Depression of Excitatory Amino Acid Neurotransmitters in Brain During Carbon Dioxide Narcosis, Anesthesia, and Hypoxia: Glutamic Acid and Aspartic Acid

Abstract

Application of the excitatory amino acid neurotransmitters aspartic acid and glutamic acid to respiratory center neurons in the medulla causes an increase in neuron output (Toleikis et al., 1979). When neurotransmitter amino acids are delivered to the surface of the medulla by means of ventriculocisternal perfusion or application directly to the ventral surface, glutamic acid increases ventilation and gammaaminobutyric acid (GABA) depresses ventilation (Hoop et al., 1985; Systrom et al., 1985; Gatti et al., 1985). The present investigation was undertaken to determine whether hypercapnia at levels associated with CO2 narcosis in man is accompanied by changes in the concentration of endogenous amino acid neurotransmitters in dorsal and ventral medulla of the brain. The aim of this study is to provide support for the hypothesis that reduction of glucose-derived endogenous excitatory amino acid neurotransmitters and elevation of depressant amino acid neurotransmitters contribute to impairment and even depression of the ventilatory response to carbon dioxide at higher inhaled CO2 concentrations (Eisele et al., 1967).