General anesthetics and neurotransmitter release

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Actions of general anesthetics on the brain electrical activities can be differentiated two characteristic types. The first type is characterized by the suppression of the spontaneous firing of the reticular neurons in dose dependent manner. Agents that induce this type of suppression are barbiturate, halothane, and isoflurane. The other type is characterized by the enhancement of the reticular neuronal firing in the clinical doses. The anesthetics that induce this enhancement are ether, ketamine, and nitrous oxide. In the central nervous system(CNS), neurotransmitters are separated into two general classes : excitatory transmitters, such as glutamate(GLU), acetylcholine(Ach), and dopamine(DA), and inhibitory ones, such as gamma-aminobutylic acid(GABA) and glycine. To provide a neurochemical basis for the different CNS actions of anesthetics, we investigated the relation of the different types of anesthetics and the release of the different classes of neurotransmitters.We studied the e … More ffects of pentobarbital, isoflurane, ketamine, and nitrous oxide on the release of various neurotransmitters at the cerebral cortex and the striatum using the microdialysis method in rats. Pentobarbital did not affect the release of GLU, GABA, and glycine, but suppressed the striatal Ach release. Isoflurane also decreased Ach release in the cerebral cortex and the striatum. Ketamine and nitrous oxide did not change the striatal Ach release. Thus, inhibitory action of pentobarbital and isoflurane might be produced by the attenuation of the release of excitatory transmitter, Ach. We studied the changes of brain monoamines and their metabolites during nitrous oxide inhalation in rats. Nitrous oxide increased the content of 3,4-dihydroxyphenylacetic acid, the metabolite of dopamine, but not dopamine, in the cerebral cortex and the medulla, which indicated the enhancement of dopaminergic neuronal activities. The euphorigenic and emetic properties of nitrous oxide may be a reflection of the activation of dopaminergic systems. Less