Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
N-type voltage-dependent calcium channels mediate the nicotinic enhancement of GABA release in chick brain
Autore:
Tredway, TL; Guo, JZ; Chiappinelli, VA;
Indirizzi:
George20037ington Univ, Sch Med & Hlth Sci, Dept Pharmacol, Washington, DCGeorge Washington Univ Washington DC USA 20037 Pharmacol, Washington, DC
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 2, volume: 81, anno: 1999,
pagine: 447 - 454
SICI:
0022-3077(199902)81:2<447:NVCCMT>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACETYLCHOLINE-RECEPTORS; OMEGA-CONOTOXIN; NEURONS; MODULATION; CELLS; RAT; PERMEABILITY; SENSITIVITY; CURRENTS; NUCLEUS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Guo, JZ George Washington Univ, Sch Med & Hlth Sci, Dept Pharmacol, 2300 Eye St NW, George Washington Univ 2300 Eye St NW Washington DC USA 20037 NW,
Citazione:
T.L. Tredway et al., "N-type voltage-dependent calcium channels mediate the nicotinic enhancement of GABA release in chick brain", J NEUROPHYS, 81(2), 1999, pp. 447-454

Abstract

The role of voltage-dependent calcium channels (VDCCs) in the nicotinic acetylcholine receptor (nAChR)-mediated enhancement of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) was investigated in chick brain slices. Whole cell recordings of neurons in the lateral spiriform (SpL) and ventral lateral geniculate (LGNv) nuclei showed that cadmium chloride (CdCl2) blocked the carbachol-induced increase of spontaneous GABAergic IPSCs, indicating that VDCCs might be involved. To conclusively show a role for VDCCs, the presynaptic effect of carbachol on SpL and LGNv neurons was examinedin the presence of selective blockers of VDCC subtypes. omega-Conotoxin GVIA, a selective antagonist of N-type channels, significantly reduced the nAChR-mediated enhancement of gamma-aminobutyric acid (GABA) release in the SpL by 78% compared with control responses. Nifedipine, an L-type channel blocker, and omega-Agatoxin-TK, a P/Q-type channel blocker, did not inhibit the enhancement of GABAergic IPSCs. In the LGNv, omega-Conotoxin GVIA also significantly reduced the nAChR-mediated enhancement of GABA release by 71% from control values. Although omega-Agatoxin-TK did not block the nicotinicenhancement, L-type channel blockers showed complex effects on the nAChR-mediated enhancement. These results indicate that the nAChR-mediated enhancement of spontaneous GABAergic IPSCs requires activation of N-type channels in both the SpL and LGNv.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 00:49:04