Ca2+ channels and synaptic transmission at the adult, neonatal, and P/Q-type deficient neuromuscular junction

Different types of voltage-activated Ca2+ channels have been established based on their molecular structure and pharmacological and biophysical properties. One of them, the P/Q-type, is the main channel involved in nerve-evoked neurotransmitter release at neuromuscular junctions and the immunologica...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autor principal: Nudler, S.
Otros Autores: Piriz, J., Urbano, F.J, Rosato-Siri, M.D, Piedras Renteria, E.S, Uchitel, O.D
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: New York Academy of Sciences 2003
Materias:
Acceso en línea:Registro en Scopus
DOI
Handle
Registro en la Biblioteca Digital
Aporte de:Registro referencial: Solicitar el recurso aquí
LEADER 12665caa a22018137a 4500
001 PAPER-4817
003 AR-BaUEN
005 20230518203425.0
008 190411s2003 xx ||||fo|||| 00| 0 eng|d
024 7 |2 scopus  |a 2-s2.0-0141636208 
024 7 |2 cas  |a immunoglobulin, 9007-83-4; nitrendipine, 39562-70-4; okadaic acid, 78111-17-8; potassium, 7440-09-7; Calcium Channels, L-Type; Calcium Channels, N-Type; Neurotransmitter Agents; Potassium, 7440-09-7 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a ANYAA 
100 1 |a Nudler, S. 
245 1 0 |a Ca2+ channels and synaptic transmission at the adult, neonatal, and P/Q-type deficient neuromuscular junction 
260 |b New York Academy of Sciences  |c 2003 
270 1 0 |m Uchitel, O.D.; Depto. Fisiol., Biol. Molec. y Cel., Fac. de Ciencias Exactas y Naturales, Ciudad Universitaria, Pabellón II piso 2, Buenos Aires 1428, Argentina; email: odu@fbmc.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
504 |a Katz, B., (1969) The Release of Neural Transmitter Substances, , Liverpool University Press. Liverpool 
504 |a Llinas, R., Steinberg, I.Z., Walton, K., Presynaptic calcium currents and their relation to synaptic transmission: Voltage clamp study in squid giant synapse and theoretical model for the calcium gate (1976) Proc. Natl. Acad. Sci. USA, 73, pp. 2913-2922 
504 |a Llinas, R., Moreno, H., Local Ca2+ signaling in neurons (1998) Cell Calcium, 24, pp. 359-366 
504 |a Catterall, W.A., Structure and regulation of voltage-gated Ca2+ channels (2000) Annu. Rev. Cell Dev. Biol., 16, pp. 521-555 
504 |a Uchitel, O.D., Toxins affecting calcium channels in neurons (1997) Toxicon, 35, pp. 1161-1191 
504 |a Ertel, E.A., Nomenclature of voltage-gated calcium channels (2000) Neuron, 25, pp. 533-535 
504 |a Hans, M., Functional consequences of mutations in the human alpha1A calcium channel subunit linked to familial hemiplegic migraine (1999) J. Neurosci., 19, pp. 1610-1619 
504 |a Kraus, R.L., Familial hemiplegic migraine mutations change alpha1A Ca2+ channel kinetics (1998) J. Biol. Chem., 273, pp. 5586-5590 
504 |a Toru, S., Spinocerebellar ataxia type 6 mutation alters P-type calcium channel function (2000) J. Biol. Chem., 275, pp. 10893-10898 
504 |a Jen, J., Calcium channelopathies in the central nervous system (1999) Curr. Opin. Neurobiol., 9, pp. 274-280 
504 |a Ophoff, R.A., P/Q-type Ca2+ channel defects in migraine, ataxia, and epilepsy (1998) Trends Pharmacol. Sci., 19, pp. 121-127 
504 |a Zhuchenko, O., Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the alpha1A-voltage-dependent calcium channel (1997) Nat. Genet., 15, pp. 62-69 
