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Titolo:
Human fear conditioning is related to dopaminergic and serotonergic biological markers
Autore:
Garpenstrand, H; Annas, P; Ekblom, J; Oreland, L; Fredrikson, M;
Indirizzi:
Uppsala Univ, Dept Psychol, SE-75142 Uppsala, Sweden Uppsala Univ Uppsala Sweden SE-75142 t Psychol, SE-75142 Uppsala, Sweden Uppsala Univ, Dept Neurosci, SE-75142 Uppsala, Sweden Uppsala Univ Uppsala Sweden SE-75142 Neurosci, SE-75142 Uppsala, Sweden
Titolo Testata:
BEHAVIORAL NEUROSCIENCE
fascicolo: 2, volume: 115, anno: 2001,
pagine: 358 - 364
SICI:
0735-7044(200104)115:2<358:HFCIRT>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
MONOAMINE-OXIDASE ACTIVITY; ANXIETY-RELATED TRAITS; PLATELET MAO ACTIVITY; A GENE PROMOTER; DEPRESSED-PATIENTS; NOVELTY SEEKING; POLYMORPHISM; PERSONALITY; ASSOCIATION; BEHAVIOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Fredrikson, M Uppsala Univ, Dept Psychol, POB 1225, SE-75142 Uppsala, Sweden Uppsala Univ POB 1225 Uppsala Sweden SE-75142 psala, Sweden
Citazione:
H. Garpenstrand et al., "Human fear conditioning is related to dopaminergic and serotonergic biological markers", BEHAV NEURO, 115(2), 2001, pp. 358-364

Abstract

Biological markers for acquisition and extinction of fear conditioning were studied in 40 individuals selected for displaying either good or poor acquisition of fear conditioning, as estimated by the skin conductance response. Participants with a short serotonin transporter (5-HTT) promoter allele or low monoamine oxidase activity in platelets (trbc-MAO) displayed better acquisition than those with only long alleles or high trbc-MAO. whereas participants with a long dopamine D4 receptor (D4DR) exon III allele showed delayed extinction compared with those with only short alleles. The findings,that D4DR exon III and 5-HTT promoter genotypes and trbc-MAO activity are related to human fear conditioning, a basic form of associative learning, are consistent with animal studies suggesting a genetic contribution to fearconditioning. The authors suggest that in humans these genetic mechanisms are partly dopaminergic and serotonergic in origin.

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Documento generato il 25/01/20 alle ore 06:21:56