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Titolo:
PREFERENTIAL BLOCKADE OF CHOLECYSTOKININ-8S-INDUCED INCREASES IN ASPARTATE AND GLUTAMATE LEVELS BY THE CCKB RECEPTOR ANTAGONIST, L-365,260,IN RAT-BRAIN
Autore:
GE J; LONG SK; KILPATRICK IC;
Indirizzi:
SCI DEV GRP,DEPT PHARMACOL,ORGANON LABS NEWHOUSE LANARK ML1 5SH SCOTLAND UNIV BRISTOL,SCH MED SCI,DEPT PHARMACOL BRISTOL BS8 1TD AVON ENGLAND SOLVAY DUPHAR BV,DEPT CNS PHARMACOL NL-1380 DA WEESP NETHERLANDS
Titolo Testata:
European journal of pharmacology
fascicolo: 2, volume: 345, anno: 1998,
pagine: 163 - 170
SICI:
0014-2999(1998)345:2<163:PBOCII>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
IN-VIVO MICRODIALYSIS; AMINO-ACIDS; NEUROTRANSMITTER RELEASE; CORTICOSTRIATAL PATHWAY; NUCLEUS-ACCUMBENS; CEREBRAL-CORTEX; LOCALIZATION; NEOSTRIATUM; MODULATION; DOPAMINE;
Keywords:
ASPARTATE; GLUTAMATE; CCK-8S; L-365,260; L-364,718; FRONTAL CORTEX, RAT; CAUDATE-PUTAMEN, RAT; MICRODIALYSIS, IN VIVO;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
J. Ge et al., "PREFERENTIAL BLOCKADE OF CHOLECYSTOKININ-8S-INDUCED INCREASES IN ASPARTATE AND GLUTAMATE LEVELS BY THE CCKB RECEPTOR ANTAGONIST, L-365,260,IN RAT-BRAIN", European journal of pharmacology, 345(2), 1998, pp. 163-170

Abstract

In the present studies, the ability of a locally delivered cholecystokinin (CCK) receptor agonist and systemically delivered antagonists tomodulate extracellular levels of aspartate and glutamate in the frontal cortex of anaesthetised rats and frontal cortex caudate-putamen of freely moving rats was investigated using an in vivo microdialysis technique. In the anaesthetised rats, local application of sulphated CCK octapeptide (CCK-8S, 10 mu M) into the frontal cortex enhanced extracellular aspartate levels to a maximum of 265 +/- 16% of the basal levels, whereas glutamate levels were increased to a maximum of 168 +/- 7% of the basal levels. Given 10 min prior to the cortical perfusion of 10 mu M of CCK-8S, the CCKB receptor antagonist. L-36,.260 (20 mg/kg, s.c.), limited the rise in cortical aspartate by over half to 170 +/- 10% of the basal levels. However, this same dose of L-365,760 still allowed CCK-8S to increase glutamate by 44 +/- 15% above the basal levels. Whereas the enhanced glutamate levels were totally unaffected by systemic administration of the CCKA receptor antagonist, L-364,718 (70 mg/kg, -40 min: s.c.), this treatment was able to limit the elevation inaspartate to 220 +/- 4% of the basal levels. In the freely moving rats, local perfusion of CCK-8S (10 mu M) increased aspartate and glutamate levels to maxima of 275 +/- 12% and 225 +/- 14% of the basal levels, respectively: in the frontal cortex. In the caudate-putamen, aspartate and glutamate levels were also elevated by CCK-8S (10 mu M) to 245 /- 15% and 185 +/- 12% of the basal levels, respectively. The respective increase in aspartate and glutamate induced by CCK-8S (10 mu M) were limited to 140 +/- 10% and 121 +/- 6% (frontal cortex), of the basal levels, and 162 +/- 15% and 143 +/- 88 (caudate-putamen), by 40 min pretreatment with L-365,260 (20 mg/kg, s.c.). In conclusion, CCK-8S a as able to enhance both aspartate and glutamate overflow in the frontal cortex of anaesthetised rats, and frontal cortex and caudate-putamenof freely, moving rats. These increases were preferentially offset bythe selective CCKB receptor antagonist, L-365,260, since no influencecould be discerned using the selective CCKA receptor antagonist, L-364,718. (C) 1998 Elsevier Science B.V.

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Documento generato il 28/11/20 alle ore 23:51:29