Role of carbon dioxide fixation, blood aspartate and glutamate in the adaptation of amphibian brain tissues to a hyperosmotic internal environment.

Mechanisms have been examined by which hyperosmotic blood plasma might elevate the levels of aspartate and glutamate in the brain of the toad Bufo boreas. CO2 fixation was assessed by two in vivo methods using [2-14 C]glucose injected intracisternally. Thirty minutes after injection, the 14C labeling of glutamate and aspartate was more than 100 times greater in brain than in liver. In brain tissues, 40 + % of 14C atoms appeared to be incorporated into aspartate via the pyruvate carboxylase pathway. Brain tissues of control toads and toads adapting or adapted to hyperosmotic plasma osmolality revealed no differences in the rate of CO2 fixation as related to glucose utilization or tissue pool sizes of glutamate and aspartate. Elevated levels of these amino acids in blood plasma preceded increases in brain tissues. Carbon atoms required during hyperosmotic adaptation for expansion of amino acid pools in brain tissues may, in part, originate from amino acids in blood but apparently not from CO2 fixation in brain.