Open AccessInhibition by Intravenously Administered Sodium Bicarbonate of Neuronal Activity in Medial Vestibular Nucleus Neurons
Author(s) -
Atsuhiko Kawabata,
Takuzo Kishimoto,
Hisamitsu Ujihara,
Masashi Sasa,
Shuji Takaori
Publication year - 1990
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.54.383
Subject(s) - medial vestibular nucleus , chemistry , premovement neuronal activity , vestibular nuclei , vestibular system , sodium bicarbonate , glutamate receptor , bicarbonate , pharmacology , lateral vestibular nucleus , chloralose , anesthesia , medicine , endocrinology , cats , neuroscience , biology , biochemistry , receptor , organic chemistry
The effects of 7% sodium bicarbonate on medial vestibular nucleus (MVN) neurons were examined to elucidate the mechanism underlying its anti-vertigo action, using alpha-chloralose-anesthetized cats. Intravenous injection of the drug at 1, 2 and 4 ml/kg every 10 min dose-dependently inhibited rotation- and glutamate-induced firing of type 1 neurons, although a low dose of the drug enhanced firing in a few neurons. However, microiontophoretic application of bicarbonate ions did not inhibit rotation- or glutamate-induced firing. After injection of the drug, the Po2 level in arterial blood did not differ from previous levels, but the bicarbonate ion levels dose-dependently increased concomitantly with an increase in pH, as compared with previous levels. These results suggest that the intravenous injection of 7% sodium bicarbonate directly inhibits the neuronal activity of the MVN, although the lower dose may enhance neuronal activity by acting on the peripheral vestibule.