Modulation of 5-hydroxytryptamine release by presynaptic inhibitory ?2-adrenoceptors in the human cerebral cortex

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Abstract
Slices and synaptosomes from human cerebral cortex (which had to be removed to reach deeply located tumours) and, for comparison, synaptosomes from guinea-pig and rat cerebral cortex were preincubated with [3H]5-hydroxytryptamine and superfused with physiological salt solution containing an inhibitor of 5-hydroxytryptamine uptake. The effects of α-adrenoceptor agaonists and antagonists on the electrically (slices) or potassium-evoked (synaptosomes) tritium overflow were studied. In human cerebral cortical slices, the electrically-evoked [3H] overflow was inhibited by noradrenaline (pIC25 value: 6.35); the non-selective α-adrenoceptor antagonist phentolamine, at a concentration of 0.32 μmol/l, strongly antagonized the inhibitory effect of noradrenaline (apparent pA2 value: 8.19) but did not affect the evoked overflow by itself. In synaptosomes from humans, guinea-pigs and rats, noradrenaline also inhibited the K+-evoked[3H] overflow in a concentration dependent manner; the α2-adrenoceptor clonidine (1 μmol/l), but not the α1-adrenoceptor agonist methoxamine (1 μmol/l), mimicked the effects of noradrenaline; the effect of noradrenaline (0.3 μmol/l) was abolished by the α2-but not by the α1-adrenoceptor antagonist prazosin (1 μmol/l). It is concluded that release-inhibiting adrenoceptors of the α2-subtype exist on 5-hydrpxytryptamine terminals innervating the cerebral cortex in human and guinea-pig brain.

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