| Summary: | 碩士 === 中國醫藥學院 === 醫學研究所 === 91 === Our previously study indicated that the inhibitory effect of adenosine on feeding is not mediated by oxytocin neurons. The purpose of the present study was to investigate the role of NPY neurons in adenosine receptor agonist-induced anorexia. We found that intracerebral co-administration of 10 μg/5ul N6-cyclopentyladenosine（CPA, A1 receptor agonist）or 1 μg/5ul CGS21680（CGS, A2a receptor agonist）with 10 μg/5ul NPY did not block the inhibitory effect of CPA or CGS-on food intake in overnight fasted rats（P＞0.05）. Another set of animals were sacrificed 2h after icv injection of CPA or CGS（1, 5 and 10 μg）and brain tissues were subjected to immunocytochmistry of NPY . The results showed that adenosine failed to alter NPY levels in the hypothalamic Arcuate（ARC）and Paraventricular（PVN）nuclei. These data reveal that the anorectic effect of adenosine is not mediated by NPY neurons. In order to investigate whether NPY cell bodies express adenosine receptors, double-label immunocytochemistry was performed in brain tissues obtained from icv cholchicin-treated animals. The result showed that although NPY was in close apposition with adenosine receptor immunoreactivity, there was no evidence of colocalization of both antigens. To further investigate the role of endogenous adenosine in the modulation of food intake, satiated rats were treated icv with 1, 5 or 10 μg DPCPX（A1 receptor antagonist）or ZM-2413851（ZM, A2a receptor antagonist）. I found that 10ug DPCPX significantly increased food intake（P＜0.05）, but ZM failed to alter the feeding behavior （P＞0.05）. The data suggest that endogenous adenosine A1 receptor plays a role in normal feeding behavior and adenosine via A1 receptors may have the same target as NPY in PVN. However, exogenous adenosine-induced anorexia is not mediated by orexigenic NPY neurons.
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