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Effects of riluzole on rat cortical neurones: an in vitro electrophysiological study
Author(s) -
Siniscalchi Antonio,
Bonci Antonello,
Mercuri Nicola B,
Bernardi Giorgio
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0700905
Subject(s) - riluzole , depolarization , electrophysiology , neuroscience , membrane potential , tetrodotoxin , chemistry , glutamate receptor , calcium in biology , cortical spreading depression , calcium , pharmacology , biophysics , anesthesia , biology , medicine , receptor , biochemistry , organic chemistry , migraine
The electrophysiological effects of riluzole on rat prefrontal and frontal cortical neurones were investigated by using both extracellular (field) and intracellular recording techniques in brain slices. Bath applied riluzole (3–200 μ m ) depressed the cortico‐cortical stimulus‐evoked field potential in a concentration‐related manner (EC 50 =29.5 μ m ). Riluzole (3–100 μ m ) reduced the tonic firing of the neocortical neurones which was caused by intracellular current injection, while it did not have any effect on the resting membrane potential and apparent input resistance of these cells. In the presence of tetrodotoxin (1 μ m ) and tetraethylammonium (30 m m ), the injection of a depolarizing current step generated a calcium spike in the neocortical neurones. Riluzole (30 μ m ) abolished this calcium‐dependent action potential. However, when the amount of the depolarizing current was increased the calcium‐dependent regenerative potential was evoked again. The depolarization of the membrane (10–20 mV) caused by brief (8–15 s) bath applications of glutamate (300 μ m –1 m m ) were not changed in the presence of riluzole (30 μ m ). It is concluded that riluzole has direct actions on rat neocortical neurones: (a) it blocks the repetitive discharge of sodium action potentials and (b) it increases the threshold for the generation of the calcium spike. These two cellular mechanisms might at least in part account for the depression of the cortico‐cortical field potential caused by this drug.British Journal of Pharmacology (1997) 120 , 225–230; doi: 10.1038/sj.bjp.0700905