Depolarisation-evoked release of dopamine and histamine from brain tissue and studies on presynaptic dopamine-histamine interaction.

The inhibitory dopamine (DA) presynaptic receptors which are localized on dopaminergic nerve terminals, so called DA autoreceptors, modulate the neurotransmitter release and synthesis by means of negative feedback mechanism. DA agonists decrease and DA antagonists facilitate stimulation-evoked calcium-dependent DA release. DA auto-receptors correspond to D2-subtype DA receptors. They are chemically stereoselective and their sensitivity change when exposed chronically to DA receptor blockers. It is thought that presynaptic inhibitory DA autoreceptors play crucial role in physiological regulation of the neurotransmitter release from nerve terminals. Accumulating evidence indicates that, in analogy to the dopaminergic system in the brain, histaminergic neurons take up radioactive histamine (HI), and when exposed to depolarizing stimuli, they release the neurotransmitter in a calcium-dependent manner. Recent experiments showed that exogenous HI is able to inhibit potassium-stimulated release of 3H-HI from brain slices prelabelled previously with 3H-1-histidine. A suggestion has been put forward that HI release from nerve terminals may be autoregulated by a new class of HI receptors, so called H3 autoreceptors (which are pharmacologically different from both H1 and H2 receptors), in a way very similar to dopaminergic autoregulatory mechanisms. Literature data and our own findings suggest the existence of HI receptors localized on the striatal dopaminergic nerve terminals, through which HI could modulate depolarization-evoked DA release. The inability of DA agonist (apomorphine) and DA antagonists (haloperidol and s-sulpiride) to affect the electrically-evoked 3H-HI release from the rabbit hypothalamic slices suggests that there are no DA presynaptic receptors modulating HI release.