[Presynaptic receptor systems in central noradrenergic neurons]

Slices of rat occipital cortex, hypothalamus or cerebellar cortex were stimulated either electrically or by high potassium (in few experiments by tyramine). 1. Electrical or potassium stimulation elicit physiologically noradrenaline release in contrast to tyramine. 2. Stimulation-induced overflow of tritium, reflecting noradrenaline release, was diminished by a) alpha-adrenoceptor agonists, b) morphine and enkephaline, c) prostaglandin E1. The effect of agonists was abolished only by specific antagonists. Metabolism of 3H-noradrenaline was unchanged. 3. It is concluded that transmitter release from the noradrenergic neurones of several brain areas is modulated by drugs acting on alpha-adrenoceptors, opiate receptors and prostaglandin receptors. In contrast to other tissues there was no evidence obtained for presynaptic dopamine, beta-, muscarine, nicotine and angiotensin receptors. It seems likely that the receptors, involved in the modulation of noradrenaline release, are located at the noradrenergic nerve ending themselves, i.e. that they are presynaptic receptors.