Output of [14C]adenine nucleotides and their derivatives from cerebral tissues. Tetrodotoxine-resistant and calcium ion-requiring components

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Abstract
1. Neocortical tissues, exposed briefly to [14C]adenine and containing over 98% of their14C as adenine nucleotides, when superfused with glucose–bicarbonate salines released about 0.1% of their14C content/min to the superfusate. 2. Addition of unlabelled adenosine to the superfusing fluid increased the14C output three- to four-fold; half-maximal increase was given by about 40μm-adenosine, and reasons are adduced for considering the activity of adenosine kinase to be a major factor in conditioning the14C output. Adenosine similarly increased the enhanced14C output caused by electrical excitation of the superfused tissue; it brought about only a small increase in tissue glycolysis. 3. Output of14C from the [14C]adenine-labelled tissues was increased when Ca2+was omitted from the superfusing fluids, but electrical stimulation did not then liberate more14C. Nevertheless, such tissues still responded to electrical stimulation by increased glycolysis, and their14C output again became susceptible to increase by electrical stimulation when Ca2+was restored. 4. The six-fold increase in tissue glycolysis caused by electrical excitation was almost completely inhibited by tetrodotoxin at 0.1μm and above, but this was associated with about 50% inhibition only in the output of14C from tissues preincubated with [14C]adenine. The14C-labelled compounds of which output was most inhibited by tetrodotoxin were adenosine, inosine and hypoxanthine whereas output in a nucleotide fraction was little affected.