Arachidonic acid metabolites as mediators of synaptic modulation

Détails

ID Serval
serval:BIB_D89AC7DA7289
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Arachidonic acid metabolites as mediators of synaptic modulation
Périodique
Cell Biology International Reports
Auteur(s)
Volterra  A.
ISSN
1065-6995
ISSN-L
0309-1651 (Print)
Statut éditorial
Publié
Date de publication
12/1989
Volume
13
Numéro
12
Pages
1189-99
Notes
Journal Article Review --- Old month value: Dec
Résumé
The neurotransmitters histamine, dopamine and the peptide Phe-Met-Arg-Phe-NH2 (FMRFa) cause presynaptic inhibition in the nervous system of the marine mollusk Aplysia Californica by combined down-modulation of a Ca++ conductance and up-modulation of a K+ conductance. The action of FMRFa on the S-type K+ channels of Aplysia sensory neurons is mediated by a metabolite of the 12-lipoxygenase pathway of arachidonic acid, possibly 12-HPETE. A Pertussis toxin-sensitive GTP binding protein couples FMRFa receptor to the activation of the arachidonic cascade. Once produced, 12-HPETE does not require ATP- or GTP-dependent processes to act on the K+ channels, but it may directly modulate the channel via an external membrane receptor. Based on this observation, a role for eicosanoids as possible intercellular messengers in the C.N.S. is discussed.
Mots-clé
Animals Aplysia/*physiology Arachidonic Acid Arachidonic Acids/*metabolism Synapses/*physiology Synaptic Transmission/*drug effects
Pubmed
Web of science
Création de la notice
24/01/2008 14:37
Dernière modification de la notice
20/08/2019 15:58
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