N-acyldopamines control striatal input terminals via novel ligand-gated cation channels

• Tipo: Artigo em Revista Científica Internacional
• Data: 2009

Autores

Ferreira, SG (Autor) Outra; Lomaglio, T (Autor) Outra; António Avelino Silva (Autor) FMUP; Francisco Cruz (Autor) FMUP; Oliveira, CR (Autor) Outra; Cunha, RA (Autor) Outra; Kofalvi, A (Autor) Outra

Revista

Título: Neuropharmacology

Vol. 56

Páginas: 676-683

ISSN: 0028-3908

Editora: Elsevier

Indexação

ISI Web of Knowledge - 17 Citações

Scopus - 17 Citações

Classificação Científica

CORDIS: Ciências da Saúde

Outras Informações

ID Authenticus: P-003-N0F

DOI: 10.1016/j.neuropharm.2008.12.001

Abstract (EN): Endogenous analogues of capsaicin, N-acyldopamines, were previously identified from striatal extracts, but the putative presynaptic role of their receptor, the TRPV(1)R (formerly: vanilloid or capsaicin receptor) in the caudate-putamen is unclear. We found that the endogenous TRPV(1)R agonists, N-arachidonoyldopamine (NADA) and oleoyldopamine (OLDA) with EC(50) values in the nanomolar range, as well as the synthetic TRPV(1)R activator 2-aminoethoxydiphenylborane (2APB), and palmytoyldopamine (PALDA, another endogenous N-acyldopamine inactive at the TRPV(1)R), but not capsaicin or other endogenous and synthetic cannabinoids, triggered a rapid Ca(2+) entry with the concomitant stimulation of glutamate and dopamine release. These effects persisted in the TRPV(1)R null-mutant mice, and were insensitive to antagonists of common ionotropic receptors, to several TRPV(1)R antagonists and to the absence of K(+). Furthermore, these N-acyldopamine receptors in glutamatergic and dopaminergic terminals are different based on their different sensitivity to anandamide, capsazepine and Gd(3+) at nanomolar concentrations. Altogether, novel ion channels instead of the TRPV(1)R mediate the presynaptic action of N-acyldopamines in the striatum of adult rodents.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 8