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Titolo:
NEUROBIOLOGICAL MECHANISMS INVOLVED IN ANTIDEPRESSANT THERAPIES
Autore:
BRILEY M; MORET C;
Indirizzi:
CTR RECH PIERRE FABRE,DIV NEUROBIOL 1,17 AVE JEAN MOULIN F-81100 CASTRES FRANCE
Titolo Testata:
Clinical neuropharmacology
fascicolo: 5, volume: 16, anno: 1993,
pagine: 387 - 400
SICI:
0362-5664(1993)16:5<387:NMIIAT>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSTSYNAPTIC SEROTONERGIC RECEPTORS; TERMINAL 5-HT AUTORECEPTORS; IMIPRAMINE BINDING-SITES; RAT-BRAIN; FRONTAL-CORTEX; PHARMACOLOGICAL CHARACTERIZATION; 5-HYDROXYTRYPTAMINE RELEASE; ELECTROCONVULSIVE SHOCK; REGIONAL DISTRIBUTION; INVIVO MICRODIALYSIS;
Keywords:
SEROTONIN AUTORECEPTORS; MICRODIALYSIS; ELECTROPHYSIOLOGY; SYNAPTIC CONCENTRATIONS OF SEROTONIN;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
60
Recensione:
Indirizzi per estratti:
Citazione:
M. Briley e C. Moret, "NEUROBIOLOGICAL MECHANISMS INVOLVED IN ANTIDEPRESSANT THERAPIES", Clinical neuropharmacology, 16(5), 1993, pp. 387-400

Abstract

Selective serotonin reuptake inhibitors (SSRIs) are effective in alleviating the symptoms of depression. However, clinical improvement is only obtained after several weeks of treatment. SSRIs, when administered acutely to animals, have little effect on synaptic levels of serotonin. This suggests the existence of one or more regulatory mechanisms controlling serotonergic neurotransmission. The firing rate of dorsal raphe serotonergic neurons is under the control of somatodendritic 5-hydroxytryptamine1A (5-HT1A) autoreceptors, the release of serotonin from nerve terminals is under the control of 5-HT autoreceptors (5-HT1B subtype in rodents, 5-HT1D in other species), whereas the control of the activity of tryptophan hydroxylase, the rate-limiting enzyme of serotonin synthesis, is complex, involving 5-HT1A but possibly other 5-HT receptors including the 5-HT1B/D subtype. During prolonged administration with a SSRI, these three feedback systems become desensitized and their regulatory effects on serotonergic neurotransmission are weakened or lost. This has the effect of allowing the synaptic levels of serotonin to rise with a consequently increased stimulation of one or moretypes of postsynaptic 5-HT receptor. Thus, it is only after prolongedadministration that the pharmacological activity of SSRI is fully expressed in terms of synaptic serotonin levels. This may explain the latency of antidepressant action seen with these drugs in humans. Variousother classes of antidepressant therapies (tricyclic antidepressants and monoamine oxidase inhibitor drugs, electroconvulsive therapy) havelong-term effects on one or more of the feedback mechanisms such thatan increase in synaptic concentrations of serotonin may be a common mechanism of many antidepressant therapies.

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Documento generato il 10/07/20 alle ore 01:11:28