ORIGINAL ARTICLE Nesfatin-1 Influences the Excitability of Paraventricular Nucleus

Recent attempts to find novel molecules involved with regulating appetite and energy balance have identified nesfatin-1 as a potent inhibitor of feeding activity (1). This peptide, arising from cleavage of the calcium-binding protein nucleobindin2, is expressed in many hypothalamic nuclei, including the paraventricular (PVN), arcuate, lateral hypothalamic and supraoptic nuclei (1). Significantly, in starved rats, nesfatin-1 levels decreased only in the PVN, a nucleus with a well known association with the control of feeding behav-iour and metabolism (2, 3). These data identify the PVN as a loca-tion where signals associated with the depletion of energy reserves are received, resulting in the inhibition of the synthesis of this satiety signal (1). Although the PVN has been identified as a source for nesfatin-1, to date, no information is available regard-ing the roles of nesfatin-1 in controlling the excitability of the neurones in this vital hypothalamic autonomic control centre. Therefore, using whole-cell patch-clamp recordings from PVN neurones in rat brain slices, we performed experiments examining the effect of nesfatin-1 on the membrane potential and excitability of PVN neurones. Materials and methods Slice preparatio