurons, providing new contex

SUBMITTER: Beeson KA 

PROVIDER: S-EPMC8724408 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature