Linked Life Data

2554206

Source:http://linkedlifedata.com/resource/pubmed/id/2554206

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1989-11-27
pubmed:abstractText
The hippocampus is widely used in investigations of different forms of synaptic plasticity, including long-term potentiation and kindling. Receptors for excitatory amino acids (EAAs) play a prominent role in these phenomena. Recently, is has been demonstrated that exposure of hippocampal slices to EAAs and related agonists produces biphasic effects on excitatory synaptic transmission: initial blockade of synaptic responses is followed by a delayed recovery. The recovered responses demonstrate altered pharmacological properties: they acquire sensitivity to N-methyl-D-aspartate (NMDA) antagonists during L-glutamate (Glu) exposure and lose sensitivity to both NMDA and non-NMDA antagonists under L-aspartate (Asp). These changes persist for many hours. It was suggested that this form of hippocampal plasticity may involve transitions between distinct states of synaptic functioning. To explore this possibility, we investigated several properties of synaptic transmission in the initial and EAA-modified states. Here we report that hippocampal postsynaptic potentials (PSPs) evoked under Glu or Asp exposure completely lose sensitivity to omega-conotoxin GVIA (omega-CgTX), a potent, specific, and irreversible blocker of certain types of neuronal calcium channels. After washout of the EAA, sensitivity to the toxin is regained. These results indicate that prolonged EAA exposure induces profound changes in the machinery of synaptic transmission, which include, but are not limited to, changes in calcium channel functioning.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
197-204
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Hippocampal synaptic plasticity induced by excitatory amino acids includes changes in sensitivity to the calcium channel blocker, omega-conotoxin.
pubmed:affiliation
A.A. Bogomoletz Institute of Physiology, Kiev, U.S.S.R.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't