INVOLVEMENT OF CHOLECYSTOKININ IN FOOD-INTAKE .3. ESTRADIOL POTENTIATES THE INHIBITORY EFFECT OF CHOLECYSTOKININ OCTAPEPTIDE ON FOOD-INTAKE IN OVARIECTOMIZED RATS

The role of cholecystokinin in a model of hypophagia, oestradiol-treated ovarlectomized rats, was investigated, implantation of oestradiol-filled constant-release implants in rats made obese by ovarlectomy potentiated the inhibitory effect of intraperitoneal injection of cholecystokinin octapeptide on food intake after 24 h of food deprivation. The alterations in the concentration of cholecystokinin in plasma and of cholecystokinin-like immunoreactivity in cerebrospinal fluid produced by deprivation of food for 24 h and subsequent food intake for 1 h were unaffected by the oestradiol treatment as was the amount of food consumed during 1 h. Oestradiol-treated rats deprived of food for 6 h, however, consumed less food during a 15-min test than controls. Treatment with oestradiol blunted the decrease in the concentration of cholecystokinin-limke immunoreactivity in the cerebrospinal fluid in response to 6 h of food deprivation. No alterations in the concentration of cholecystokinin in plasma occurred after this period of food deprivation and subsequent feeding during 15 min in either oestradiol-treated or control rats. Thus, treatment with oestradiol enhances responsivity to exogenous cholecystokinin octapeptide and changes the response of endogenous levels of cholecystokinin-like immunoreactivity in the cerebrospinal fluid to a short period of food deprivation. It is suggested that these effects are caused by an action of oestradiol on cholecystokinin pathways in the brain. The results support the suggestion that hunger in the rat is inversely related to the decrease in the concentration of cholecystokinin-like immunoreactivity in the cerebrospinal fluid.