Linked Life Data

18702724

Source:http://linkedlifedata.com/resource/pubmed/id/18702724

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-8-15
pubmed:abstractText
Hippocampal pyramidal neurons express various extrasynaptic glutamate receptors. When glutamate spillover was facilitated by blocking glutamate uptake and fast synaptic transmission was blocked by antagonists of AMPA- and NMDA-type glutamate receptors and an ionotropic GABA receptor blocker, repetitive synaptic stimulation evoked a persistent membrane depolarization that consisted of an early Ca(2+)-independent component and a late Ca(2+)-dependent component. The early component, which we refer to as a plateau potential, had a half-width of 770 +/- 160 ms and a steady peak level of -9.54 +/- 3.50 mV. It was accompanied by an increase in membrane conductance, the I-V relationship of which showed a peak at -19.91 +/- 2.18 mV and reversal of the current at -4.32 +/- 2.13 mV, and was suppressed by high concentration of an NMDA receptor (NMDAR) antagonist d-APV, or an NMDAR glycine-binding site antagonist 5,7-dCK. After blocking synaptically located NMDARs using MK801, the potential was still evoked synaptically when spillover was facilitated. A sustained depolarization was evoked by iontophoretic application of glutamate in the presence or absence of a glutamate uptake blocker. This potential was not affected by Na(+) or Ca(2+) channel blockers, but was suppressed by 5,7-dCK, leaving an unspecified depolarizing potential. Iontophoresis of NMDA evoked a sustained depolarization that was blocked by a high concentration of d-APV or 5,7-dCK. The I-V relationship of the current during this potential was similar to that obtained during the synaptically induced plateau potentials. These results show that CA1 pyramidal neurons generate plateau potentials mediated most likely by activation of extrasynaptic NMDARs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1460-9568
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
521-34
pubmed:meshHeading
pubmed-meshheading:18702724-Action Potentials, pubmed-meshheading:18702724-Animals, pubmed-meshheading:18702724-Calcium, pubmed-meshheading:18702724-Calcium Channel Blockers, pubmed-meshheading:18702724-Excitatory Amino Acid Antagonists, pubmed-meshheading:18702724-Excitatory Postsynaptic Potentials, pubmed-meshheading:18702724-Glutamic Acid, pubmed-meshheading:18702724-Hippocampus, pubmed-meshheading:18702724-Male, pubmed-meshheading:18702724-N-Methylaspartate, pubmed-meshheading:18702724-Neurons, pubmed-meshheading:18702724-Patch-Clamp Techniques, pubmed-meshheading:18702724-Rats, pubmed-meshheading:18702724-Rats, Wistar, pubmed-meshheading:18702724-Receptors, Glutamate, pubmed-meshheading:18702724-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:18702724-Sodium Channel Blockers, pubmed-meshheading:18702724-Synaptic Transmission
pubmed:year
2008
pubmed:articleTitle
A plateau potential mediated by the activation of extrasynaptic NMDA receptors in rat hippocampal CA1 pyramidal neurons.
pubmed:affiliation
Laboratory of Cellular Neurobiology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo 192-0392, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't