Characterisation of extracellular amino acids in striatum of freely moving rats by in vivo microdialysis

Abstract

To investigate the characteristics of extracellular amino acids released from the striatum, we performed in vivo microdialysis in non-anaesthetised, freely moving rats. Amino acids were determined after precolumn derivatisation with o-phthalaldehyde by high-performance liquid chromatography and fluorescence detection. The omission of Ca2+ in the perfusion medium partially decreased the basal concentration of aspartate and glutamate. This shows that a small fraction of basal concentration of aspartate and glutamate is of neuronal origin. The effect of high K+ and veratrine stimulation was evaluated in the presence or absence of Ca2+ or tetrodotoxin (1 microM). High K+ and veratrine caused a remarkable increase in the aspartate and glutamate efflux. The omission of Ca2+ only partially decreased K(+)-stimulated aspartate and glutamate efflux. Tetrodotoxin completely antagonised veratrine-stimulated aspartate and glutamate efflux. Although glycine and taurine releases were stimulated by high K+ and veratrine, their release was not always antagonised with Ca2+ omission or tetrodotoxin inclusion. Thus, the neuronal origin of stimulated release of glycine and taurine is unclear. Although tetrodotoxin sensitivity and Ca2(+)-dependency are regarded as a basic criterion for classical neurotransmitters in microdialysis experiments, they should not be adapted to the physiological characteristics of the release of amino acids.

The voltage-gated sodium channel activator veratrine induces anxiogenic-like behaviors in rats

“…Veratrine, a sodium channel activator, evokes presynaptic glutamate release though the opening of voltage-gated sodium channels. This notion is corroborated by the findings of a microdialysis study in rats [7][8][9] and a study using rat synaptosomes [10]. Recently, we also reported that the local perfusion of veratrine in the prelimbic medial prefrontal cortex of mice increased extracellular glutamate levels [11].…”

The source of physiologically stimulated glutamate efflux from the striatum of conscious rats.

“…There is conflicting evidence concerning the origin of the extracellular glutamate measured by microdialysis. High K+ solutions lead to a parallel increase in both glutamate and aspartate, suggesting a cytoplasmic origin; however, the K+-evoked release is reduced by replacement of Ca2P with Mg2+ (Semba, Kito & Toru, 1995), which is a criterion for exocytotic release. Similarly, the origin of basal glutamate is not clear.…”

Taurine infused intrastriatally elevates, but intranigrally decreases striatal extracellular dopamine concentration in anaesthetised rats

“…These findings support the neurotransmitter/neuromodulatory role of taurine in the striatonigral pathway. However, basal release of striatal taurine has not been found to be sensitive to tetrodotoxin (Westerink et al, 1987;Semba et al, 1995).…”