Abstract：
:Voltage-gated Ca2+ (CaV) channels couple membrane depolarization to Ca2+ influx, triggering a range of Ca2+-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. GPCR-dependent mechanisms that downregulate CaV channel expression levels are observed in many neurons but are, by comparison, less studied. Here we show that the growth hormone secretagogue receptor type 1a (GHSR), a GPCR, can inhibit the forwarding trafficking of several CaV subtypes, even in the absence of agonist. This constitutive form of GPCR inhibition 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.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Mustafá ER,López Soto EJ,Martínez Damonte V,Rodríguez SS,Lipscombe D,Raingo Jdoi
10.1242/jcs.207886subject
Has Abstractpub_date
2017-11-15 00:00:00pages
3907-3917issue
22eissn
0021-9533issn
1477-9137pii
jcs.207886journal_volume
130pub_type
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