18 results on '"Amifampridine"'
Search Results
2. Reply.
- Author
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Sanders DB, Harati Y, Juel VC, Lou JS, Marburger T, Pascuzzi RM, Peltier AC, Richman DP, and Smith AG
- Subjects
- Humans, Amifampridine, Lambert-Eaton Myasthenic Syndrome
- Published
- 2018
- Full Text
- View/download PDF
3. 3,4-diaminopyridine base effectively treats the weakness of Lambert-Eaton myasthenia.
- Author
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Sanders DB, Juel VC, Harati Y, Smith AG, Peltier AC, Marburger T, Lou JS, Pascuzzi RM, Richman DP, Xie T, Demmel V, Jacobus LR, Aleš KL, and Jacobus DP
- Subjects
- Adult, Aged, Aged, 80 and over, Double-Blind Method, Female, Humans, Lambert-Eaton Myasthenic Syndrome complications, Maintenance Chemotherapy, Male, Middle Aged, Muscle Weakness etiology, Young Adult, Amifampridine therapeutic use, Deprescriptions, Lambert-Eaton Myasthenic Syndrome drug therapy, Muscle Weakness drug therapy, Neuromuscular Agents therapeutic use
- Abstract
Introduction: 3,4-diaminopyridine has been used to treat Lambert-Eaton myasthenia (LEM) for 30 years despite the lack of conclusive evidence of efficacy., Methods: We conducted a randomized double-blind placebo-controlled withdrawal study in patients with LEM who had been on stable regimens of 3,4-diaminopyridine base (3,4-DAP) for ≥ 3 months. The primary efficacy endpoint was >30% deterioration in triple timed up-and-go (3TUG) times during tapered drug withdrawal. The secondary endpoint was self-assessment of LEM-related weakness (W-SAS)., Results: Thirty-two participants were randomized to continuous 3,4-DAP or placebo groups. None of the 14 participants who received continuous 3,4-DAP had > 30% deterioration in 3TUG time versus 72% of the 18 who tapered to placebo (P < 0.0001). W-SAS similarly demonstrated an advantage for continuous treatment over placebo (P < 0.0001). Requirement for rescue and adverse events were more common in the placebo group., Discussion: This trial provides significant evidence of efficacy of 3,4-DAP in the maintenance of strength in LEM. Muscle Nerve 57: 561-568, 2018., (© 2017 The Authors Muscle & Nerve Published by Wiley Periodicals, Inc.)
- Published
- 2018
- Full Text
- View/download PDF
4. Effect of 3,4-diaminopyridine at the murine neuromuscular junction.
- Author
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Ng F, Lee DC, Schrumpf LA, Mazurek ME, Lee Lo V, Gill SK, and Maselli RA
- Subjects
- 4-Aminopyridine pharmacology, Acetamides pharmacology, Amifampridine, Animals, Calcium metabolism, Dose-Response Relationship, Drug, Female, In Vitro Techniques, Membrane Potentials drug effects, Mice, Mice, Inbred C57BL, Synaptic Transmission drug effects, 4-Aminopyridine analogs & derivatives, Diaphragm drug effects, Neuromuscular Junction drug effects, Potassium Channel Blockers pharmacology
- Abstract
Introduction: We investigated the effects of 3,4-diaminopyridine (3,4-DAP) and its acetylated metabolite, N-(4-amino-pyridin-3-yl) acetamide (3-Ac), at the mammalian neuromuscular junction., Methods: Quantal release of acetylcholine was studied in diaphragm muscles of mice, using in vitro intracellular microelectrode recordings., Results: Under conditions of low probability of release, 3,4-DAP produced a 1,000% increase in quantal release, but 3-Ac had no effect. Under conditions of normal probability of release, the effect of 3,4-DAP was modest and limited by concurrent depletion of synaptic vesicles, especially with high concentrations of 3,4-DAP and high frequencies of nerve stimulation., Conclusions: These findings predict 3,4-DAP is most effective in conditions with low probability of quantal release, such as Lambert-Eaton myasthenic syndrome. A beneficial effect is also expected in disorders of neuromuscular transmission in which the effect of 3,4-DAP on quantal release is not limited by depletion of synaptic vesicles, such as postsynaptic congenital myasthenic syndromes. Muscle Nerve, 2016 Muscle Nerve 55: 223-231, 2017., (© 2016 Wiley Periodicals, Inc.)
