Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-4-6
pubmed:abstractText
The peptides neuropeptide Y (NPY) and bradykinin (BK) both inhibited Ca2+ currents in rat dorsal root ganglion neurons (DRG) in vitro. The effects of both peptides were completely blocked by treatment of cells with pertussis toxin. Based on antigenic determinants, DRG cells contained at least two pertussis toxin substrates, alpha o (Mr, 39 kd) and alpha i2 (Mr, 40 kd). We examined the ability of three purified bovine alpha subunits (identified with antibodies as alpha o, alpha i1, and alpha i2) to reconstitute the inhibitory effects of NPY and BK. Reconstitution of NPY effects occurred according to the potency series alpha o greater than alpha i1 much greater than alpha i2. However, in the case of BK all three G proteins were approximately equally effective. Whereas complete reconstitution of NPY effects could be obtained with alpha o, no single alpha subunit produced complete reconstitution of BK. Combinations of alpha o and alpha i2, however, were able to completely reconstitute the effects of BK. Thus several G proteins can effect the regulation of Ca2+ channels in these cells. However, neurotransmitters may be selective in the G proteins or combinations of G proteins utilized to achieve this regulation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0896-6273
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1185-93
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Differential G protein-mediated coupling of neurotransmitter receptors to Ca2+ channels in rat dorsal root ganglion neurons in vitro.
pubmed:affiliation
Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't