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Electrically evoked purine release from rat cerebral cortical slices was evaluated, using a HPLC analysis combined with radioactivity measurement of the identified fractions. Two different pools of released purines have been identified: one probably related to cell metabolism and the other strictly linked to the nervous transmission. Since a linear increase, due to the stimulation frequencies, was found for the purines released from this second pool, a possible dependence on sodium and calcium transmembrane fluxes was evaluated. Pretreatment of the slices with TTX (5 x 10(-7) M) caused only a partial inhibitory effect on purine release (50%). This effect was probably related to the drug activity on the neuronal component of slices, since TTX induces an almost complete inhibition of purine release from isolated neurons "in cultures" and does not affect it from glial cells. Verapamil (1 x 10(-4) M), a calcium-channel blocker at glial and neuronal level, and TEA (3 x 10(-2) M), a specific inhibitor of calcium-mediated potassium efflux from glial cells, administered to the slices alone or in combination, showed a partial calcium-dependence of purine release. These results suggest a glial role in modulation of electrically-evoked purine release. These cells could exert a "buffering action" that regulates the calcium-mediated potassium availability, by which neuronal activity might be influenced.
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P Di Iorio, and
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