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
Language
- eng
Conference Location
- United States