{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T11:56:07Z","timestamp":1791028567760,"version":"4.1.0"},"reference-count":58,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,1,23]],"date-time":"2013-01-23T00:00:00Z","timestamp":1358899200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2013,3]]},"abstract":"<jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>In mammals, satiety\u2010controlling mechanisms develop before the switch from ingestive behaviour from milk suckling to regular food intake; however, the underlying mechanisms are currently unknown.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We show that absence of the cholecystokinin\u20101 (CCK\u20101) receptor gene significantly increases suckling pup weight, regardless of maternal genotype in mice.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>CCK\u20101 receptor expression was observed in satiety\u2010controlling regions such as the hypothalamus, caudal brainstem, nodose ganglion and pylorus, which is consistent with suggested receptor function in adults, whereas corresponding receptor expression was low to non\u2010existent at pre\u2010weanling stages.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Third ventricle ependymal tanycyte\u2010like cells transiently expressed CCK\u20101 receptors at critical developmental stages, and gastrointestinal milk filling upregulated cFos expression in these cells.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Localized blocking of ependymal CCK\u20101 receptors was sufficient to produce overweight pups, suggesting that the ependymal CCK\u20101 receptor is an infant\u2010specific satiety controller.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><jats:p><jats:bold>Abstract\u2002<\/jats:bold> Cholecystokinin (CCK) is a hypothetical controller for suckling and infancy body weight, although the underlying mechanisms remain unclear. Therefore, the present study analysed the mechanisms using mice lacking the CCK\u20101 receptor (CCK1R\u2013\/\u2013). Although CCK1R\u2013\/\u2013 mice displayed normal weights at birth and adulthood, CCK1R\u2013\/\u2013 pups had enlarged adipocytes and were overweight from the first to second week after birth, regardless of maternal genotype. The lacZ reporter gene assay and\/or calcium imaging analysis demonstrated that CCK\u20101 receptors were abundant in satiety\u2010controlling regions such as the hypothalamus, brainstem, nodose ganglion and pylorus in adults, whereas these signals were few to lacking at pre\u2010weanling stages. At postnatal day (PD) 6, the increase in cFos expression in the medullary nucleus tractus solitarius was similarly triggered by gastrointestinal milk\u2010 or saline filling in both genotypes, further indicating immature CCK\u20101 receptor function in an ascending satiety\u2010controlling system during infancy. Conversely, third ventricle ependymal tanycyte\u2010like cells expressed CCK\u20101 receptors with expression peaking at PD6. At PD6, wild\u2010type but not CCK1R\u2013\/\u2013 mice had increased cFos immunoreactivity in ependymal cells following gastrointestinal milk filling whereas the response became negligible at PD12. In addition, ependymal cFos was not increased by saline filling, indicating that these responses are dependent on CCK\u20101 receptors, developmental stage and nutrients. Furthermore, body weights of wild\u2010type pups were transiently increased by blocking ependymal CCK receptor function with microinjection of a CCK\u20101 antagonist, but not a CCK\u20102 antagonist. Hence, we demonstrate <jats:italic>de novo<\/jats:italic> functions of ependymal CCK\u20101 receptors and reveal a new aspect of infant satiety\u2010controlling mechanisms.<\/jats:p>","DOI":"10.1113\/jphysiol.2012.247676","type":"journal-article","created":{"date-parts":[[2012,12,25]],"date-time":"2012-12-25T04:24:55Z","timestamp":1356409495000},"page":"1295-1312","source":"Crossref","is-referenced-by-count":16,"title":["Infant satiety depends on transient expression of cholecystokinin\u20101 receptors on ependymal cells lining the third ventricle in 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