The behavioral and neuroendocrine effects of the adipose tissue-derived circulating protein, leptin, appear to be mediated by the hypothalamus. We have investigated whether the leptin receptor gene is expressed in hindbrain regions known to be involved in the processing of satiety and energetic signals of peripheral origin. In the mouse, gene expression was detected in the nucleus of the solitary tract, lateral parabrachial nucleus, and medullary reticular nucleus and diffusely elsewhere by in situ hybridization. Receptor messenger RNA in these neuronal areas consisted largely, if not exclusively, of the long splice variant, Ob-Rb. Presumed short receptor splice variants were abundantly expressed in the leptomeninges and the choroid plexus of the fourth ventricle. Similar levels of leptin receptor gene expression were present in the hindbrain of lean and obese (ob/ob) mice. The leptin receptor gene was expressed comparatively weakly in the nucleus of the solitary tract of the rat and was not detectable in the lateral parabrachial nucleus. However, by contrast with the mouse, a high level of receptor gene expression was observed in the cerebellum of the rat. A number of rodent hindbrain sites expressing the leptin receptor gene are activated by circulating leptin and may form a monitoring/signaling pathway to complement more direct hypothalamic interactions.