| Ethanol, one of the most abused drugs, exerts its action by affecting multiple targets in the central nervous system. It has been shown to interact with almost all identified neurotransmitter systems. Some studies suggested ethanol can alter directly or indirectly the brain extracelluar concentrations of some amino acids. Acetaldehyde (AcH) is the main and primary metabolite of ethanol. It has long been suggested to be involved in a number of ethanol's pharmacological and behavioral effects, however, the role of acetaldehyde in ethanol's effects has been an extremely controversial topic. Conflicting evidence has also been published. Studies in rats, monkeys and humans have shown that the prefrontal cortex contributes to executive functioning. Or in other words, the prefrontal cortex can make set of cognitive control processes that are necessary for optimal scheduling of complex sequences of behaviour. The anterior cingulate cortex (ACC) and lateral cortex (LO) are part of the prefrontal cortex. In recent years some evidence indicates that they are closely involved in drug abuse. Studies have indicated that amino acids in the frontal cortex are also involved in the central actions of the abused drugs. The present studies, therefore, investigated the actions of ethanol and acetaldehyde on the release of some excitatory (glutamate) and inhibitory (taurine, GABA) amino acids in the ACC and LO.The role of ethanol and acetaldehyde on the release of amino acids (glutamate, taurine and GABA) in the ACC and LO were studied by using microdialysis coupled to high performance liquid chromatography (HPLC) with fluorescence detection. The results showed that both ethanol (3g/kg, i.p.) and acetaldehyde (100mg/kg), decrease glutamate release significantly, increse taurine release significantly, but have no changes to GABA at any time points assayed. The microdialysis technique followed by gas chromatography (GC) was used... |
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