Linked Life Data

8113813

Source:http://linkedlifedata.com/resource/pubmed/id/8113813

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-3-28
pubmed:abstractText
The effects of the divalent cations Ca2+, Sr2+, Ba2+, Mg2+, Mn2+, and Cd2+ were studied on gamma-aminobutyric acidA (GABAA) responses in rat cerebral cortical synaptoneurosomes. The divalent cations produced bidirectional modulation of muscimol-induced 36Cl- uptake consistent with their ability to permeate and block Ca2+ channels. The order of potency for inhibition of muscimol responses was Ca2+ > Sr2+ > Ba2+, similar to the order for permeation of Ca2+ channels in neurons. The order of potency for enhancement of muscimol responses was Cd2+ > Mn2+ > Mg2+, similar to the order for blockade of Ca2+ channels in neurons. Neither Ca2+ nor Mg2+ caused accumulation of GABA in the extravesicular space due to increased GABA release or decreased reuptake of GABA by the synaptoneurosomes. The inhibition of muscimol responses by Ca2+ was most likely via an intracellular site of action because additional inhibition could be obtained in the presence of the Ca2+ ionophore, A23187. This confirms electrophysiologic findings in cultured neurons from several species. In contrast, the effects of Cd2+, Mn2+, and Mg2+ may be mediated via blockade of Ca2+ channels or by intracellular sites, although the results of these studies do not distinguish between the two loci. The effects of Zn2+ were also studied, because this divalent cation is reported to have widely divergent effects on GABAA responses. In contrast to other studies, we demonstrate that Zn2+ inhibits GABAA responses in an adult neuronal preparation. Zn2+ produced a concentration-dependent inhibition (limited to 40%) of muscimol responses with an EC50 of 60 microM. The inhibition of muscimol-induced 36Cl- uptake by Zn2+ was noncompetitive.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
62
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
916-22
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Bidirectional modulation of GABA-gated chloride channels by divalent cations: inhibition by Ca2+ and enhancement by Mg2+.
pubmed:affiliation
Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't