Linked Life Data

9247137

Source:http://linkedlifedata.com/resource/pubmed/id/9247137

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-9-11
pubmed:abstractText
Spinal cord motoneurons (MNs) undergo a process of cell death during embryonic development and are the target of lethal acquired or inherited disorders, such as the amyotrophic lateral sclerosis. Therefore, the identification of mechanisms leading to MN survival is of crucial importance. Elevations in intracellular Ca2+ promote chicken MN survival during the embryonic period of naturally occurring cell death. We have recently demonstrated that the alpha7 nicotinic acetylcholine receptor (nAChR) mediates significant increases in free Ca2+ concentration at membrane potentials at which other pathways for Ca2+ influx are inactive. Although it is possible that Ca2+ influx through alpha7 nAChR promotes cell survival, the relation between alpha7 nAChR activation, cytosolic free Ca2+ and mammalian spinal cord MN survival has not been established. In the present study we have now demonstrated that Ca2+ influx through the alpha7-subunit is sufficient to rescue a significant number of cultured spinal cord MNs from programmed cell death induced by trophic factor deprivation. This is the first demonstration that neuronal nAChRs are involved in the regulation of MN survival.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
411
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
32-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Activation of alpha7 nicotinic acetylcholine receptor promotes survival of spinal cord motoneurons.
pubmed:affiliation
Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't