- Published
- 2017
- Full Text
- View/download PDF
5. A response to a recent editorial by concerned physicians on 3,4-diaminopyridine.
- Author
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McEnany PJ
- Subjects
- Amifampridine, Humans, 4-Aminopyridine analogs & derivatives, Orphan Drug Production
- Published
- 2017
- Full Text
- View/download PDF
6. Amifampridine phosphate in congenital myasthenic syndrome.
- Author
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Verma S, Mazell SN, and Shah DA
- Subjects
- 4-Aminopyridine therapeutic use, Amifampridine, Child, Preschool, Electroencephalography, Female, Humans, Male, Mutation genetics, Receptors, Nicotinic genetics, 4-Aminopyridine analogs & derivatives, Myasthenic Syndromes, Congenital drug therapy, Potassium Channel Blockers therapeutic use
- Published
- 2016
- Full Text
- View/download PDF
7. Amifampridine phosphate (Firdapse(®)) is effective and safe in a phase 3 clinical trial in LEMS.
- Author
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Oh SJ, Shcherbakova N, Kostera-Pruszczyk A, Alsharabati M, Dimachkie M, Blanco JM, Brannagan T, Lavrnić D, Shieh PB, Vial C, Meisel A, Komoly S, Schoser B, Sivakumar K, and So Y
- Subjects
- 4-Aminopyridine therapeutic use, Adult, Aged, Aged, 80 and over, Amifampridine, Calcium Channels immunology, Double-Blind Method, Female, Humans, Lambert-Eaton Myasthenic Syndrome immunology, Male, Middle Aged, Treatment Outcome, Young Adult, 4-Aminopyridine analogs & derivatives, Lambert-Eaton Myasthenic Syndrome drug therapy, Muscle Strength, Phosphates therapeutic use, Potassium Channel Blockers therapeutic use
- Abstract
Objective: We evaluated the efficacy and safety of amifampridine phosphate (Firdapse(®)) for symptomatic treatment in Lambert-Eaton myasthenic syndrome (LEMS)., Methods: Phase 3, randomized, double-blind, study. Patients were treated initially with amifampridine phosphate for 7-91 days, followed by randomization to continue amifampridine phosphate for 14 days or placebo (7-day taper, 7-day placebo). The primary efficacy endpoints were changes from baseline at day 14 in Quantitative Myasthenia Gravis and Subject Global Impression scores., Results: The coprimary efficacy end points and 1 of the secondary efficacy end points were met, showing a significant benefit of aminfampridine phosphate over placebo at Day 14. All 5 primary, secondary, and tertiary endpoints achieved statistical significance at Day 8. Amifampridine phosphate was well tolerated; the most common adverse events were oral and digital paresthesias, nausea, and headache., Conclusions: This study provides Class I evidence of efficacy of amifampridine phosphate as a symptomatic treatment for LEMS., (© 2016 Wiley Periodicals, Inc.)
- Published
- 2016
- Full Text
- View/download PDF
8. Editorial by concerned physicians: Unintended effect of the orphan drug act on the potential cost of 3,4-diaminopyridine.
