Abstract
Most of the major anticonvulsants including phenytoin, phenobarbital and carbamazepine are known to have presynaptic actions that affect evoked transmitter release (1–6). Most of these substances also have postsynaptic actions. In the case of phenytoin, the presynaptic actions are of special interest because it has long been held that the depression or elimination by phenytoin of post-tetanic potentiation is the experimental analog of its anticonvulsant properties (7) and post tetanic potentiation is very much a result of presynaptic effects (8). We have studied the actions of phenytoin at the neuromuscular synapse and found that its actions there were complex and were dependent on the calcium concentration of the external media (5–7). In normal media containing 1.8mM calcium, phenytoin inhibited evoked release. In low calcium (0.2mM) media, the drug increased evoked release. The drug was found to increase spontaneous release, which is to say it increased the frequency of miniature endplate potentials (mepps), irrespective of the calcium concentration of the media. In normal media it did so and in media containing no added calcium but with EGTA it also increased mepp frequency. To explain these differing effects, it was suggested that phenytoin reduced calcium influx during stimulation and also inhibited some portion of the calcium sequestration or extrusion process.
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© 1986 Martinus Nijhoff Publishing, Boston
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Pincus, J. (1986). Phenytoin, Transmitter Release and Calcium Flux. In: Rahamimoff, R., Katz, B. (eds) Calcium, Neuronal Function and Transmitter Release. Topics in the Neurosciences, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2307-5_27
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DOI: https://doi.org/10.1007/978-1-4613-2307-5_27
Publisher Name: Springer, Boston, MA
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