Nicotine-induced release of noradrenaline from hypothalamic synaptosomes

In order to elucidate the functional role of nicotinic receptors in the hypothalamus, the drug-induced release of noradrenaline from hypothalamic synaptosomes was studied utilizing [3H]noradrenaline ([3H]NA). The release of [3H]NA from synaptosomes was significantly increased with an increase of the dose of nicotine, carbamylcholine chloride, reserpine or tyramine hydrochloride added to the medium, whereas arecoline, atropine sulfate or mecamylamine hydrochloride had no significant effect. Mecamylamine hydrochloride completely inhibited the nicotine- or carbamylcholine-induced release of [3H] at the concentration of 10(-4) M, but had on effect on the reserpine- or tyramine-induced release of [3H]NA. A high concentration of potassium in the medium which depolarizes the synaptosome membrane significantly enhanced the release of [3H]NA. These results strongly suggest that there exist nicotinic cholinergic receptors in brain synaptic regions which play an important role in the function of hypothalamus by releasing noradrenaline and that the release mechanism of noradrenaline induced by nicotine is different from that induced by reserpine and tyramine. Although the existence of postsynaptic nicotinic receptor sites could not be reled out, the present studies indicate the importance of presynaptic cholinergic receptors in the brain.