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چکیده:  

Carbon dioxide (CO2) and ether are administered as light anesthetized agents. However, little is known about side effects of its actions. In addition, in all our previous works on regulatory mechanisms of hypothalamus in food intake including the effect of PVN D1 and D2 dopamine receptors and glucosensitive neurons, the drug injections were performed under brief ether anesthesia.  In current study, we address the hypothesis which demonstrates that CO2 and ether as light anesthetic agents affect the stimulatory effect of PVN dopamine receptors and glucosensitive neurons in feeding behavior.

Male Wistar rats were implanted with guide cannula directed to the PVN. Glucose (0.8 µg), SKF38393 (D1 agonist, 0.5 µg), quinpirole (D2 agonist, 0.3 µg) and saline (0.3 µl) were microinjected. Food intake was measured over 1 hour. Our results showed that CO2 but not ether decreased food intake compared to intact animals. The PVN injections of glucose, SKF38393 and quinpirole increased food intake under brief anesthetized ether. In contrast, the PVN microinjected glucose- and dopamine receptors agonists-induced food intake inhibited under light CO2 anesthesia. We suggest that light anesthetized CO2 and ether affect food intake. This effect is probably mediated, at least in part, by PVN glucosensing neurons and dopamine receptors

نوع مطالعه: Original | موضوع مقاله: Behavioral Neuroscience
دریافت: ۱۳۹۶/۱/۲۸ | پذیرش: ۱۳۹۶/۵/۸ | انتشار: ۱۳۹۷/۳/۵

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