- Author
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Burns TM, Smith GA, Allen JA, Amato AA, Arnold WD, Barohn R, Benatar M, Bird SJ, Bromberg M, Chahin N, Ciafaloni E, Cohen JA, Corse A, Crum BA, David WS, Dimberg E, Sousa EA, Donofrio PD, Dyck PJ, Engel AG, Ensrud ER, Ferrante M, Freimer M, Gable KL, Gibson S, Gilchrist JM, Goldstein JM, Gooch CL, Goodman BP, Gorelov D, Gospe SM Jr, Goyal NA, Guidon AC, Guptill JT, Gutmann L, Gutmann L, Gwathmey K, Harati Y, Harper CM Jr, Hehir MK, Hobson-Webb LD, Howard JF Jr, Jackson CE, Johnson N, Jones SM, Juel VC, Kaminski HJ, Karam C, Kennelly KD, Khella S, Khoury J, Kincaid JC, Kissel JT, Kolb N, Lacomis D, Ladha S, Larriviere D, Lewis RA, Li Y, Litchy WJ, Logigian E, Lou JS, MacGowen DJ, Maselli R, Massey JM, Mauermann ML, Mathews KD, Meriggioli MN, Miller RG, Moon JS, Mozaffar T, Nations SP, Nowak RJ, Ostrow LW, Pascuzzi RM, Peltier A, Ruzhansky K, Richman DP, Ross MA, Rubin DI, Russell JA, Sachs GM, Salajegheh MK, Saperstein DS, Scelsa S, Selcen D, Shaibani A, Shieh PB, Silvestri NJ, Singleton JR, Smith BE, So YT, Solorzano G, Sorenson EJ, Srinivasen J, Tavee J, Tawil R, Thaisetthawatkul P, Thornton C, Trivedi J, Vernino S, Wang AK, Webb TA, Weiss MD, Windebank AJ, and Wolfe GI
- Subjects
- 4-Aminopyridine therapeutic use, Amifampridine, Humans, Neuromuscular Junction Diseases economics, 4-Aminopyridine analogs & derivatives, Neuromuscular Junction Diseases drug therapy, Orphan Drug Production economics, Orphan Drug Production methods, Physicians psychology, Potassium Channel Blockers therapeutic use
- Published
- 2016
- Full Text
- View/download PDF
9. Acute and chronic effects of botulinum neurotoxin a on the mammalian neuromuscular junction.
- Author
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Baskaran P and Thyagarajan B
- Subjects
- 4-Aminopyridine analogs & derivatives, 4-Aminopyridine pharmacology, Acetylcholine metabolism, Acetylcholinesterase metabolism, Amifampridine, Animals, Calcium Ionophores pharmacology, Cell Line, Tumor, Electric Stimulation, Electromyography, In Vitro Techniques, Ionomycin pharmacology, Mice, Mice, Inbred C57BL, Neuroblastoma pathology, Neuromuscular Junction metabolism, Potassium Channel Blockers pharmacology, Reflex drug effects, Time Factors, Botulinum Toxins, Type A toxicity, Evoked Potentials, Motor drug effects, Neuromuscular Agents toxicity, Neuromuscular Junction drug effects
- Abstract
Introduction: Botulinum neurotoxin A (BoNT/A) cleaves SNAP-25 and inhibits acetylcholine (ACh) release at the neuromuscular junctions (NMJ) to cause neuroparalysis. Previous reports indicate a dyssynchrony between the inhibitory effect of BoNT/A on ACh release and SNAP-25 cleavage., Methods: We tested the in vitro (acute; 90 min) and in vivo (chronic; 12 h) effects of BoNT/A on stimulus-evoked ACh release (SEAR), twitch tension, and SNAP-25 cleavage in isolated extensor digitorum longus (EDL) nerve-muscle preparations (NMP)., Results: In vitro or in vivo BoNT/A poisoning inhibited SEAR and twitch tension. Conversely, SNAP-25 cleavage and inhibition of spontaneous release frequency were observed only in NMP poisoned with BoNT/A in vivo. Moreover, chronic treatment of BoNT/A inhibited ionomycin stimulated Ca(2+) signals in Neuro 2a cells., Conclusions: These results demonstrate that the inhibition of SEAR precedes SNAP-25 cleavage and suggest involvement of a more complex mechanism for the inhibitory effect of BoNT/A at the NMJ., (Copyright © 2013 Wiley Periodicals, Inc.)
- Published
- 2014
- Full Text
- View/download PDF
10. 3,4-Diaminopyridine is more effective than placebo in a randomized, double-blind, cross-over drug study in LEMS.
