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Pala

"New research on cannabis as a gateway drug"

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A while ago we had posted on the forum a link to an announcement that a reseach paper was soon to published in which it was to be showed that cannabis is a gateway drug, specifically for heroin. The article wrote that it showed this relationship by observing that those rats given THC, would become more heroin addicts than the control group (not given THC).

OR NOT!

Apparently, all that the paper showed was that those rats exposed to THC would later be more sensitive to its effects. That is to say, both groups were as likely to become addicted, but the exposed group would on average use a higher dosage.

Here's the main concluding bit (although its all worthwhile):

The difference between the groups came post-addiction: For the first 15 heroin sessions, both sets used generally equal amounts of heroin. Then the control rats leveled off. But the pot rats kept taking more of the drug, leveling off at about a 25 percent higher dosage. This increased use was evidence of their greater sensitivity to heroin.

Hurd says that because the marijuana-exposed rats demonstrated this heightened sensitivity, she expected them to be more motivated in pursuing the drug. But they weren't. The control rats paced their cages and repeatedly pressed the active bars even when the light indicating availability wasn't on. The pot rats, on the other hand, figured out that the heroin was available only at certain times, and that pacing and tapping the bar incessantly wasn't worth the trouble. When heroin was available, the marijuana rats took more of it. But when it wasn't, they chilled in the corner.

((The rest of the article writes about another study that failed to find a link between regular MJ use and cancer.))

Edited by Pala

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Nice link.

Would've been interesting to see what had happened if there was a cannabis and heroin bar for the rats to press...

i.e. Same experiment, but include a third set of rats that have been exposed to pot and have the choice of either heroin or cannabis...

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It would have been good to post tihs in the original thread, but since it is not, please post a link from the other thread to this one. It's important to debunk bad science and it's not a good idea to have a thread floating around that makes a wrong record.

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Thanks for the paper. :)

Heroin was administered one week after the administration session of THC. It was suggested that elevated expression of the PENK gene may have been involved in the difference between the groups. It would be interesting to find a relationship between amount of PENK mRNA and time after ceasing THC administration. It does mention this:

THC stimulates CB1 receptors, which similar to mORs, are coupled to Gi/o G-proteins (Pertwee and Ross, 2002) that should inhibit PENK transcription. Thus, increased PENK mRNA expression following the drug-free period into adulthood could reflect an allostatic response to counteract a potential downregulation of the PENK during THC exposure.
Which only supports the need for such a project.

Re the whole CB1 thing: While looking around to determine CB1's funtion, came across this, which includes:

The selective blockade of CB1 receptors by SR 141716 impaired the perception of the appetitive value of positive reinforcers (food, cocaine, morphine) and reduced the motivation for sucrose, beer and alcohol consumption, indicating that positive incentive and/or motivational processes could be under a permissive control of CB1-related mechanisms.
...which might explain that thing I read a while ago about MJ users enjoyed food, etc more than the rest of the population.

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there is a diet pill to hit the market which is based on a CB1 blocker. ie, it's an anti munchies pill.

it will also block cannabis activity at CB1, so might be useful if you want to quit smoking pot.

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