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Titolo:
DOPAMINE D-1 RECEPTOR-STIMULATED RELEASE OF ACETYLCHOLINE IN RAT STRIATUM IS MEDIATED INDIRECTLY BY ACTIVATION OF STRIATAL NEUROKININ(1) RECEPTORS
Autore:
ANDERSON JJ; KUO S; CHASE TN; ENGBER TM;
Indirizzi:
NINCDS,EXPTL THERAPEUT BRANCH,BLDG 10,ROOM 5C215,9000 ROCKVILLE PIKE BETHESDA MD 20892
Titolo Testata:
The Journal of pharmacology and experimental therapeutics
fascicolo: 3, volume: 269, anno: 1994,
pagine: 1144 - 1151
SICI:
0022-3565(1994)269:3<1144:DDRROA>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
FREELY MOVING RATS; P NK1 RECEPTOR; SUBSTANCE-P; CHOLINERGIC NEURONS; GENE-EXPRESSION; MESSENGER-RNA; PHENOTYPICAL CHARACTERIZATION; STRIATOPALLIDAL NEURONS; STRIATONIGRAL NEURONS; BASAL FOREBRAIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
J.J. Anderson et al., "DOPAMINE D-1 RECEPTOR-STIMULATED RELEASE OF ACETYLCHOLINE IN RAT STRIATUM IS MEDIATED INDIRECTLY BY ACTIVATION OF STRIATAL NEUROKININ(1) RECEPTORS", The Journal of pharmacology and experimental therapeutics, 269(3), 1994, pp. 1144-1151

Abstract

Activation of dopamine D-1 receptors is thought to stimulate release of striatal acetylcholine (ACh) indirectly, possibly through local release of substance P which, in turn, may enhance release of ACh. To test this hypothesis, in vivo microdialysis was used to assess the effectof neurokinin(1) (NK1) receptor blockade on D-1 agonist-induced increases in ACh release in the striatum of awake, freely moving rats with and without a unilateral 6-hydroxydopamine-induced lesion of the nigrostriatal pathway. Local perfusion with the D-1 agonist nyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride (SKF 38393; 1-25 mu M for 20 min) increased striatal ACh release in both intact rats and rats with a 6-hydroxydopamine-induced lesion, although the increase wasgreater in magnitude in rats with a lesion. Local application of the NK1 antagonist, oxyphenyl)methyl]-1-azabicyclo[2.2.2]octan-3-amine (CP-96,345; 10 and 25 mu M), but not its less active enantiomer oxyphenyl)methyl]-1-azabicyclo[2.2.2]octan-3-amine (CP-96,344; 10 and 25 mu M),decreased the elevation in ACh induced by SKF 38393 in both intact rats and rats treated with 6-hydroxydopamine. Systemic administration ofthe NK1 antagonist -a-androstanol[3.2-b]pyrimidol[1,2-a]benzimidazolehydrochloride (WIN 51,708; 20 mg/kg i.p.) also reduced the increase in ACh release induced by local perfusion of SKF 38393. These results indicate that antagonism of striatal NK1 receptors reduces D-1 receptor-stimulated release of striatal ACh and suggest that increases in ACh release induced by D-1 agonists may be mediated indirectly through local release of substance P acting at NK1 receptors on striatal cholinergic neurons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 20:20:55