Science Focus
original post »The regulation of appetite by the nervous system is a hot area of research due to the raging obesity/diabetes epidemic. An international team of researchers interested in the subject—none of whom hail from either Colorado or Amsterdam—astutely noticed that "the phenomenon of cannabis-triggered feeding in a state of satiety is a hallmark of marijuana use in humans." So they injected cannabinoids into sated mice to see how the drugs affected neurons in the hypothalamus known to regulate satiety, the feeling of fullness. They figured that the cannabinoids would decrease the activity of these neurons. They figured totally wrong.
The researchers used two different molecules that stimulate cannabinoid receptor 1 (CB1R). When injected into mice, both molecules induced feeding in well-fed animals. POMC neurons in the hypothalamus are known to promote satiety, so the researchers assumed that activation of cannabinoid signaling would decrease the activity of these neurons, allowing the mice to start feeding again.
Paradoxically, they found that CB1R signaling hyperactivated the POMC neurons. And not only that; these neurons were essential in driving the feeding response to cannabinoids. When the researchers suppressed POMC activity, the stoned mice didn't eat.
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» see original post http://feeds.arstechnica.com/~r/arstechnica/science/~3/ghV_UF2cc3c/
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