MOTIVATION, EMOTION, FEEDING, DRINKINGLesion of area postrema attenuated hyperphagic responses to glucoprivation, but not transcriptional activation of the neuropeptide Y gene in ratsOzawa, Yoshiharua; Arima, Hiroshia; Banno, Ryoichia; Ito, Yoshihiroa; Goto, Motomitsua; Morishita, Yoshiakia; Sugimura, Yoshihisaa; Ozaki, Nobuakia; Nagasaki, Hiroshib; Oiso, YutakaaAuthor Information Departments of aEndocrinology and Diabetes bMetabolic Medicine, Nagoya University School of Medicine, Showa-ku, Nagoya, Japan Correspondence to Hiroshi Arima, Department of Endocrinology and Diabetes, Nagoya Graduate University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan Tel: +81 52 744 2142; fax: +81 52 744 2206; e-mail: [email protected] Received April 28, 2012 Accepted May 1, 2012 NeuroReport: August 1, 2012 - Volume 23 - Issue 11 - p 673-675 doi: 10.1097/WNR.0b013e3283556676 Buy Metrics Abstract The area postrema (AP) is a circumventricular organ that lacks a blood–brain barrier. Previous studies have shown that the lesion of AP (APX) attenuated hyperphagic responses to glucoprivation. As the orexigenic neuropeptide Y (NPY) neurons have been implicated in the regulation of food intake, we examined whether the activation of NPY neurons by glucoprivation is mediated through the AP as well. In agreement with previous studies, hyperphagic responses to an injection of 2-deoxy-D-glucose that blocks glucose utilization were significantly attenuated in the APX group compared with the sham-operated (Sham) group. However, the expression levels of NPY heteronuclear RNA, a sensitive indicator for the gene transcription, were significantly increased in the arcuate nucleus by a 2-deoxy-D-glucose injection in both the APX and the Sham groups, and there were no significant differences in the values between groups. These data suggest that the hyperphagic response to glucoprivation, but not the activation of NPY gene transcription in the arcuate nucleus, was mediated through the AP in the hindbrain. © 2012 Lippincott Williams & Wilkins, Inc.