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Titolo:
The central aromatic amino acid DOPA decarboxylase inhibitor, NSD-1015, does not inhibit L-DOPA-induced circling in unilateral 6-OHDA-lesioned-rats
Autore:
Treseder, SA; Rose, S; Jenner, P;
Indirizzi:
Univ London Kings Coll, Guys Kings & St Thomas Sch Biomed Sci, Neurodegenerat Dis Res Ctr, Div Pharmacol & Therapeut, London SE1 1UL, England Univ London Kings Coll London England SE1 1UL t, London SE1 1UL, England
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 1, volume: 13, anno: 2001,
pagine: 162 - 170
SICI:
0953-816X(200101)13:1<162:TCAAAD>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HYPOTHALAMIC SLICES; B MONOAMINE-OXIDASE; TETRODOTOXIN-SENSITIVE RELEASE; MEDIATED LOCOMOTOR ACTIVITIES; STRIATAL SLICES; CONSCIOUS RATS; IN-VIVO; 6-HYDROXYDOPAMINE-TREATED RATS; ENDOGENOUS NORADRENALINE; BIPHASIC ACTIONS;
Keywords:
central AADC inhibition; contralateral circling behaviour; monoamine oxidase inhibition; Wistar rats;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Jenner, P Univ London Kings Coll, Guys Kings & St Thomas Sch Biomed Sci, Neurodegenerat Dis Res Ctr, Div Pharmacol & Therapeut, Guys Campus, London SE1 1UL, England Univ London Kings Coll Guys Campus London England SE1 1UL gland
Citazione:
S.A. Treseder et al., "The central aromatic amino acid DOPA decarboxylase inhibitor, NSD-1015, does not inhibit L-DOPA-induced circling in unilateral 6-OHDA-lesioned-rats", EUR J NEURO, 13(1), 2001, pp. 162-170

Abstract

The centrally acting aromatic amino acid dopa decarboxylase (AADC) inhibitor, 3-hydroxybenzyl hydrazine (NSD-1015), is widely used to study the neurotransmitter-like actions of L-DOPA. However, the effects of NSD-1015 on L-DopA-induced motor activity are unclear as both increases and decreases havebeen reported. We now investigate the effects of NSD-1015 on L-DOPA-induced contralateral circling behaviour in 6-OHDA-lesioned rats and on striatal levels of L-DOPA, 3-O-methyl-DOPA (3-OMD), dopamine, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) using microdialysis techniques. NSD-1015 (50-200 mg/kg i.p.) inhibited AADC activity both in the liver and striatum of normal rats. Administration of NSD-1015 (50-200 mg/kg i.p.), delayed the onset of circling produced by administration of L-DOPA (25 mg/kg i.p.) and carbidopa (12.5 mg/kg i.p.), suggesting blockade of central AADC activity. However, the duration of the L-DOPA-induced circling was prolonged and overall no inhibition of circling behaviour occurred. L-DOPA (25 mg/kg i.p.) plus carbidopa (12.5 mg/kg i.p.) increased extracellular levels of L-DOPA, 3-OMD, dopamine, DOPAC and HVA in the 6-OHDA-lesioned striatum. Pretreatment of rats with the central AADC inhibitor, NSD-1015 (100 mg/kg i.p.),potentiated the increase in dialysate levels of L-DOPA and 3-OMD. However,it did not reduce striatal dopamine levels in the 6-OHDA-lesioned hemisphere, which were elevated following L-DOPA administration. The increases in DOPAC and HVA levels were abolished by NSD-1015 pretreatment. These results suggest that, while NSD-1015 blocks central AADC activity, it also acts as a monoamine oxidase inhibitor so maintaining striatal dopamine concentration by reducing dopamine metabolism. NSD-1015,therefore, may not be an appropriate tool for the study of brain AADC activity and for assessing the neuromodulatory role of L-DOPA.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 20:15:26