- Author
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Oh SJ, Claussen GG, Hatanaka Y, and Morgan MB
- Subjects
- 4-Aminopyridine therapeutic use, Adult, Aged, Amifampridine, Cross-Over Studies, Double-Blind Method, Female, Humans, Lambert-Eaton Myasthenic Syndrome physiopathology, Male, Middle Aged, Placebos, Prospective Studies, 4-Aminopyridine analogs & derivatives, Lambert-Eaton Myasthenic Syndrome drug therapy
- Abstract
The purpose of this study was to investigate the clinical and electrophysiological efficacy of 3,4-diaminopyridine (DAP) in patients with Lambert-Eaton myasthenic syndrome (LEMS) in a randomized, double-blind, cross-over drug trial. The diagnosis of LEMS was made based on the combination of fluctuating muscle weakness, diminished or absent reflexes, and more than 60% increment of the compound muscle action potential (CMAP) amplitude after brief exercise or 50-HZ stimulation on a repetitive nerve stimulation (RNS) test. Evaluations were done at baseline, with placebo, and with 3,4-DAP (up to 75-80 mg/day). Assignment of placebo or 3,4-DAP was done in a double-blinded manner. Measurements included subjective symptoms score, objective clinical measurements [LEMS classification, muscle strength score, quantitative myasthenia gravis (QMG) score] and RNS test and single-fiber electromyography (SFEMG). The differences between placebo and baseline values (placebo change) were compared with the differences between 3,4-DAP and baseline or placebo values (DAP change). Seven patients with LEMS (QMG score >9) participated in the study. One patient had major side-effects with 3,4-DAP and withdrew from the study. Statistically significant efficacy was noted with DAP change (N = 13) compared with placebo change (N = 7) according to the subjective symptoms score (P = 0.01), LEMS classification (P < 0.001), muscle strength score (P < 0.006), QMG score (P = 0.02), and CMAP (P = 0.03). For long-term treatment, 2 patients preferred 3,4-DAP, 1 chose guanidine hydrochloride, 1 preferred pyridostigmine, and 2 chose no treatment. A randomized, double-blind, cross-over drug trial of 3,4-DAP showed significant efficacy over placebo in patients with LEMS. As a long-term treatment, however, not all patients preferred this drug.
- Published
- 2009
- Full Text
- View/download PDF
11. Long-lasting in vivo inotropic effects of the K(+) channel blocker 3,4-diaminopyridine during fatigue-inducing stimulation.
- Author
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Van Lunteren E, Moyer M, and Pollarine J
- Subjects
- 4-Aminopyridine pharmacology, Amifampridine, Animals, Electric Stimulation, Evoked Potentials, Motor drug effects, Isometric Contraction, Rats, Rats, Sprague-Dawley, 4-Aminopyridine analogs & derivatives, Cardiotonic Agents, Muscle Fatigue physiology, Potassium Channel Blockers pharmacology
- Abstract
Blocking K(+) channels with aminopyridines enhances muscle contractile performance in vitro, but the improvements are relatively short-lasting during fatigue-inducing stimulation. We hypothesized that in vivo inotropic actions persist over long periods of fatigue-inducing stimulation. The effects of 3,4-diaminopyridine (DAP) were evaluated for rat extensor digitorum longus (EDL) muscle. DAP increased twitch force by 105%. There was a significant leftward shift in the force-frequency relationship, with force values being increased at frequencies up to and including 20 HZ. During repetitive fatigue-inducing 20-HZ stimulation, DAP-induced force increases were large and persisted significantly for at least 30 minutes. Thus, DAP substantially improves contractile performance of EDL muscle in vivo for much longer periods during fatigue-inducing contractions than in vitro. These data provide support for a potential role for aminopyridines as inotropic agents in applications such as functional electrical stimulation, in which low to medium stimulation frequencies are typically utilized.
- Published
- 2008
- Full Text
- View/download PDF
12. Myasthenia gravis and Lambert-Eaton myasthenic syndrome in the same patient.
- Author
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Sha SJ and Layzer RB
- Subjects
- 4-Aminopyridine analogs & derivatives, 4-Aminopyridine therapeutic use, Adolescent, Amifampridine, Cholinesterase Inhibitors therapeutic use, Electrodiagnosis methods, Female, Humans, Lambert-Eaton Myasthenic Syndrome diagnosis, Lambert-Eaton Myasthenic Syndrome therapy, Myasthenia Gravis diagnosis, Myasthenia Gravis therapy, Potassium Channel Blockers therapeutic use, Pyridostigmine Bromide therapeutic use, Thymectomy methods, Lambert-Eaton Myasthenic Syndrome complications, Myasthenia Gravis complications
- Abstract
An 18-year-old-woman developed symptoms of generalized myasthenia gravis (MG). Antibodies to the acetylcholine receptor were found in her serum, but electrodiagnostic testing showed abnormalities typical of the Lambert-Eaton myasthenic syndrome (LEMS). Following thymectomy, the thymus gland showed thymic hyperplasia typical of MG, and the patient responded to treatment with 3,4-diaminopyridine and pyridostigmine. There have been few reports in the literature of MG and LEMS coexisting in the same patient. In this case, electrodiagnostic tests, antibody studies, thymus pathology, and response to treatment suggest that both disorders contributed to the patient's symptoms. Thymic hyperplasia, so far only known to be associated with MG, provides strong evidence that both diseases were symptomatic.
