Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1995-8-22
pubmed:abstractText
The non-phosphorylated neurofilament marker, SMI-32, identifies ventral horn motor neurons in spinal cord slice. We show here that SMI-32 marks a subset of spinal cord neurons in culture. Many of these neurons ('large SMI-32(+) neurons') have morphological characteristics of identified motor neurons in vitro: large cell body size (> 20 microns), extensive neuritic arborization and, generally, one particularly long process. These neurons are preferentially injured by brief (40 min) kainate exposures, but not by NMDA exposures. This rapidly triggered damage to large SMI-32(+) neurons is Ca2+ dependent. In addition, most of the SMI-32(+) neurons exhibit kainate-stimulated Co2+ uptake, a histochemical technique which marks neurons possessing Ca(2+)-permeable AMPA/kainate receptor-gated channels. The unusual vulnerability of large SMI-32(+) spinal neurons to kainate toxicity may result from rapid Ca2+ entry through Ca(2+)-permeable AMPA/kainate channels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0959-4965
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
945-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
In vitro kainate injury to large, SMI-32(+) spinal neurons is Ca2+ dependent.
pubmed:affiliation
Department of Neurology, University of California Irvine 92717-4290, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't