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HA-966 - Potentially the best supplement to cannabis that you've never heard of.

cannabis ha-966 966 weed marijuana memory working spatial hippocampus

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#1 Lobotomy

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Posted 29 June 2014 - 02:05 PM


 

From  http://en.wikipedia....ible_prevention :

 

One study has shown that the effects of THC on working memory could be diminished by the enantiomers of HA966, which is a glycine site partial agonist.[36] To explain, a study was conducted on rats, where their performance on spatial working memory tasks was impaired by administration of THC, but it was not impaired when the THC was accompanied by HA966.[36] This study suggests that the behavioural effects of THC on spatial working memory could be diminished moderated by the administration of HA966.[36]

 

I was doing some research on cannabis' effects on memory, and I eventually ended up here.

 

The pyrrolidone nucleus and the effects of the drug make it look like a straight up racetam in terms of action. It is reported to aid the loss of memory associated with cannabis.

 

 

I dunno, might be worth checking out.


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#2 branks

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Posted 29 June 2014 - 03:44 PM

Its sedative hypnotic effects are supposed to rival that of GHB's, but the mode of action in how it induces such effects is completely unknown. As far as they know it has almost zero interaction with GABA. A very strange substance indeed.

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#3 goodman

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Posted 29 June 2014 - 04:27 PM

what if the damage is already done, can it reverse it?

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#4 Metagene

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Posted 29 June 2014 - 05:00 PM

I concur.

http://www.ncbi.nlm....pubmed/5157720/

1-Hydroxy-3-amino-pyrrolidone-2(HA-966): a new GABA-like compound, with potential use in extrapyramidal diseases.

AuthorsBonta IL, et al. Show allJournal
Br J Pharmacol. 1971 Nov;43(3):514-35.
Affiliation
Abstract
1. The drug HA-966 (1-hydroxy-3-amino-pyrrolidone-2), which chemically resembles the cyclic form of GABA, has been studied for neuro-pharmacological properties and for effects on the catecholamine content of the corpus striatum.2. The acute effects on spontaneous behaviour of rodents included flaccid catalepsy and reversible tranquillization in doses which were 5% or less of the lethal dose. Long lasting depression of the CNS, followed by complete recovery, was produced in the cat and the dog. In the monkey HA-966 caused periodical sleeping episodes.3. The exploratory behaviour and the amphetamine-induced motor activity in mice were blocked by HA-966. The toxicity of amphetamine in aggregated mNice was only moderately reduced, suggesting that HA-966 differs from neuroleptics.4. Tremors induced by chemical agents (nicotine, zinc and tremorine) were markedly inhibited by HA-966. The muscarinic effects of tremorine were not reduced by HA-966, indicating a selective central antitremor effect.5. HA-966 elevated the threshold to strychnine convulsions and abolished the ipsilateral flexor reflex, while not having motor endplate blocking properties. It is suggested that HA-966 depresses central internuncial neurones.6. In rats and rabbits HA-966 produced synchronous EEG and inhibited the sensory arousal in doses not causing sedation. In the monkey the drug caused a periodical dissociation between ;sleep-EEG' and behaviour.7. In rat brain, HA-966 selectively elevated the dopamine content in the corpus striatum, while no changes in noradrenaline and 5-hydroxytryptamine contents could be demonstrated. The effect was still present when dopa synthesis was inhibited with alpha-methyl-p-tyrosine.8. Several effects of intravenously administered HA-966 became manifest after an appreciable delay and in hepatectomized mice the effects were much reduced. It is postulated that HA-966 is converted to a pharmacologically active metabolite.9. The results are discussed in the light of current views on drug therapy in extrapyramidal conditions and a GABA-related hypothesis as to the mode of action of HA-966 is presented.

http://www.ncbi.nlm....ubmed/18177675/

The glycine site-specific NMDA antagonist (+)-HA966 enhances the effect of morphine and reverses morphine tolerance via a spinal mechanism.

AuthorsAdam F, et al. Show allJournal
Neuropharmacology. 2008 Mar;54(3):588-96. doi: 10.1016/j.neuropharm.2007.11.013. Epub 2007 Nov 28.

