Measurement of amino acid neurotransmitters in vestibular nucleus in albino rat by microdialysis and high pressure liquid chromatography

Abstract

The present study was performed in an attempt to identify and quantify amino acids which act as the afferent vestibular transmitter by using microdialysis technique and HPLC. Effect of electrical stimulation and lesion of vestibular nerve including effect of high potassium stimulation on amino acids release (aspartic acid, Asp: glutamic acid. Glu; serine. Ser; glutamine, Gln; glycine. Gly; taurine, Tau; alanine. Ala; y-aminobutyric acid, GABA) were investigated. It was found that electrical stimulation of vestibular nerve produced a significant increase of release Asp and Glu at p < 0.05 while no significant increase in efflux of the others was observed. In acute lesioned rats. slightly initial increase was observed in the case of Asp, Glu, Ala and Tau content with subsequent decrease found gradually following prolong sample collection. In 3 days post lesioned rats, it was found that the rats showed abnormal equilibrium and ataxic movement and there was a marked reduction in Glu, Gln, Ala and Tau levels in vestibular nuclei of the lesioned side compared to those of the contralateral side (p<0.05). In addition, it was found that after stimulating the vestibular nerve terminal with high potassium (100 mM) solution, the potassium evoked release of almost all of amino acids except glycine in lesioned rats was lower than in normal rats and the greatest decrease was observed in Glu release. In 7 days post lesioned rats, there were no significantly different in all amino acids release between lesioned and contralateral sides. However, there was also a slight trend for mean Glu levels to be decreased. While mean Asp showed a slight increasing trend and also found abnormal equilibrium and ataxic movement. These results suggest that the excitatory amino, glutamate, acts as vestibular primary afferent transmitter. Lesioning this nerve causes imbalance in neurotransmitter release which produces an abnormal equilibrium and ataxic movement, however. compensatory mechanism from other parts will play an important role in vestibular compensation.