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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1-2
|
| pubmed:dateCreated |
1993-10-5
|
| pubmed:abstractText |
Reductions in cortical somatostatin (SRIH) and choline acetyl-transferase (ChAT) are major biochemical deficits in Alzheimer disease (AD). SRIH and ChAT were measured in fetal rat cerebral neurons after exposure to the glutamate agonists N-methyl-D-aspartate (NMDA), kainate (KA), and quisqualate (Q). NMDA (96 h incubation) stimulated SRIH release and content in a dose-dependent manner with a Bmax of 10(-5)M and EC50 of 2-3 x 10(-6)M. KA showed a small stimulation in SRIH levels at 10(-5)M, but produced marked inhibition at 10(-4)M. Q decreased both intracellular and secreted SRIH. KA (51-76% of basal) and Q (27-56% of basal) but not NMDA (91-114% of basal) also inhibited the incorporation of [35S]methionine into proteins. In similar experiments 10(-4)M Q (23 +/- 9% of basal) and KA (20 +/- 3% of basal) but not NMDA (80 +/- 16% of basal) reduced ChAT levels in hypothalamic/septal cultures. These inhibitory actions on ChAT activity by KA and Q were reversed by gamma-glutamyltaurine (GT) but not by 2-amino-5-phosphonopentanoic acid (AP5). Chronic NMDA exposure partially inhibited muscarinic acetylcholine receptor (mAChR) mediated inositol phospholipid (PI) turnover, whereas it was abolished after KA and Q pretreatment. These findings suggest that in cerebral cell cultures, NMDA has a stimulatory action on somatostatinergic neurons and non-NMDA receptor agonism could play an important role in EAA-mediated neural damage.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Choline O-Acetyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamates,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol Phosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Kainic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/N-Methylaspartate,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Quisqualic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholinergic,
http://linkedlifedata.com/resource/pubmed/chemical/Somatostatin
|
| pubmed:status |
MEDLINE
|
| pubmed:issn |
1044-7393
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
19
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
107-20
|
| pubmed:dateRevised |
2003-11-14
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| pubmed:meshHeading |
pubmed-meshheading:8103332-Animals,
pubmed-meshheading:8103332-Brain,
pubmed-meshheading:8103332-Cell Survival,
pubmed-meshheading:8103332-Cells, Cultured,
pubmed-meshheading:8103332-Choline O-Acetyltransferase,
pubmed-meshheading:8103332-Female,
pubmed-meshheading:8103332-Glutamates,
pubmed-meshheading:8103332-Glutamic Acid,
pubmed-meshheading:8103332-Inositol Phosphates,
pubmed-meshheading:8103332-Kainic Acid,
pubmed-meshheading:8103332-Kinetics,
pubmed-meshheading:8103332-N-Methylaspartate,
pubmed-meshheading:8103332-Nerve Tissue Proteins,
pubmed-meshheading:8103332-Neurons,
pubmed-meshheading:8103332-Parasympathetic Nervous System,
pubmed-meshheading:8103332-Pregnancy,
pubmed-meshheading:8103332-Quisqualic Acid,
pubmed-meshheading:8103332-Rats,
pubmed-meshheading:8103332-Receptors, Cholinergic,
pubmed-meshheading:8103332-Somatostatin
|
| pubmed:articleTitle |
Differential responses of rat cerebral somatostatinergic and cholinergic cells to glutamate agonists.
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| pubmed:affiliation |
Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff, UK.
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| pubmed:publicationType |
Journal Article
|