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Cannabinoid antagonists for memory encoding?


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#1 gamesguru

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Posted 12 May 2010 - 09:07 PM


We all know that THC (an exogenous cannabinoid) significantly compromises working memory in humans and in animals. However, what's not yet know is to what extent endogenous cannabinoids are designed to downregulate working memory. Some speculate that the intricate endogenous cannabinoid system is evolutionarily adaptive to help forget the "less important things", so that our brains don't go insane with trying to store information. Therefore inhibiting the cannabinoid system to an extent, will theoretically induce modest improvements in short-memory/memory consolidation.

I found this study (and a few others I didn't post) demonstrating that rimonabant (a cannabinoid receptor antagonist) improves short-term memory, and therefore memory consolidation.

The cannabinoid CB(1) receptor antagonist CE prolongs spatial memory duration in a rat delayed radial arm maze memory task.
Wise LE, Iredale PA, Lichtman AH.

Department of Pharmacology and Toxicology, Virginia Commonwealth University, 410 North 12th Street, PO Box 98061, Richmond, VA 23298, USA.
Abstract
The cannabinoid receptor system plays an integral role in learning and memory. Moreover, the cannabinoid CB(1) receptor antagonist rimonabant has been found to improve performance in a variety of animal memory models. The present study tested whether a novel and potent cannabinoid CB(1) receptor antagonist, CE, would prolong the duration of spatial memory. Rats were trained in a two-phase radial arm maze procedure, consisting of acquisition and retrieval tests, which were separated by an 18 h delay. CE was administered 30 min before the acquisition phase, immediately after the acquisition phase, or 30 min before the retrieval test to assess its effects on acquisition and retrieval processes. CE administered before and immediately after the acquisition phase significantly decreased the number of errors committed during the retrieval test. On the other hand, CE administered 30 min before the retrieval test had no effect on the number of errors committed. These findings demonstrate that CE improves memory by acting on consolidation, rather than retrieval, processes and further suggest that the endocannabinoid system has an important role in modulating memory duration.


Thoughts on rimonabant as a nootropic?

Edited by dasheenster, 12 May 2010 - 09:23 PM.

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#2 LabRat84

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Posted 12 May 2010 - 10:10 PM

I have an exam tomorrow and a cram session ahead of me tonight... I'll try it. Can't use it as a controlled experiment though, as I've been taking my well-tested nootropics for the past few days.

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#3 Stan100

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Posted 12 May 2010 - 10:29 PM

If you check the Wikipedia page, you'll note that it was pulled for making people suicidal:

In October, 2008, the European Medicines Agency recommended that doctors not prescribe the drug due to the risk of serious psychiatric problems and even suicide. The drug was subsequently suspended.

Shortly after market introduction, press reports and independent studies suggest that side-effects occur stronger and more commonly than shown by the manufacturer in their clinical studies. Reports of severe depression are frequent. This is deemed to result from the drug's being active in the central nervous system, an area of human physiology so complex that the effects of a drug are extremely difficult to predict or anticipate.

On June 15, 2007, BBC News reported[11] that a committee advising the U.S. FDA had voted not to recommend the drug's approval because of concerns over suicidality, depression, and other related side-effects associated with use of the drug.


After that, you can see the part hypothesizing about better memory, including a link to a study where rats did better.

#4 tlm884

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Posted 13 May 2010 - 03:46 AM

If you check the Wikipedia page, you'll note that it was pulled for making people suicidal:

In October, 2008, the European Medicines Agency recommended that doctors not prescribe the drug due to the risk of serious psychiatric problems and even suicide. The drug was subsequently suspended.

Shortly after market introduction, press reports and independent studies suggest that side-effects occur stronger and more commonly than shown by the manufacturer in their clinical studies. Reports of severe depression are frequent. This is deemed to result from the drug's being active in the central nervous system, an area of human physiology so complex that the effects of a drug are extremely difficult to predict or anticipate.

