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Titolo:
Coupling of L-type calcium channels to neurotransmitter release at mouse motor nerve terminals
Autore:
Urbano, FJ; Depetris, RS; Uchitel, OD;
Indirizzi:
Univ Buenos Aires, Fac Ciencias Exactas & Nat, Lab Fisiol & Biol Mol, RA-1428 Buenos Aires, DF, Argentina Univ Buenos Aires Buenos Aires DF Argentina RA-1428 Aires, DF, Argentina
Titolo Testata:
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
fascicolo: 6, volume: 441, anno: 2001,
pagine: 824 - 831
SICI:
0031-6768(200103)441:6<824:COLCCT>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
SQUID GIANT SYNAPSE; PROTEIN-KINASE-C; TRANSMITTER RELEASE; CA2+ CHANNELS; TYROSINE PHOSPHORYLATION; NEUROMUSCULAR-JUNCTION; CHROMAFFIN CELLS; BOTULINUM TOXIN; IN-VITRO; P/Q-TYPE;
Keywords:
calcium channel; motor nerve terminal; cell-permeant calcium buffers; BAPTA-AM; EGTA-AM; serine/threonine phosphorylation; okadaic acid;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Uchitel, OD Univ Buenos Aires, Fac Ciencias Exactas & Nat, Lab Fisiol & Biol Mol, Ciudad Univ,Pabellon 2,2do Piso, RA-1428 Buenos Aires, DF, Argentina Univ Buenos Aires Ciudad Univ,Pabellon 2,2do Piso Buenos Aires DF Argentina RA-1428
Citazione:
F.J. Urbano et al., "Coupling of L-type calcium channels to neurotransmitter release at mouse motor nerve terminals", PFLUG ARCH, 441(6), 2001, pp. 824-831

Abstract

Previously, we have presented evidence for the presence of L-type voltage-dependent Ca2+ channels (VDCC) in 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, (acetoxymethyl)ester (BAPTA-AM)-incubated motor nerve terminals (MNTs) of the levator auris muscle of mature mice. The aim of the present work was to study the coupling of these L-type VDCC to neurotransmitter release by inhibiting protein phosphatases. We thus studied the effects of the protein phosphatase inhibitors okadaic acid (OA) and pervanadate on quantal content (QC) of transmitter release with the P/Q-type channels fullyblocked. The QC was not significantly different under the three experimental conditions tested: incubation with dimethylsulphoxide (DMSO), ethylene-glycerol-bis(beta -aminoethylether)-N,N,N',N'-tetraacetic acid, (acetoxymethyl)ester (ECTA-AM) and BAPTA-AM. After preincubation with OA (1 muM), but not with pervanadate, QC increased substantially in the BAPTA-AM-incubated (up to 400%) MNT, but not in those incubated with DMSO or EGTA-AM. The OA-induced increment of QC was attenuated greatly (similar to 95% reduction) by preincubation with either nitrendipine (10 muM) or calciseptine (300 nM). The effect of OA (1 muM) and pervanadate (0.1 mM) on spontaneous neurotransmitter release was also studied. After preincubation with OA, but not pervanadate, miniature end-plate potential (MEPP) frequency increased only in theBAPTA-AM-incubated MNT (up to 700% increment). This response was attenuated (by similar to 80%) by nitrendipine (10 muM) or calciseptine (300nM). In contrast, neither omega -agatoxin IVA (120 nM) nor omega -conotoxin GVIA (1muM) affected this OA-induced increment significantly. We also evaluated the relationship between QC and extracellular [Ca2+] ([Ca2+](i)) in BAPTA-AM-incubated MNT Under conditions in which only P/Q-type VDCC were available to participate in neurotransmitter release, QC increased as [Ca2+](0) was raised from 0.5 to 2 mM. However, when only L-type VDCC were available, QC increased when [Ca2+], increased from 0.5 to 1 mM, but decreased significantly at 2 mM. The mean latency for P/Q-type VDCC-mediated EPP was 1.7-1.9 ms;for L-type VDCC-mediated EPP, 1.9-2.5 ms. The rise time of the L-type VDCCmediated EPP was significantly slower than that mediated by P/Q-type VDCC. Preincubation with H-7 (100 CIM), a potent inhibitor of protein kinase C (PKC) and adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase (PKA), attenuated the OA-induced increment of both QC and MEPP frequency(50% and 70% decrement, respectively), suggesting the participation of at least these two protein kinases in the coupling of L-type VDCC. In summary,our results show coupling of L-type VDCC to neurotransmitter release when protein phosphatases are inhibited and intracellular [Ca2+] is buffered by the fast chelator BAPTA.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 19:26:25