hey smoke this shit & you gonna wanna go down to the 7-11 and eat 12 Snickers bars & Milky Way & 3 Musketeers &
The High Non-Junk Science Council of Vleeptron is indebted to coydogsrock, the last human being on Earth still using webtv for e-mail and Internet, for calling our attention to this scientific paper.
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Neuron [scientific journal]Volume 48, Issue 6, 22 December 2005, Pages 1055-1066
Abstract
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doi:10.1016/j.neuron.2005.10.021
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Article
Integration of Endocannabinoid
and Leptin Signaling
in an Appetite-Related
Neural Circuit
and Leptin Signaling
in an Appetite-Related
Neural Circuit
Young-Hwan Jo1, 4, Corresponding Author Contact Information, E-mail The Corresponding Author, Ying-Jiun J. Chen1, Streamson C. Chua, Jr.2, 3, 4, David A. Talmage2, 3 and Lorna W. Role1
1Department of Pathology and Cell Biology in the Center for Neurobiology and Behavior, Columbia University, College of Physicians and Surgeons, New York, New York 10032
2Department of Pediatrics, Columbia University, College of Physicians and Surgeons, New York, New York 10032
3The Institute of Human Nutrition, Columbia University, College of Physicians and Surgeons, New York, New York 10032
Received 17 March 2005; revised 22 July 2005; accepted 5 October 2005. Published: December 21, 2005. Available online 21 December 2005.
Summary
Recently developed therapeutics for obesity, targeted against cannabinoid receptors, result in decreased appetite and sustained weight loss. Prior studies have demonstrated CB1 receptors (CB1Rs) and leptin modulation of cannabinoid synthesis in hypothalamic neurons. Here, we show that depolarization of perifornical lateral hypothalamus (LH) neurons elicits a CB1R-mediated suppression of inhibition in local circuits thought to be involved in appetite and "natural reward." The depolarization-induced decrease in inhibitory tone to LH neurons is blocked by leptin. Leptin inhibits voltage-gated calcium channels in LH neurons via the activation of janus kinase 2 (JAK2) and of mitogen-activated protein kinase (MAPK). Leptin-deficient mice are characterized by both an increase in steady-state voltage-gated calcium currents in LH neurons and a CB1R-mediated depolarization-induced suppression of inhibition that is 6-fold longer than that in littermate controls. Our data provide direct electrophysiological support for the involvement of endocannabinoids and leptin as modulators of hypothalamic circuits underlying motivational aspects of feeding behavior.
Corresponding Author Contact InformationPh: 718 430 2987; Fax: 718 430 8557
4 Present address: Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10467.
posted by Vleeptron Dude | 14:03
4 Comments:
Wait...I thought smoking marijuana gave you the munchies, not suppressed the munchies.
I ate an entire box of ritz crackers in seven minutes once when I still lived with my college roomate Dave, after sampling some of Hawaii's golden finest.
Yes yes what you said ... BUT ...
the recent (within last decade) discovery of endocannabinoids -- molecules and receptor sites in the brain which intimately resemble the Fun biochemicals in cannabis -- have now led to this research in mice. What this guy is doing is showing how endocannabinoids in the brain can be manipulated and suppressed, promising to the opposite of The Munchies: a significant appetite suppression effect. And considering that Obesity is now being acknowledged as just about The Major Life-Threatening Health Condition in the USA ... this could open up an entire new pharmaceutical strategy for dealing with obesity.
At least that's what I made of it. AMY!!!!! AMY!!!! What's it all mean?
hmm. so, can they genetically modify pot so that it still gets you way stoned, but also supresses your appetite? Just imagine! Toke the Fat Away! America's newest diet craze! You get baked but don't want anything baked! Smoke some and you'll wake up four pounds lighter tomorrow and no hangover!
well, i think this researcher is Beyond Pot. (He probably wishes that he didn't even have to use that word with "cannabi" in it.)
My guess is, Pfizer is already sending a limo up to the Bronx to bring him (through the NYC transit strike) to a lovely lunch at the best French restaurant in Midtown to discuss the practical human implications of his discovery with the mice.
My guess is, four or five years from now, a Pill. You take it once a day, you just don't want to eat nearly as much. The Anti-Munchies.
In his TV series "The Nature of Things," the Canadian biologist Suzuki noted that medical researchers have been recording serum cholesterol levels since about 1900 -- in individuals AND national averages.
Only once since then did a nation's average serum cholesterol go DOWN ... during the years when the Nazis occupied most of Europe, and shipped all the meat animals of the occupied nations back to Germany -- thus forcing most of Europe to become vegetarians against their will. And what the impoverished diet didn't do, Forced Labor did the rest.
Sadly, during any prosperous time, a nation will just tend to eat itself silly and become couch potatoes. Shame on them, but so natural and human a thing to do.
But there's going to be a HUGE profitable market for a pill that can really effectively suppress appetite. By the time it's available on prescription, Pfizer will have erased every trace of its original biochemical link to That Naughty Stuff.
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