On June 15, 2007, BBC News reported[11] that a committee advising the U.S. FDA had voted not to recommend the drug's approval because of concerns over suicidality, depression, and other related side-effects associated with use of the drug.


After that, you can see the part hypothesizing about better memory, including a link to a study where rats did better.


Where do you get rimonabant

#5 Guacamolium

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Posted 13 May 2010 - 05:00 AM

I've never really thought CB agonists were that bad, it was just their selectivity. (hint hint, nootropic CB)

I always thought that scientists would study CB agonists that don't attach to the parietal lobes, but attach to the others.

Seems kind of, needed, to me - as seeing CB enhancement could reshape our whole perceptiveness a bit, without influencing STM.

But to your topic inquiry, CB1 and 2 parietal antagonists seems like a great idea, scientists.....

#6 chrono

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Posted 13 May 2010 - 05:25 AM

Very interesting idea. Can you link to those other relevant studies, if you made note of them?

Are there other CB1 antagonists we know of which might be more convenient?

#7 medievil

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Posted 13 May 2010 - 02:43 PM

If you check the Wikipedia page, you'll note that it was pulled for making people suicidal:

In October, 2008, the European Medicines Agency recommended that doctors not prescribe the drug due to the risk of serious psychiatric problems and even suicide. The drug was subsequently suspended.

Shortly after market introduction, press reports and independent studies suggest that side-effects occur stronger and more commonly than shown by the manufacturer in their clinical studies. Reports of severe depression are frequent. This is deemed to result from the drug's being active in the central nervous system, an area of human physiology so complex that the effects of a drug are extremely difficult to predict or anticipate.

On June 15, 2007, BBC News reported[11] that a committee advising the U.S. FDA had voted not to recommend the drug's approval because of concerns over suicidality, depression, and other related side-effects associated with use of the drug.


After that, you can see the part hypothesizing about better memory, including a link to a study where rats did better.

Yes, but it may be worth a try as an accasional study aid. I dont know how much the incidence of those side effects was tough.

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#8 gamesguru

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Posted 13 May 2010 - 08:44 PM

Very interesting idea. Can you link to those other relevant studies, if you made note of them?

Are there other CB1 antagonists we know of which might be more convenient?


Short-term memory is modulated by the spontaneous release of endocannabinoids: evidence from hippocampal population codes.
Deadwyler SA, Goonawardena AV, Hampson RE.

Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157-1083, USA. sdeadwy@wfubmc.edu
Abstract
Population codes derived from ensembles of hippocampal neurons were assessed to determine whether endocannabinoids were active when rats performed a delayed-nonmatch-to-sample (DNMS) short-term memory task. Multivariate discriminant analyses of the firing patterns of ensembles of CA1 and CA3 hippocampal neurons extracted representations of information encoded at the time of the sample response (SmR codes) during individual DNMS trials. The 'strength' or distinctiveness of trial-specific SmR codes in normal sessions was compared with sessions in which either rimonabant, the well-characterized cannabinoid CB1 receptor antagonist, or WIN 55212-2 (WIN-2), a cannabinoid CB1 receptor agonist, were administered. Results show that performance on trials with delay intervals longer than 10 s was facilitated by rimonabant (2.0 mg/kg) owing to a significantly increased frequency of trials with stronger SmR codes. In contrast, WIN-2 (0.35 mg/kg) suppressed the strength of SmR codes necessary to perform trials with delays greater than 10 s. The positive influence of rimonabant on performance indicated that the action of endocannabinoids was to reduce SmR code strength, resulting in trials that were at risk for errors if the delay exceeded 10 s. Thus endocannabinoids, like exogenously administered cannabinoids, reduced hippocampal encoding necessary to perform long-delay trials. The findings therefore indicate a direct relationship between the actions of endocannabinoids on hippocampal processes and the ability to encode information into short-term memory.


I'm sure there are more you could find by searching around (primarily google scholar), but I'm too busy with school for the time being.


And also, of course there are more CB1 antagonists or inverse agonists.
http://en.wikipedia....te:Cannabinoids




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