Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker
In order to search for early changes induced by the application of human immunoglobulin G (IgG) on motor nerve terminals, IgG from patients with amyotrophic lateral sclerosis (ALS) and control subjects was injected subcutaneously into the levator auris muscle of mice. A week or a month after the las...
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| Formato: | Capítulo de libro |
| Lenguaje: | Inglés |
| Publicado: |
2000
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| Acceso en línea: | Registro en Scopus DOI Handle Registro en la Biblioteca Digital |
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| LEADER | 12510caa a22014297a 4500 | ||
|---|---|---|---|
| 001 | PAPER-20936 | ||
| 003 | AR-BaUEN | ||
| 005 | 20230518205222.0 | ||
| 008 | 190411s2000 xx ||||fo|||| 00| 0 eng|d | ||
| 024 | 7 | |2 scopus |a 2-s2.0-0034082626 | |
| 024 | 7 | |2 cas |a Calcium Channel Blockers; Calcium Channels, L-Type; Immunoglobulin G; Nitrendipine, 39562-70-4; omega-Agatoxin IVA; omega-Conotoxin GVIA, 92078-76-7 | |
| 040 | |a Scopus |b spa |c AR-BaUEN |d AR-BaUEN | ||
| 030 | |a MUNED | ||
| 100 | 1 | |a Fratantoni, S.A. | |
| 245 | 1 | 0 | |a Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker |
| 260 | |c 2000 | ||
| 270 | 1 | 0 | |m Uchitel, O.D.; Inst. de Fisiol./Biologia Molecular, Facultad de Ciencias Exactas, Pab. II, Capital Federal 1428, Argentina; email: odu@bg.fcen.uba.ar |
| 506 | |2 openaire |e Política editorial | ||
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| 504 | |a Smith, D.O., Conklin, M.W., Jensen, P.J., Atchison, W.D., Decreased calcium currents in motor nerve terminals of mice with Lambert-Eaton myasthenic syndrome (1995) J Physiol (Lond), 15 (487), pp. 115-123 | ||
| 504 | |a Smith, R.G., Siklos, L., Alexianu, M.E., Engelhardt, J.I., Mosier, D.R., Colom, L., Habib Mohamed, A., Appel, S.H., Autoimmunity and ALS (1996) Neurology, 47 (SUPPL.), pp. S40-S46 | ||
| 504 | |a Uchitel, O.D., Appel, S.H., Crawford, F., Szczupak, L., Immunoglobulins from amyotrophic lateral sclerosis patients enhance spontaneous transmitter release from motor nerve terminals (1988) Proc Natl Acad Sci USA, 85, pp. 7371-7374 | ||
| 504 | |a Uchitel, O.D., Protti, D.A., Sánchez, V., Cherksey, B.D., Sugimori, M., Llinás, R., P-type voltage-dependent calcium channel mediate presynaptic calcium influx and transmitter release in mammalian synapses (1992) Proc Natl Acad Sci USA, 89, pp. 3330-3333 | ||
| 504 | |a Uchitel, O.D., Scornik, F., Protti, D.A., Fumberg, C.G., Alvarez, V., Appel, S.H., Long-term neuromuscular dysfunction produced by passive transfer of amyotrophic lateral sclerosis immunoglobulins (1992) Neurology, 42, pp. 2175-2180 | ||
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| 504 | |a El escorial world federation of neurología criteria for the diagnosis of amyotrophic lateral sclerosis (1994) J Neurol Sci, 124 (SUPPL.), pp. 96-107 | ||
| 504 | |a Zar, J.H., (1996) Biostatistical Analysis, 3rd Ed., , Englewood Cliffs, NJ: Prentice-Hall | ||