- Published
- 2007
- Full Text
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13. Improvement of dy/dy dystrophic diaphragm by 3,4-diaminopyridine.
- Author
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van Lunteren E and Moyer M
- Subjects
- 4-Aminopyridine analogs & derivatives, Amifampridine, Animals, Disease Models, Animal, Electric Stimulation methods, Homozygote, In Vitro Techniques, Isometric Contraction drug effects, Laminin deficiency, Male, Mice, Muscle Contraction drug effects, Muscle Fatigue drug effects, Stress, Mechanical, Time Factors, 4-Aminopyridine pharmacology, Diaphragm drug effects, Diaphragm physiopathology, Muscular Dystrophy, Animal physiopathology, Potassium Channel Blockers pharmacology
- Abstract
Concerns have been raised that inotropic agents may worsen function of dystrophic muscle due to structural fragility. Studies tested the hypothesis that force increments elicited by potassium (K(+)) channel blockade can be maintained during the course of repetitive stimulation. In vitro twitch force of dy/dy dystrophic mouse diaphragm was significantly lower than normal (796 versus 1271 g/cm(2)). 3,4-Diaminopyridine (DAP) increased twitch force of dystrophic diaphragm by 111 +/- 12% (P <.0001) and increased force at stimulation frequencies of 5-50 Hz by 41-77%. During fatigue-inducing stimulation, force augmentation by DAP was well maintained in dystrophic muscle throughout 25 Hz (P =.0047) and 50 Hz (P =.0059) stimulation. These findings indicate that the K(+) channel blocker DAP augments the force of dystrophic muscle to values close to that of normal muscle over a range of stimulation frequencies. Furthermore, these functional increments can be achieved without causing force to eventually deteriorate below that of untreated dystrophic muscle during fatiguing stimulation. It is possible that DAP may be useful for the clinical management of a variety of disorders causing muscle weakness., (Copyright 2002 Wiley Periodicals, Inc.)
- Published
- 2002
- Full Text
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14. Effect of 3,4-diaminopyridine on the time course of decay of compound muscle action potential augmentation in the Lambert-Eaton myasthenic syndrome.
- Author
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Maddison P, Newsom-Davis J, and Mills KR
- Subjects
- 4-Aminopyridine therapeutic use, Action Potentials drug effects, Adult, Aged, Amifampridine, Female, Fingers, Humans, Male, Middle Aged, Muscle Contraction physiology, Reaction Time, 4-Aminopyridine analogs & derivatives, Lambert-Eaton Myasthenic Syndrome drug therapy, Lambert-Eaton Myasthenic Syndrome physiopathology, Muscle, Skeletal drug effects, Muscle, Skeletal physiopathology
- Abstract
3,4-Diaminopyridine (3,4-DAP) is known to be beneficial in the symptomatic treatment of the Lambert-Eaton myasthenic syndrome (LEMS). The effects of 3,4-DAP on the decay of postexercise augmentation were observed in 6 patients with LEMS. After 10 s maximal voluntary contraction, the amplitude of the compound muscle action potential (CMAP) recorded from abductor digiti minimi decayed exponentially after an initial rise. The rate of decay in CMAP amplitude was increased after treatment with 3,4-DAP, suggesting that this drug has an effect on the efflux of calcium ions from the presynaptic nerve terminal.
- Published
- 1998
- Full Text
- View/download PDF
15. Single-fiber electromyography improvement with 3,4-diaminopyridine in Lambert-Eaton myasthenic syndrome.
- Author
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Kim DS, Claussen GC, and Oh SJ
- Subjects
- 4-Aminopyridine administration & dosage, Aged, Amifampridine, Humans, Lambert-Eaton Myasthenic Syndrome physiopathology, Male, Potassium Channel Blockers, 4-Aminopyridine analogs & derivatives, Electromyography methods, Lambert-Eaton Myasthenic Syndrome diagnosis, Lambert-Eaton Myasthenic Syndrome drug therapy, Muscle Fibers, Skeletal physiology