504 |a Fletcher, C.F., Absence epilepsy in tottering mutant mice is associated with calcium channel defects (1996) Cell, 87, pp. 607-617 
504 |a Doyle, J., Mutations in the Cacnl1a4 calcium channel gene are associated with seizures, cerebellar degeneration, and ataxia in tottering and leaner mutant mice (1997) Mamm. Genome, 8, pp. 113-120 
504 |a Jun, K., Ablation of P/Q-type Ca(2+) channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the alpha(1A)-subunit (1999) Proc. Natl. Acad. Sci. USA, 96, pp. 15245-15250 
504 |a Reuter, H., Diversity and function of presynaptic calcium channels in the brain (1996) Curr. Opin. Neurobiol., 6, pp. 331-337 
504 |a Catterall, W.A., Structure and function of neuronal Ca2+ channels and their role in neurotransmitter release (1998) Cell Calcium, 24, pp. 307-323 
504 |a Uchitel, O.D., P-type voltage-dependent calcium channel mediates presynaptic calcium influx and transmitter release in mammalian synapses (1992) Proc. Natl. Acad. Sci. USA, 89, pp. 3330-3333 
504 |a Protti, D.A., Uchitel, O.D., Transmitter release and presynaptic Ca2+ currents blocked by the spider toxin omega-Aga-IVA (1993) Neuroreport, 5, pp. 333-336 
504 |a Protti, D.A., Calcium channel blockers and transmitter release at the normal human neuromuscular junction (1996) Neurology, 46, pp. 1391-1396 
504 |a Katz, E., Effects of Ca2+ channel blocker neurotoxins on transmitter release and presynaptic currents at the mouse neuromuscular junction (1997) Br. J. Pharmacol., 121, pp. 1531-1540 
504 |a Vincent, A., Beeson, D., Lang, B., Molecular targets for autoimmune and genetic disorders of neuromuscular transmission (2000) Eur. J. Biochem., 267, pp. 6717-6728 
504 |a Urbano, F.J., Uchitel, O.D., L-type calcium channels unmasked by cell-permeant Ca2+ buffer at mouse motor nerve terminals (1999) Pflüg. Arch., 437, pp. 523-528 
504 |a Urbano, F.J., Depetris, R.S., Uchitel, O.D., Coupling of L-type calcium channels to neurotransmitter release at mouse motor nerve terminals (2001) Pflüg. Arch., 441, pp. 824-831 
504 |a Xu, Y.F., Hewett, S.J., Atchison, W.D., Passive transfer of Lambert-Eaton myasthenic syndrome induces dihydropyridine sensitivity of ICa in mouse motor nerve terminals (1998) J. Neurophysiol., 80, pp. 1056-1069 
504 |a Fratantoni, S.A., Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker (2000) Muscle Nerve, 23, pp. 543-550 
504 |a Katz, E., Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction (1996) J. Physiol., 497 (3 PART), pp. 687-697 
504 |a Santafe, M.M., Multiple types of calcium channels mediate transmitter release during functional recovery of botulinum toxin type A-poisoned mouse motor nerve terminals (2000) Neuroscience, 95, pp. 227-234 
504 |a Rosato-Siri, M.D., Uchitel, O.D., Calcium channels coupled to neurotransmitter release at neonatal rat neuromuscular junctions (1999) J. Physiol., 514 (2 PART), pp. 533-540 
504 |a Rosato-Siri, M.D., Differential Ca2+-dependence of transmitter release mediated by P/Q- and N-type calcium channels at neonatal rat neuromuscular junctions (2002) Eur. J. Neurosci., 15, pp. 1874-1880 
504 |a Urbano, F.J., Short term facilitation and Ca2+ dependence of transmitter release are altered at the neuromuscular junction of P/Q Ca2+ channel knock out mice (2001) Biophys. J., 80, pp. 234a 
504 |a Depetris, R.S., Loss of temporal precision of neurotransmitter release at neuromuscular junctions of mice lacking P/Q-type Ca2+ channels (2001) Soc. Neurosci. 
