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

• Type: Article in International Scientific Journal
• Date: 2009

Authors

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

Journal

Title: Neuropharmacology

Vol. 56

Pages: 676-683

ISSN: 0028-3908

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 17 Citations

Scopus - 17 Citations

Scientific classification

CORDIS: Health sciences

Other information

Authenticus ID: 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.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 8