Linked Life Data

9630481

Source:http://linkedlifedata.com/resource/pubmed/id/9630481

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1999-3-29
pubmed:abstractText
Glutamatergic neurotransmission through NMDA receptors is critical for both neurogenesis and mature function of the central nervous system (CNS), and is thought to be one target for developmentally-induced damage by alcohol to brain function. In the current study we examined Ca2+ signaling linked to NMDA receptor activation as a potential site for alcohol's detrimental effects on the developing nervous system. We compared Ca2+ signals to NMDA in granule neurons cultured from cerebella of rat neonates exposed to alcohol (ethanol) during development with responses to NMDA recorded in separated control groups. Alcohol exposure was by the vapor chamber method on postnatal days 4-7. An intermittent exposure paradigm was used where the pups were exposed to alcohol vapor for 2. 5 h/day to produce peak BALs of approximately 320 mg%. Control pups were placed in an alcohol-free chamber for a similar time period or remained with their mother. After culture under alcohol-free conditions for up to 9 days, Ca2+ signaling in response to NMDA was measured using fura-2 Ca2+ imaging. Results show that the peak amplitude of the Ca2+ signal to NMDA was significantly smaller in cultured granule neurons obtained from alcohol-treated pups compared to granule neurons from control pups. In contrast, the Ca2+ signal to K+ depolarization was not depressed by the alcohol treatment. Resting Ca2+ levels were also altered by the alcohol treatment. These results show that intermittent alcohol exposure during development in vivo can induce long-term changes in CNS neurons that affect the Ca2+ signaling pathway linked to NMDA receptors and resting Ca2+ levels. Such changes could play an important role in the CNS dysfunction associated with alcohol exposure during CNS development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-8993
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Elsevier Science B.V.
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
793
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
12-20
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Neonatal alcohol exposure reduces NMDA induced Ca2+ signaling in developing cerebellar granule neurons.
pubmed:affiliation
Department of Neuropharmacology and Alcohol Research Center, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. gruol@scripps.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.