504 |a Newcomb, R., Selective peptide antagonist of the class E calcium channel from the venom of the tarantula Hysterocrates gigas (1998) Biochemistry, 37, pp. 15353-15362 
504 |a Adler, E.M., Alien intracellular calcium chelators attenuate neurotransmitter release at the squid giant synapse (1991) J. Neurosci., 11, pp. 1496-1507 
520 3 |a Different types of voltage-activated Ca2+ channels have been established based on their molecular structure and pharmacological and biophysical properties. One of them, the P/Q-type, is the main channel involved in nerve-evoked neurotransmitter release at neuromuscular junctions and the immunological target in Eaton-Lambert Syndrome. At adult neuromuscular junctions, L- and N-type Ca2+ channels become involved in transmitter release only under certain experimental or pathological conditions. In contrast, at neonatal rat neuromuscular junctions, nerve-evoked synaptic transmission depends jointly on both N- and P/Q-type channels. Synaptic transmission at neuromuscular junctions of the ataxic P/Q-type Ca2+ channel knockout mice is also dependent on two different types of channels, N- and R-type. At both neonatal and P/Q knockout junctions, the K +-evoked increase in miniature endplate potential frequency was not affected by N-type channel blockers, but strongly reduced by both P/Q- and R-type channel blockers. These differences could be accounted for by a differential location of the channels at the release site, being either P/Q- or R-type Ca2+ channels located closer to the release site than N-type Ca2+ channels. Thus, Ca2+ channels may be recruited to mediate neurotransmitter release where P/Q-type channels seem to be the most suited type of Ca2+ channel to mediate exocytosis at neuromuscular junctions.  |l eng 
593 |a Lab. de Fisiol. y Biol. Molecular, Depto. Fisiol., Biol. Molec. y Cel., IFIBYNE-CONICET, Buenos Aires, Argentina 
593 |a Dept. of Molec./Cellular Physiology, Stanford University, Stanford, CA, United States 
593 |a Dept. of Physiology and Neuroscience, NYU School of Medicine, 550 First Avenue, New York, NY 10016, United States 
593 |a Biophysics Sector, S.I.S.S.A./I.S.A.S., Via Beirut 2-4, 34014 Trieste, Italy 
593 |a Department of Physiology, Loyola University Chicago, Maywood, IL 60153, United States 
593 |a Depto. Fisiol., Biol. Molec. y Cel., Fac. de Ciencias Exactas y Naturales, Ciudad Universitaria, Pabellón II piso 2, Buenos Aires 1428, Argentina 
690 1 0 |a CALCIUM CHANNELS 
690 1 0 |a CALCIUM DEPENDENCE 
690 1 0 |a MINIATURE ENDPLATE POTENTIALS 
690 1 0 |a NEUROMUSCULAR JUNCTION 
690 1 0 |a TRANSMITTER RELEASE 
690 1 0 |a CALCIUM CHANNEL 
690 1 0 |a CALCIUM CHANNEL BLOCKING AGENT 
690 1 0 |a CALCIUM CHANNEL L TYPE 
690 1 0 |a CALCIUM CHANNEL N TYPE 
690 1 0 |a CALCIUM CHANNEL P TYPE 
690 1 0 |a CALCIUM CHANNEL Q TYPE 
