Linked Life Data

9712657

Source:http://linkedlifedata.com/resource/pubmed/id/9712657

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
1998-9-9
pubmed:abstractText
Nicotine has many effects on CNS functions, presumably through its action on neuronal nicotinic acetylcholine receptors (AChRs). One subclass of AChRs that binds the snake venom toxin alpha-bungarotoxin (alpha-Bgt-AChRs) has been shown to modulate neurotransmission in the brain. We now show that alpha-Bgt-AChR activation by low doses of nicotine results in apoptotic cell death of both primary and immortalized hippocampal progenitor cells. In HC2S2-immortalized hippocampal progenitors, nicotine is cytotoxic to undifferentiated cells, whereas it spares the same cells once differentiation has been induced. The activation of alpha-Bgt-AChRs by nicotine results in the induction of the tumor suppressor protein p53 and the cdk inhibitor p21. The cytotoxic effect of nicotine is dependent on extracellular calcium levels and is probably attributable to the poor ability of undifferentiated progenitors to buffer calcium loads. The major calcium buffer in these cells, calbindin D28K, is present only after differentiation has been induced. Furthermore transfection of undifferentiated cells with calbindin results in dramatic protection against the cytotoxic effects of nicotine. These results show that nicotine abuse could have significant effects on the survival of progenitor populations in the developing and adult brain and also suggest an endogenous role for alpha-Bgt-AChRs in neuronal development and differentiation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0270-6474
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6871-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Nicotinic receptor-induced apoptotic cell death of hippocampal progenitor cells.
pubmed:affiliation
Laboratory of Genetics, The Salk Institute, La Jolla, California 92037, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.