Effects of 4-aminopyridine on neuromuscular transmission
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Cited by (140)
4-Aminopyridine ameliorates mobility but not disease course in an animal model of multiple sclerosis
2013, Experimental NeurologyCitation Excerpt :Therefore it may be speculated that 4-AP induces the expression of ion channels that facilitates action potential conduction in demyelinated fibers. Alternative mechanisms of actions of 4-AP including increased presynaptic transmitter release, which in turn enhance postsynaptic response, have been discussed (Kim et al., 1980; Lundh, 1978; Smith et al., 2000). The finding that 4-AP potentiates neuromuscular transmission by targeting the voltage-activated Ca2 + channel β subunit raises the possibility that 4-AP may directly stimulate Ca2 + channel in addition to its effect on KV channels thereby exerting synergistic effects (Wu et al., 2009).
The Safety Profile of Dalfampridine Extended Release in Multiple Sclerosis Clinical Trials
2012, Clinical TherapeuticsCitation Excerpt :Although it has been extensively used for the investigation and characterization of potassium channels in laboratory studies for many decades, most of this work has involved millimolar concentrations that are not directly relevant to clinical experience, which is associated with plasma concentrations typically <1 μM. A number of laboratory studies have suggested that dalfampridine is able to relieve conduction block in demyelinated axons,9–12 as well as potentiate synaptic and neuromuscular transmission in some conditions,13–15 although the concentration dependence of these effects has not been fully elucidated. During the past 30 years, published studies have reported on the use of dalfampridine, initially in simple, immediate-release (IR) formulations, for treatment of various neurologic conditions.16–26