Linked Life Data

9439798

Source:http://linkedlifedata.com/resource/pubmed/id/9439798

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1998-2-24
pubmed:abstractText
The mechanism by which (1S,3R)-ACPD, a metabotropic glutamate receptor agonist, induces burst firing in lateral septal neurons of the rat was investigated in coronal brainstem slices. Membrane currents were characterized in voltage clamp using whole-cell recordings. In the presence of (1S,3R)-ACPD, following depolarizing voltage jumps, repolarization towards the holding potential generated an inward aftercurrent. It could have a plateau-like phase and decayed exponentially. This (1S,3R)-ACPD-dependent inward aftercurrent was accompanied by an increase in cell conductance and was reduced following partial replacement of extracellular sodium by N-methyl-D-glucamine. It was unaffected by TEA or barium, and persisted in Cs-loaded neurons or following partial replacement of extracellular chloride by isethionate. This suggests that it was mainly carried by sodium. Loading neurons with the calcium chelator, BAPTA, or blocking transmembrane calcium currents, suppressed the (1S,3R)-ACPD-dependent aftercurrent. By contrast, partial replacement of extracellular sodium by lithium did not affect it. Thus, this current was dependent upon calcium influx but was not due to a sodium/calcium exchanger. It was probably mediated by G protein activation. Indeed, in neurons loaded with GTP-gamma-S, following depolarizing voltage jumps, repolarization towards the holding potential revealed an inward aftercurrent having properties similar to those of the (1S,3R)-ACPD-dependent current. We suggest that (1S,3R)-ACPD induced calcium-activated non-selective channels. In the presence of this agonist, a depolarization-evoked calcium influx could thus evoke a cationic inward current. This current probably promotes the burst firing observed in lateral septal neurons in current clamp.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
776
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
75-87
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9439798-Age Factors, pubmed-meshheading:9439798-Animals, pubmed-meshheading:9439798-Animals, Newborn, pubmed-meshheading:9439798-Cycloleucine, pubmed-meshheading:9439798-Electric Conductivity, pubmed-meshheading:9439798-GTP-Binding Proteins, pubmed-meshheading:9439798-Gluconates, pubmed-meshheading:9439798-Guanosine 5'-O-(3-Thiotriphosphate), pubmed-meshheading:9439798-Male, pubmed-meshheading:9439798-Membrane Potentials, pubmed-meshheading:9439798-Neuroprotective Agents, pubmed-meshheading:9439798-Patch-Clamp Techniques, pubmed-meshheading:9439798-Rats, pubmed-meshheading:9439798-Rats, Sprague-Dawley, pubmed-meshheading:9439798-Receptors, Metabotropic Glutamate, pubmed-meshheading:9439798-Septal Nuclei, pubmed-meshheading:9439798-Sodium, pubmed-meshheading:9439798-Sodium Channels, pubmed-meshheading:9439798-Tetrodotoxin
pubmed:year
1997
pubmed:articleTitle
Action of a metabotropic glutamate receptor agonist in rat lateral septum: induction of a sodium-dependent inward aftercurrent.
pubmed:affiliation
Department of Physiology, University Medical Centre, Geneva, Switzerland. mario.raggenbass@medecine.unige.ch
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't