Constitutive activity of the Ghrelin receptor reduces surface expression of voltage-gated Ca2+ channels in a CaVβ-dependent manner
Voltage-gated Ca2+ (CaV) channels couple membrane depolarization to Ca2+ influx, triggering a range ofCa2+-dependent cellular processes. CaV channels are, therefore, crucial in shaping neuronal activity and function, depending on their individual temporal and spatial properties. Furthermore, many ne...
| Autores: | , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2017 |
| País: | Argentina |
| Institución: | Universidad Nacional de La Plata |
| Repositorio: | SEDICI (UNLP) |
| Idioma: | inglés |
| OAI Identifier: | oai:sedici.unlp.edu.ar:10915/87538 |
| Acceso en línea: | http://sedici.unlp.edu.ar/handle/10915/87538 |
| Access Level: | acceso abierto |
| Palabra clave: | Biología CaVβ GPCR Voltage-gated calcium (Ca2+) channels |
| Sumario: | Voltage-gated Ca2+ (CaV) channels couple membrane depolarization to Ca2+ influx, triggering a range ofCa2+-dependent cellular processes. CaV channels are, therefore, crucial in shaping neuronal activity and function, depending on their individual temporal and spatial properties. Furthermore, many neurotransmitters and drugs that act through G protein coupled receptors (GPCRs), modulate neuronal activity by altering the expression, trafficking, or function of CaV channels. GPCRdependent mechanisms that downregulate CaV channel expression levels are observed in many neurons but are, by comparison, less studied. Herewe showthat the growth hormone secretagogue receptor type 1a (GHSR), a GPCR, can inhibit the forwarding trafficking of severalCaV subtypes, even in the absence of agonist. This constitutive form ofGPCRinhibition of CaV channels depends on the presence of a CaVβ subunit. CaVβ subunits displace CaVα1 subunits from the endoplasmic reticulum. The actions of GHSR on CaV channels trafficking suggest a role for this signaling pathway in brain areas that control food intake, reward, and learning and memory. |
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