690 1 0 |a CALCIUM CHANNEL R TYPE 
690 1 0 |a IMMUNOGLOBULIN 
690 1 0 |a NEUROTRANSMITTER 
690 1 0 |a NITRENDIPINE 
690 1 0 |a OKADAIC ACID 
690 1 0 |a OMEGA AGATOXIN 
690 1 0 |a OMEGA AGATOXIN GVIA 
690 1 0 |a OMEGA AGATOXIN IVA 
690 1 0 |a SNX 482 
690 1 0 |a UNCLASSIFIED DRUG 
690 1 0 |a AGENTS INTERACTING WITH TRANSMITTER, HORMONE OR DRUG RECEPTORS 
690 1 0 |a CALCIUM CHANNEL N TYPE 
690 1 0 |a POTASSIUM 
690 1 0 |a ATAXIA 
690 1 0 |a CHEMICAL STRUCTURE 
690 1 0 |a CONFERENCE PAPER 
690 1 0 |a DRUG EFFECT 
690 1 0 |a DYSTONIA 
690 1 0 |a EATON LAMBERT SYNDROME 
690 1 0 |a ELECTRIC POTENTIAL 
690 1 0 |a ELECTROPHYSIOLOGY 
690 1 0 |a ENDPLATE POTENTIAL 
690 1 0 |a EXOCYTOSIS 
690 1 0 |a EXPERIMENT 
690 1 0 |a GENETIC ANALYSIS 
690 1 0 |a GENETIC CODE 
690 1 0 |a HUMAN 
690 1 0 |a IMMUNE SYSTEM 
690 1 0 |a KNOCKOUT MOUSE 
690 1 0 |a NERVE ENDING 
690 1 0 |a NERVE POTENTIAL 
690 1 0 |a NEUROMUSCULAR SYNAPSE 
690 1 0 |a NEUROTRANSMITTER RELEASE 
690 1 0 |a NONHUMAN 
690 1 0 |a PATHOPHYSIOLOGY 
690 1 0 |a STRUCTURE ANALYSIS 
690 1 0 |a SYNAPTIC TRANSMISSION 
690 1 0 |a ADULT 
690 1 0 |a AGING 
690 1 0 |a ANIMAL 
690 1 0 |a CLASSIFICATION 
690 1 0 |a FETUS 
690 1 0 |a GENETICS 
690 1 0 |a METABOLISM 
690 1 0 |a MOUSE 
690 1 0 |a NEUROMUSCULAR JUNCTION DISORDER 
690 1 0 |a NEWBORN 
690 1 0 |a PHYSIOLOGY 
690 1 0 |a RAT 
690 1 0 |a REVIEW 
690 1 0 |a SECRETION 
690 1 0 |a SYNAPTIC MEMBRANE 
690 1 0 |a ATAXIA 
690 1 0 |a ADULT 
690 1 0 |a AGING 
690 1 0 |a ANIMALS 
690 1 0 |a ANIMALS, NEWBORN 
690 1 0 |a CALCIUM CHANNELS, L-TYPE 
690 1 0 |a CALCIUM CHANNELS, N-TYPE 
690 1 0 |a FETUS 
690 1 0 |a HUMANS 
690 1 0 |a MICE 
690 1 0 |a NEUROMUSCULAR JUNCTION 
690 1 0 |a NEUROMUSCULAR JUNCTION DISEASES 
690 1 0 |a NEUROTRANSMITTER AGENTS 
690 1 0 |a POTASSIUM 
690 1 0 |a RATS 
690 1 0 |a SYNAPTIC MEMBRANES 
690 1 0 |a SYNAPTIC TRANSMISSION 
653 0 0 |a snx 482 
700 1 |a Piriz, J. 
700 1 |a Urbano, F.J. 
700 1 |a Rosato-Siri, M.D. 
700 1 |a Piedras Renteria, E.S. 
700 1 |a Uchitel, O.D. 
773 0 |d New York Academy of Sciences, 2003  |g v. 998  |h pp. 11-17  |p Ann. New York Acad. Sci.  |x 00778923  |w (AR-BaUEN)CENRE-1541  |t Annals of the New York Academy of Sciences 
856 4 1 |u https://www.scopus.com/inward/record.uri?eid=2-s2.0-0141636208&doi=10.1196%2fannals.1254.003&partnerID=40&md5=274eded5e6b05ead4bc588daa097ef89  |y Registro en Scopus 
856 4 0 |u https://doi.org/10.1196/annals.1254.003  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_00778923_v998_n_p11_Nudler  |y Handle 
856 4 0 |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00778923_v998_n_p11_Nudler  |y Registro en la Biblioteca Digital 
961 |a paper_00778923_v998_n_p11_Nudler  |b paper  |c PE 
962 |a info:eu-repo/semantics/article  |a info:ar-repo/semantics/artículo  |b info:eu-repo/semantics/publishedVersion 
963 |a VARI 
999 |c 65770