Sheriff ST, Xiao C, Chance WT, Kasckow JW, Balasubramaniam A (2002) Selective lesion of neuropeptide Y (NPY)-receptor neurons in hypothalamus inhibit food intake and reduces body weight in rats. Neuroscience 2002 Abstracts 384.1. Society for Neuroscience, Orlando, FL.
Summary: Administration of NPY into hypothalamic areas elicits a most powerful feeding response in rats. The neuronal cell type mediating this orexigenic signal is not clearly understood. To determine the role of NPY-responsive neurons in feeding behavior, we selectively lesioned NPY-receptor neurons by using avidinylated saporin (Av-Sap) mixed with biotinylated NPY. Av-Sap-Biotin NPY complex (ASBN 2.5ug/5ul CSF) or saporin (2ug/4ul CSF) was injected into intracerebroventricle (ICV) of Sprague Dawley rats. Food intake (FI) and body weight was monitored for seven days. On the eighth day NPY (1ug/1ul CSF) was injected into ICV and the FI was monitored for four hours. Injection of ASBN showed a severe reduction in food intake (54%) on the seventh day in comparison to saporin-treated group. ASBN-treated group showed a decrease in the body weight by 24%. The Saporin-treated group showed little body weight reduction (4%). NPY-induced food intake was also reduced in ASBN-treated group. Immunohistochemical analysis revealed a moderate reduction of Y1 receptor (Y1R) neurons in the PVN and arcuate nucleus in this group. Loss of tyrosine hydroxylase neurons in the arcuate nucleus was observed in ASBN-treated group. These results suggest that NPY-receptor neurons may be essential for maintaining the energy homeostasis.
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