Wednesday, December 21, 2005

Research: Machinery of the 'marijuana munchies'

One of the primary hazards of marijuana use is well-documented: the uncontrollable urge to consume a bag of Skittles, half of a leftover pizza, a pound of chocolate chips, and the freezer-burned date logs that have been around since Aunt Sarah came for a visit last October. Finally, some serious research on the munchies from some pointy-headed tokers at Columbia Univerisity:
In their studies, the researchers concentrated on the lateral hypothalamus (LH) of the brain, known to be a center of control of food intake. Their studies involved detailed electrophysiological measurements of the effects of specific neurons that they had identified in previous studies as being important in endocannabinoid signaling. Their studies revealed that activation of CB1 receptors, as by endocannabinoid molecules, induced these neurons to be rendered more excitable by a mechanism called "depolarization-induced suppression of inhibition" (DSI).

What's more, they found that leptin inhibits DSI. However, they found that leptin did not interfere with the CB1 receptors themselves. Rather, leptin "short-circuits" the endocannabinoid effects by inhibiting pore-like channels in the neurons that regulate the flow of calcium into the neurons. Such calcium is necessary for the synthesis of endocannabinoids.

In further studies of mice genetically altered to be leptin deficient, the researchers found the DSI to be more prolonged than in normal mice. Thus, they said, the findings "implicate this mechanism for leptin receptor/endocannabinoid signaling in contributing to the maintenance of weight balance…." The researchers also included that "upregulation of endocannabinoid signaling in the LH may explain, at least in part, the increased body weight consistent with a prior report of elevated endocannabinoids" in such leptin-deficient mice.

The researchers concluded that their findings "are consistent with the hypothesis that the integration of endocannabinoid and leptin signaling regulates the excitability of neurons on appetite-related circuits."

Link to press release (via Boing Boing)

Tonight, let's all burn a spliff to Young-Hwan Jo, Ying-Jiun J. Chen, Streamson C. Chua, Jr., David A. Talmage, and Lorna W. Role!


mdmhvonpa said...

Hmmm, if I could genetically engineer lettuce to do the same thing, imagine the boon to medical industry by reducing obesity.

Beth said...

ooh ooh ooh- electrophysiology!

Hmmm...I'm not getting it, if leptin and canniboids had opposite effects you would expect that fat people would actually loose weight when they smoked dope. Theoretically leptin, which is made by fat cells, makes you eat less- so if your fat and you have lots of leptin and then the pot short-circuits leptin...OK I just got it. Pot inhibits you from "sensing" your fat!

mdmhvonpa- oh yes there are tons of people looking to control obesity- at first they thought leptin was the holy grail- but the problem with obesity is that they fail to respond to it- so you can inject 'em full of it and their brain is refractory. Like diabetes I guess- your body becomes refractory to insulin if it too high for too long.

Anonymous said...

wazzup doug?

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