INVOLVEMENT OF CHOLECYSTOKININ RECEPTOR TYPES IN PATHWAYS CONTROLLINGOXYTOCIN SECRETION

1 Intravenous administration of cholecystokinin (CCK) results in a tra nsient activation of oxytocin neurones in the rat, and hence to oxytoc in secretion: this activation is followed by expression of c-fos mRNA and of Fos-like immunoreactivity (Fos-LI) in magnocellular oxytocin ne urones. Fos-like immunoreactivity is also induced in the regions of th e brainstem that are thought to relay information from the periphery t o the hypothalamus. 2 Administration of the selective CCK(A) receptor antagonist MK-329, but not the CCK(B) receptor antagonist L-365,260, p rior to CCK injection, prevented oxytocin release as measured by radio immunoassay and oxytocin neuronal activation as measured by electrophy siology and by the lack of induction of c-fos mRNA. 3 MK-329 abolished the release of adrenocorticotrophic hormone (ACTH) following injectio n of CCK. 4 MK-329 prevented the expression of Fos-LI in the hypothala mic magnocellular nuclei and in the area postrema and dorsal vagal com plex of the brainstem. 5 L-365,260 had no effect on the expression of Fos-LI in the brainstem, but attenuated that seen in the hypothalamic magnocellular nuclei. 6 We conclude that CCK acts on CCK(A) receptors, either in the area postrema or on peripheral endings of the vagus ner ve, to cause the release of hypothalamic oxytocin and ACTH. Informatio n may be carried to the hypothalamus in part by CCK acting at CCK(B) r eceptors.