The focus of the present review is to reconsider the role of endogenous norepinephrine (NE) in brain, specifically within the hypothalamic paraventricular nucleus (PVN), with regard to its potential role in eliciting eating or satiety. The PVN is innervated by NE fibers and is a site at which infusion of exogenous NE elicits eating at low doses. Two subtypes of alpha-adrenergic receptors within the PVN exert antagonistic actions on eating in the rat: activation of PVN alpha(2)-adrenoceptors increases eating, whereas activation of PVN alpha(1)-adrenoceptors suppresses eating. Pharmacologic manipulations that elevate NE can increase or decrease food intake, depending on the site and type of NE manipulation. Certain antiobesity drugs may act to reduce eating via release of NE and subsequent activation of alpha(1)-adrenoceptors. The PVN exhibits a reliable rhythm in the secretion of endogenous NE over the dark-and-light cycle, and this rhythm may interact with changes in numbers of PVN alpha(1)- and alpha(2)-adrenoceptors to modulate eating during the dark-and-light cycle. Push-and-pull and microdialysis studies indicate that NE secretion is strongly associated with eating, particularly at the start of the dark phase. The present review considers potential interactions of NE with substances such as leptin and neuropeptide Y that alter eating.