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Potassium channel modulation by the pseudopeptide ochratoxin A in rat nerve fibers
Author(s) -
Carratú MariaRosaria,
Belmadani Abdelhak,
Cuomo Vincenzo,
Creppy Edmond Ekué
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980801)53:3<312::aid-jnr5>3.0.co;2-d
Subject(s) - pronase , chemistry , biophysics , conductance , potassium , sodium channel , depolarization , sodium , biochemistry , trypsin , biology , enzyme , mathematics , organic chemistry , combinatorics
Abstract Ochratoxin A (OTA), a naturally occurring mycotoxin produced by Aspergillus and Penicillium genera, blocks anion conductance in Madin‐Darby canine kidney (MDCK) cells and reduces the potassium concentration gradient in the same cells. So far, a direct effect of OTA on cation channels has not been reported. Experiments were then designed to explore the OTA action on ion channels of rat nerve fibres. Voltage clamp technique has shown that OTA (0.1–1 μM) does not significantly affect sodium current in the intact myelinated axon. After paranodal demyelination (using 0.2% pronase) large K + outward and K + tail currents are elicited upon depolarization and repolarization. OTA application on pronase treated fibres produces the following effects: 1) reduction in the amplitude of the tail current with a negligible effect on the time constant of its fast decaying component (modified by pronase application); 2) reduction in potassium conductance to 30% of the control value (i.e., the value in pronase‐treated fibres); and 3) reduction in the leakage conductance. Our findings point at the paranodal region of myelinated nerve fibres as a target for the neurotoxic pseudopeptide OTA found as contaminant in food. The uncleaved OTA is effectively acting since pronase fails to cleave it into phenylalanine and OT alpha. J. Neurosci. Res. 53:312–317, 1998. © 1998 Wiley‐Liss, Inc.