THE EFFECT OF LEAD ON DOPAMINE, GABA AND HISTIDINE SPONTANEOUS AND KCL-DEPENDENT RELEASES FROM RAT-BRAIN SYNAPTOSOMES

The effect of lead on the release of [C-14]GABA, [H-3]dopamine and [C- 14]histidine (as a precursor of histamine) was studied in synaptosomes obtained from chronically lead-treated rats and in synaptosomes with in vitro lead added. In vivo treatment of rats with lead acetate resul ts in a decrease in the K+-depolarization-dependent release of GABA an d dopamine and histidine. Lead given in vitro itself (independently of depolarizing condition) stimulated the release of previously accumula ted neurotransmitters in synaptosomes (GABA and dopamine). This effect depends on lead acetate concentration. On the other hand lead, in dif ferent concentrations, did not cause changes in the histidine release. The results show that lead can attack the synaptic neurotransmission in two ways: by depressing the Ca-KCl-evoked release of GABA, dopamine and histidine and by a selective stimulation of a spontaneous release (independent of depolarization conditions) of GABA and dopamine but n ot histidine.