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Mechanism of nerve membrane depolarization caused by grayanotoxin I
Author(s) -
Narahashi Toshio,
Seyama Issei
Publication year - 1974
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1974.sp010718
Subject(s) - depolarization , tetrodotoxin , resting potential , biophysics , chemistry , sodium , membrane potential , sodium channel , axon , voltage clamp , dissociation constant , permeability (electromagnetism) , membrane , anatomy , receptor , biology , biochemistry , organic chemistry
1. The mechanism of depolarization of squid axon membranes caused by grayanotoxin I has been studied by means of internal perfusion and voltage clamp techniques. 2. The depolarization induced by either internal or external application of grayanotoxin I was reversed by decreasing the external sodium concentration from 449 to 1 m m . 3. No depolarization was observed when both external and internal media were devoid of sodium ions, indicating that the depolarization by grayanotoxin I in normal media is due to a specific increase in resting sodium permeability. 4. The resting sodium permeability as measured by voltage clamp was increased to 1·31 × 10 −6 cm/sec by internal application of 1 × 10 −5 m grayanotoxin I, an increase by a factor of about 90. 5. The apparent dissociation constant of internally applied grayanotoxin I in increasing the resting sodium permeability was estimated to be 4·12 × 10 −5 m , and the toxin interacts with the membrane receptor on a one‐to‐one stoichiometric basis. 6. Tetrodotoxin antagonized the action of grayanotoxin I in increasing the resting sodium permeability in a non‐competitive manner.