CHOLECYSTOKININ EVOKES VASOPRESSIN RELEASE FROM PERFUSED HYPOTHALAMIC-NEUROHYPOPHYSEAL EXPLANTS

Cholecystokinin (CCK) may have a transmitter/modulator role in the hyp othalamic magnocellular neurosecretory system, In the rat, the supraop tic and paraventricular nuclei display high affinity binding for radio labelled CCK. Exogenously applied CCK depolarizes supraoptic neurons, acting at postsynaptic CCK-B type receptors. The present study evaluat ed the ability for the sulfated octapeptide of CCK (CCK-8S), which is a predominate form of this peptide in brain, to evoke release of vasop ressin from the neurohypophysis of intra-arterially perfused hypothala mic explants. 3 min applications of 1 mu M CCK-8S through the intra-ar terial perfusion medium prompted an elevation of vasopressin in sample s taken from the neurointermediate lobe in 10 of 14 preparations. Vaso pressin levels rose from undetectable baseline values to a peak of 29. 5 +/- 6.7 pg/ml (mean +/- S.E.M). This response was dose-dependent and was abolished by pituitary stalk transection (5/5 explants). Locally applied CCK-8S (25-200 pmol) through bilateral infusions onto the vent ral surface of the supraoptic nucleus also induced a dose-dependent re lease of vasopressin (5/7 explants). These observations suggest that C CK can act at receptors located on (or near) the somata of supraoptic nucleus neurons to induce neuronal discharges that are conducted to th e neural lobe where they evoke release of vasopressin from neurohypoph ysial axon terminals.