Affiliation
Abstract
Using the C-fibre reflex as a nociceptive response elicited by a wide range of stimulus intensities in the rat, we recently reported that a single treatment with (+)-HA966, a glycine site-specific NMDA receptor antagonist: (1) potentiates morphine antinociception; and (2) reverses an established morphine tolerance. We presently aimed at determining whether our observation was likely to result from a direct effect on the spinal cord or an indirect effect of supraspinal origin. In a 2x2x2 experimental design, we compared the effects of 5 mg/kg morphine in: (1) sham-operated rats or animals whose brainstems had been transected at the level of the obex; (2) rats that were implanted with pellets, either 150 mg morphine or placebo; and (3) animals injected either with saline or 10 mg/kg (+)-HA966. The control C-fibre reflexes were similar in all groups of animals. As compared to "non-tolerant" rats, the depressive effect of morphine was weaker in "morphine-tolerant" animals where the threshold did not change following morphine but the gain of the stimulus-response curve decreased, albeit to a significantly lesser extent than in the "non-tolerant" group. Whether in "non-tolerant" or "tolerant" groups, the effects of morphine were stronger in "obex-transected" than in "sham-operated" animals. In all groups, the effects of morphine were potentiated by the preliminary administration of (+)-HA966. However, in the "morphine-tolerant" group, the preliminary administration of (+)-HA966 was more potent in the "sham-operated" than in the "obex-transected" groups. Since overall effects were very similar in "sham-operated" and "obex-transected" animals, we concluded for our model that the critical site for the expression of the neuronal plastic changes associated with morphine tolerance lies in the spinal cord.


Edited by Metagene, 29 June 2014 - 05:05 PM.


#5 adamh

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Posted 29 June 2014 - 11:39 PM

Too bad its impossible to get at a reasonable cost. It sounds interesting. Perhaps the chinese will jump on the bandwagon if there is interest?



#6 FW900

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Posted 30 June 2014 - 01:07 AM

People typically consume cannabis so they can run away from memory rather than retain and confront it. Look at any writing of someone "high" on cannabis, their insights seem to include scattered thoughts that mindlessly jump from one thing to another. This begs the question, are the memories formed during cannabis usage even worth preserving? From what I gather (based mainly on reading and people I have known who've consumed cannabis), most insights gained from the drug seem to be trivial, at times deal with food, and carry an undertone of extreme paranoia. Not exactly worth preserving.

 

 


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#7 Metagene

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Posted 30 June 2014 - 01:12 AM

what if the damage is already done, can it reverse it?



You might want to look into COX-2 inhibitors

We found that COX inhibition by NS398 rescued decreased hippo- campal LTP induced by repeated in vivo exposure to D9-THC for 7 days both at CA3-CA1 synapses (Figure 3A) and perforant path synapses in the dentate gyrus (Figure S3A). Similarly, genetic inhibition of COX-2 also prevented LTP deterioration induced by D9-THC at both CA3-CA1 synapses (Figure 3B) and the perforant path (Figure S3B). To verify whether persistent overexpression of COX-2 impairs LTP, we recorded LTP in animals repeatedly treated with LPS, which increases COX-2. As we expected, repeated injection of LPS significantly reduced LTP, and this decrease was prevented by inhibition of COX-2 (Figure S3C). These data suggest that persistent elevation of COX-2 in the brain will be detrimental to integrity of synaptic structure and plasticity. Because a single dose of D9-THC pro- duced an increase in COX-2 expression, we wondered whether this increase alters synaptic function. To this end, we recorded long-term depression (LTD) induced by low-frequency stimula- tion (LFS) at hippocampal CA3-CA1 synapses and found that LTD is impaired by a single D9-THC exposure. However, LTD is normal in COX-2 knockout animals that received a single injec- tion of D9-THC (Figure S4). This information suggests that a single D9-THC exposure induces a COX-2-associated impair- ment in LTD (Mato et al., 2004, 2005).


http://www.medicinal...profen_COX2.pdf

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#8 labratdream

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Posted 06 January 2020 - 01:12 AM

It's available at newmind







Also tagged with one or more of these keywords: cannabis, ha-966, 966, weed, marijuana, memory, working, spatial, hippocampus

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