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Titolo:
Reversal of diminished inhibitory sensory gating in cocaine addicts by a nicotinic cholinergic mechanism
Autore:
Adler, LE; Olincy, A; Cawthra, E; Hoffer, M; Nagamoto, HT; Amass, L; Freedman, R;
Indirizzi:
Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA Univ Colorado Denver CO USA 80262 tr, Dept Psychiat, Denver, CO 80262 USA Vet Affairs Med Ctr, Res Serv, Denver, CO USA Vet Affairs Med Ctr Denver CO USA airs Med Ctr, Res Serv, Denver, CO USA
Titolo Testata:
NEUROPSYCHOPHARMACOLOGY
fascicolo: 6, volume: 24, anno: 2001,
pagine: 671 - 679
SICI:
0893-133X(200106)24:6<671:RODISG>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
SCHIZOPHRENIC-PATIENTS; CIGARETTE-SMOKING; DEPENDENT OUTPATIENTS; INDUCED PSYCHOSIS; AUDITORY-STIMULI; INDUCED PARANOIA; RAT HIPPOCAMPUS; NORMALIZATION; DEFICIT; SENSITIZATION;
Keywords:
cocaine abuse; psychosis; auditory evoked potential; nicotine; nicotinic receptors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Adler, LE Univ Colorado, Hlth Sci Ctr, Dept Psychiat, C-268-16,4200 E 9th Ave, Denver, CO 80262 USA Univ Colorado C-268-16,4200 E 9th Ave Denver CO USA 80262 62 USA
Citazione:
L.E. Adler et al., "Reversal of diminished inhibitory sensory gating in cocaine addicts by a nicotinic cholinergic mechanism", NEUROPSYCH, 24(6), 2001, pp. 671-679

Abstract

Cocaine addiction, as with other stimulant abuse, produces psychotic symptoms. Although often moderate to mild in severity, these symptoms are, nevertheless, associated with poorer over-all outcome. Recent studies suggest diminished nicotinic cholinergic neurotransmission as a mechanism of a physiological deficit found in schizophrenia, failure of auditory sensory inhibition. Diminished inhibitory sensory gating also occurs in cocaine addicts, probably because of their increased catecholamingeric neurotransmission, which blocks the inhibition. In the present study, 11 cocaine addicts in the first week of detoxification were recorded electrophysiologically, after which the effects of 6 mg of nicotine gum, were assessed in a double-blind placebo-controlled crossover design. The test was repeated 10 days later. Treatment with nicotine, but not placebo, briefly reversed the inhibitory abnormality on both test days. Although nicotine itself may not be a desirable therapeutic agent, because desensitization of nicotinic receptors limits thetime course of its effect, the study identifies a previously unexploited therapeutic target for new drug development of the neuropsychiatric sequelaeof cocaine addition. (C) 2001 American College of Neuropsychopharmacology. Published by Elsevier Science Inc.

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Documento generato il 20/11/19 alle ore 03:19:57