G protein-coupled receptor kinase mediates desensitization of norepinephrine-induced Ca2+ channel inhibition.

Journal Article (Journal Article)

G protein-coupled receptors are essential signaling molecules at sites of synaptic transmission. Here, we explore the mechanisms responsible for the use-dependent termination of metabotropic receptor signaling in embryonic sensory neurons. We report that the inhibition of voltage-dependent Ca2+ channels mediated by alpha2-adrenergic receptors desensitizes slowly with prolonged exposure to the transmitter and that the desensitization is mediated by a G protein-coupled receptor kinase (GRK). Intracellular introduction of recombinant, purified kinases or synthetic blocking peptides into individual neurons demonstrates the specific involvement of a GRK3-like protein. These results suggest that GRK-mediated termination of receptor-G protein coupling is likely to regulate synaptic strength and, as such, may provide one effective mechanism for depression of synaptic transmission.

Full Text

Duke Authors

Cited Authors

  • Diverse-Pierluissi, M; Inglese, J; Stoffel, RH; Lefkowitz, RJ; Dunlap, K

Published Date

  • March 1996

Published In

Volume / Issue

  • 16 / 3

Start / End Page

  • 579 - 585

PubMed ID

  • 8785055

International Standard Serial Number (ISSN)

  • 0896-6273

Digital Object Identifier (DOI)

  • 10.1016/s0896-6273(00)80077-x


  • eng

Conference Location

  • United States