Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2005-6-1
pubmed:abstractText
In order to further explore how GABA can modulate the excitability of noradrenergic neurons of the locus coeruleus (LC), we investigated the presence of GABA(A) receptors on glutamatergic nerve terminals and the functional consequences of their activation. We used mechanically dissociated immature rat LC neurons with adherent nerve terminals and patch-clamp recordings of spontaneous excitatory postsynaptic currents. Activation of presynaptic GABA(A) receptors by muscimol facilitated spontaneous glutamate release by activating tetrodotoxin-sensitive Na(+) channels and high-threshold Ca(2+) channels. Bumetanide (10 microM), a potent blocker of Na(+)-K(+)-Cl(-) cotransporter, diminished the muscimol-induced facilitatory action of glutamate release. Our results indicate that the Na(+)-K(+)-Cl(-) cotransporter accumulates Cl(-) inside the nerve terminals so that activation of presynaptic GABA(A) receptors causes depolarization. This GABA(A)-receptor-mediated modulation of spontaneous glutamatergic transmission is another mechanism by which GABA and its analogues can regulate the excitability and activity of noradrenergic neurons in the LC.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
1046
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
24-31
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Activation of presynaptic GABAA receptors increases spontaneous glutamate release onto noradrenergic neurons of the rat locus coeruleus.
pubmed:affiliation
Cellular and System Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't