- Published
- 1998
- Full Text
- View/download PDF
16. Stimulated single-fiber electromyography in Lambert-Eaton myasthenic syndrome before and after 3,4-diaminopyridine.
- Author
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Sadeh M, River Y, and Argov Z
- Subjects
- 4-Aminopyridine therapeutic use, Adult, Amifampridine, Electromyography, Female, Humans, Lambert-Eaton Myasthenic Syndrome drug therapy, Time Factors, 4-Aminopyridine analogs & derivatives, Lambert-Eaton Myasthenic Syndrome physiopathology, Motor Endplate physiopathology
- Abstract
A patient with LEMS unrelated to cancer was studied by stimulated single-fiber electromyography (SFEMG) before and 3 months after the onset of therapy with 3,4-diaminopyridine. All end-plates showed a progressive reduction in blockings and jitter with the increase in stimulation rate. Treatment significantly corrected this feature, but the overall pattern of frequency-improved jitter remained. Such widespread finding is rare but diagnostic for Lambert-Eaton myasthenic syndrome. Stimulated SFEMG can be used to monitor therapy in such patients.
- Published
- 1997
- Full Text
- View/download PDF
17. Potassium channel blockers and impulse propagation in murine motor endplate disease.
- Author
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Bournaud R and Mallart A
- Subjects
- Action Potentials drug effects, Amifampridine, Aminopyridines pharmacology, Animals, In Vitro Techniques, Ion Channels drug effects, Mice, Mice, Inbred C3H, Motor Endplate drug effects, Neuromuscular Diseases drug therapy, Tetraethylammonium, Tetraethylammonium Compounds pharmacology, 4-Aminopyridine analogs & derivatives, Ion Channels metabolism, Motor Endplate metabolism, Neuromuscular Diseases metabolism, Neuromuscular Junction metabolism, Potassium metabolism
- Abstract
An electrophysiologic study has been performed on motor nerves of mice affected with hereditary "motor endplate disease" (MED). Bath application of potassium channel blockers, such as tetraethylammonium and 3,4-diaminopyridine, which are almost without effect on the monophasic compound action potential of normal nerves, considerably enhanced the action potential duration in nerves from mutant mice. Furthermore, external current recordings from motor endings revealed an absence of the K-dependent waveform component in MED mice, which indicates a similar K current intensity in the terminal part of the endings and in the heminode. These observations suggest that in the mutant, unlike in normal mice, K channels play a role in action potential electrogenesis. Possible relationships with paranodal dysmyelination are discussed.
- Published
- 1987
- Full Text
- View/download PDF
18. Aminoglycosides and 3,4-diaminopyridine on neuromuscular block caused by botulinum type A toxin.
- Author
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Molgó J, Lemeignan M, and Thesleff S
- Subjects
- Amifampridine, Aminoglycosides pharmacology, Animals, Kinetics, Male, Membrane Potentials drug effects, Microelectrodes, Motor Endplate drug effects, Motor Endplate pathology, Motor Endplate physiopathology, Neuromuscular Junction drug effects, Neuromuscular Junction physiopathology, Rana temporaria, 4-Aminopyridine analogs & derivatives, Aminopyridines pharmacology, Anti-Bacterial Agents pharmacology, Botulinum Toxins toxicity, Neuromuscular Junction pathology
- Abstract
Impulse-evoked transmitter release was greatly reduced at frog neuromuscular junctions 3-20 days after botulinum type A toxin (BoTx) poisoning. The reduction in transmitter release was accompanied by an increased variability in the latency between the presynaptic spike and the release of transmitter. The aminoglycoside antibiotics amikacin, gentamycin, and bekanamycin, when applied at concentrations within their therapeutic levels, markedly enhanced the blockade of transmitter release in BoTx-poisoned junctions. 3,4-diaminopyridine strongly antagonized the effects of BoTx at early stages of poisoning, and the combined presynaptic effects of BoTx and aminoglycoside antibiotics provided that transmitter release was not completely blocked by the toxin. The antagonism was apparent at all frequencies of stimulation. Since the aminoglycoside antibiotics enhanced the neuromuscular block caused by BoTx, these drugs should be avoided in patients suspected of poisoning by this toxin.
- Published
- 1987
- Full Text
- View/download PDF
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