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Depression of synaptic transmission by diphenylhydantoin
Author(s) -
Yaari Yoel,
Pincus Jonathan H.,
Argov Zohar
Publication year - 1977
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410010405
Subject(s) - postsynaptic potential , neurotransmission , chemistry , biophysics , neuroscience , calcium , neuromuscular transmission , stimulation , synapse , membrane potential , phenytoin , synaptic augmentation , anesthesia , biology , biochemistry , medicine , epilepsy , receptor , organic chemistry
Diphenylhydantoin (phenytoin, DPH) depresses synaptic transmission at the frog neuromuscular synapse by presynaptic and postsynaptic mechanisms. In normal Ringer's solution the amplitude of the neurally evoked end‐plate potentials and their quantal content are reduced. Somewhat paradoxically, miniature end‐plate potential (mepp) frequency is increased by the drug. These effects could result if DPH blocked both calcium transport at the axonal membrane and intracellular calcium sequestration. Mepp amplitude is reduced, and DPH also induces nerve conduction block at high rates of stimulation. The relevance of these effects to the anticonvulsive activity of DPH is discussed.