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Titolo:
CHRONIC DOSING WITH 1-AMINOCYCLOPROPANECARBOXYLIC ACID, A GLYCINE PARTIAL AGONIST, MODULATES NMDA INHIBITION OF MUSCARINIC-COUPLED PI HYDROLYSIS IN RAT CORTICAL SLICES
Autore:
BOJE KMK; LAKHMAN SS;
Indirizzi:
SUNY BUFFALO,DEPT PHC,H517 COOKE HOCHSTETTER BUFFALO NY 14260 SUNY BUFFALO,SCH PHARM,DEPT PHARMACEUT BUFFALO NY 14260
Titolo Testata:
Neurochemical research
fascicolo: 9, volume: 23, anno: 1998,
pagine: 1167 - 1174
SICI:
0364-3190(1998)23:9<1167:CDW1AA>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYL-D-ASPARTATE; STIMULATED PHOSPHOINOSITIDE HYDROLYSIS; EXCITATORY AMINO-ACIDS; RECEPTOR COMPLEX; 7-CHLOROKYNURENIC ACID; RECOGNITION SITES; BRAIN; GLUTAMATE; CORTEX; ACCUMULATION;
Keywords:
1-AMINOCYCLOPROPANECARBOXYLIC ACID; N-METHYL-D-ASPARTATE; N-METHYL-D-ASPARTATE RECEPTORS; PHOSPHOINOSITOL HYDROLYSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
K.M.K. Boje e S.S. Lakhman, "CHRONIC DOSING WITH 1-AMINOCYCLOPROPANECARBOXYLIC ACID, A GLYCINE PARTIAL AGONIST, MODULATES NMDA INHIBITION OF MUSCARINIC-COUPLED PI HYDROLYSIS IN RAT CORTICAL SLICES", Neurochemical research, 23(9), 1998, pp. 1167-1174

Abstract

Chronic dosing with the glycine partial NMDA agonist, 1-aminocyclopropanecarboxylic acid (ACPC) elicited an altered allosteric regulation of cortical NMDA receptor binding. The present study hypothesized that these allosteric receptor binding changes would be manifest as pharmacologically functional reductions in NMDA receptor activity following chronic ACPC dosing. NMDA inhibition of carbachol-induced phosphoinositide (PI) hydrolysis was used as a functional assay to assess NMDA receptor function in rat cerebral cortex. NMDA inhibition of stimulated PIturnover was similar in naive (46% +/- 4.5%; mean +/- SE; n = 34) andACPC dosed rats (39% +/- 2.3%; n = 34). While ACPC reversed NMDA's inhibitory effects in naive rats(80% +/- 13%; n = 9), it was ineffective(P < 0.05) in ACPC pretreated rats (48% +/- 9.8%; n = 9). In contrast, the NMDA antagonists, MK-801 (ion channel), 7-chlorokynurenic acid (glycine site) and AP-7 (glutamate site), effectively reversed NMDA's inhibitory effects in naive and ACPC treated rats. The potency of theseantagonists were unaltered by prior ACPC dosing. Thus, chronic ACPC therapy does not alter the functioning of the NMDA ion channel or glutamate receptor sites, but elicits functional tolerance to ACPC's actions in the cortical NMDA complex.

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Documento generato il 29/11/20 alle ore 16:05:05