| 520 | 3 | |a In order to search for early changes induced by the application of human immunoglobulin G (IgG) on motor nerve terminals, IgG from patients with amyotrophic lateral sclerosis (ALS) and control subjects was injected subcutaneously into the levator auris muscle of mice. A week or a month after the last injection, endplate potentials were recorded. No changes in quantal content of transmitter release were observed. In control and ALS IgG-treated muscles, neurotransmitter release remained sensitive to P/Q-type and insensitive to N-type voltage-sensitive calcium channel (VSCC) blockers as in untreated muscles. In contrast, IgG from 5 of 8 different ALS patients induced a significant reduction in quantal content of the evoked response after incubation with nitrendipine, indicating that a novel sensitivity to this calcium channel blocker appears in these motor nerve terminals. These results indicate that ALS IgG induces plastic changes at nerve terminals. The expression of transmitter release coupled to L-type VSCC indicate that ALS IgGs are capable of inducing plastic changes at the nerve terminals that may participate in the process leading to neuronal death. (C) 2000 John Wiley and Sons, Inc. |l eng | |
| 593 | |a Inst. Biol. Cel. y Neurociencias P., Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina | ||
| 593 | |a Lab. de Fisiol. y Biologia Molecular, Facultad de Ciencias Exactas, Universidad de Buenos Aires, Buenos Aires, Argentina | ||
| 593 | |a Hospital Británico, Buenos Aires, Argentina | ||
| 593 | |a Inst. Fisiologia y Biologia Molec., Facultad de Ciencias Exastas, Pab. II, 2 piso, Capital Federal 1428, Argentina | ||
| 690 | 1 | 0 | |a AMYOTROPHIC LATERAL SCLEROSIS |
| 690 | 1 | 0 | |a CALCIUM CHANNELS |
| 690 | 1 | 0 | |a NEUROMUSCULAR JUNCTION |
| 690 | 1 | 0 | |a NITRENDIPINE |
| 690 | 1 | 0 | |a TRANSMITTER RELEASE |
| 690 | 1 | 0 | |a CALCIUM CHANNEL BLOCKING AGENT |
| 690 | 1 | 0 | |a IMMUNOGLOBULIN G |
| 690 | 1 | 0 | |a NITRENDIPINE |
| 690 | 1 | 0 | |a ADULT |
| 690 | 1 | 0 | |a AGED |
| 690 | 1 | 0 | |a AMYOTROPHIC LATERAL SCLEROSIS |
| 690 | 1 | 0 | |a ANIMAL CELL |
| 690 | 1 | 0 | |a ANIMAL MODEL |
| 690 | 1 | 0 | |a ANIMAL TISSUE |
| 690 | 1 | 0 | |a ARTICLE |
| 690 | 1 | 0 | |a CALCIUM TRANSPORT |
| 690 | 1 | 0 | |a CLINICAL ARTICLE |
| 690 | 1 | 0 | |a CONTROLLED STUDY |
| 690 | 1 | 0 | |a FEMALE |
| 690 | 1 | 0 | |a HUMAN |
| 690 | 1 | 0 | |a HUMAN CELL |
| 690 | 1 | 0 | |a HUMAN TISSUE |
| 690 | 1 | 0 | |a IMMUNOTHERAPY |
| 690 | 1 | 0 | |a MALE |
| 690 | 1 | 0 | |a MOUSE |
| 690 | 1 | 0 | |a NERVE CELL NECROSIS |
| 690 | 1 | 0 | |a NEUROTRANSMITTER RELEASE |
| 690 | 1 | 0 | |a NONHUMAN |
| 690 | 1 | 0 | |a PRIORITY JOURNAL |
| 690 | 1 | 0 | |a PROTEIN EXPRESSION |
| 690 | 1 | 0 | |a VOLTAGE CLAMP |
| 690 | 1 | 0 | |a ADULT |
| 690 | 1 | 0 | |a AGED |
| 690 | 1 | 0 | |a ANIMALS |
| 690 | 1 | 0 | |a CALCIUM CHANNEL BLOCKERS |
| 690 | 1 | 0 | |a CALCIUM CHANNELS, L-TYPE |
| 690 | 1 | 0 | |a EVOKED POTENTIALS |
| 690 | 1 | 0 | |a FEMALE |
| 690 | 1 | 0 | |a HUMANS |
| 690 | 1 | 0 | |a IMMUNOGLOBULIN G |
| 690 | 1 | 0 | |a MALE |
| 690 | 1 | 0 | |a MICE |
| 690 | 1 | 0 | |a MIDDLE AGED |
| 690 | 1 | 0 | |a MOTOR NEURON DISEASE |
| 690 | 1 | 0 | |a MUSCLE, SKELETAL |
| 690 | 1 | 0 | |a NEUROMUSCULAR JUNCTION |
| 690 | 1 | 0 | |a NITRENDIPINE |
| 690 | 1 | 0 | |a OMEGA-AGATOXIN IVA |
| 690 | 1 | 0 | |a OMEGA-CONOTOXIN GVIA |
| 690 | 1 | 0 | |a REFERENCE VALUES |
| 700 | 1 | |a Weisz, G. | |
| 700 | 1 | |a Pardal, A.M. | |
| 700 | 1 | |a Reisin, R.C. | |
| 700 | 1 | |a Uchitel, O.D. | |
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