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Counter cannabis effects on memory

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sativa

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Feb 7 10 9:20 PM

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I'm planning on trialing this 'stack' at some point in the near future. [source]


     Cannabis (or marijuana) is a very useful tool for creative thinking and expanded logic (Studies have shown). But Studies have also shown that, although cannabis doesn't kill brain cells, marijuana's effects reduce memory function in a few different ways.
     Some benefits of this supplement include: Reversing some tolerance, reversing memory loss, speeding detoxification of THC, correcting some hormonal effects, potientially helping immune system, and improving overall memory.

Main ways Cannabis reduces memory:
1. Residual CB1 agonist release from fatty cells
2. cAMP/ CREB (Chemical responsible for Long-Term memory potential) decrease will result in less memories being encoded.
3. NGF (Nerve Growth Factor) decrease lowers the maintenance and growth of new neurons.
4. Decrease in Glutaminergic brain activity (via GABA) (causes a lowered mental energy and could make someone lazy/tired).

Ingredients:
Dihydromyricetin Extract
     A natural proven intoxication blocker. Studies show this type of chemical diminishes all memory impairments caused by THC. Contains a chemical called ampelopsin that influences GABA(a) receptors in an inhibitory fashion. This compound not only reverses memory effects caused by GABA, it also prevents long term anxiety caused by THC. This compound can be used to reverse even non-drug induced anxiety.  8' 13'

American Ginseng
     Proven to increase metabolism of THC to its inactive version 11-nor-9-carboxy. This means american ginseng is a working detox. Prevents CB1 activation after intoxication, reducing ones tolerance. American Ginseng also contains CB1 Inverse agonist falcarinol (Studies show it reverses CB1s effects at certain sites). Some slight hormonal type improvements have also been noted. American Ginseng also increases dopamine production in certain areas of the brain improving memory and tolerance. American Ginseng also works as a choline uptake enhancer exactly as Aniracetam, Piracetam and most of the other racetams (nootropics) do. 7' 10' 11' 17'

Lysine
     This natural compound has been found to relieve anxiety and stress in the gut without effecting gaba receptors or memory! Marijuana has been shown to increase stress and anxiety aswell as weaken the immune system. Lysine helps to reverse both of these aspects.
9' 18' 19' 20' 21' 22'

Bacopa Extract
      Bacopa has been shown to increase working memory as well as long term retention. Bacopa also reduces the possibility of seizure. This makes overdose from Dihydromyricetin nearly impossible even at unsafe amounts. Bacopa has also been shown to reverse amnesia caused by gaba down regulation with an unknown mechanism. Bacopasides has also been found to thwart brain inflammation caused from smoke and lipoxygenase. 1' 6' 9'

ALCAR (Acetyl-L-Carnitine)
     Studies have shown it is very beneficial with boosting the effects of NGF. Studies show it helps ATP production. Uridine relies on ATP to exert its effects, thus proving synergistic effects between the two. Aceytl-L-Carnitine also works synergistically with l-glutamine, increasing the activation of glutaminase, the enzyme responsible with converting glutamine into glutamate (most abundant neurotransmitter in the brain). Studies also show it improves mental performance greatly. 12' 14' 16'

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#2 [url]

Feb 8 10 5:51 AM

Cannabinoid antagonize or inhibit  nmda and acetylcholine witch leading to; what was I just talking about dude ? no short term memory at all. Its creative if you use it 1 time a month causing a other persperctive of being but if its a daily addiction well you turn pothead , dumb, slient and confuse with no cognitive sharpness. Acetyl-l carnitine is VERY great especially with a big coffee--> ZOOM ZOOM !!
''Studies also show it improves mental performance greatly.'' Experience prove it :D

Consumption of caffeine antagonizes adenosine and increases activity in neurotransmission including acetylcholine, epinephrine, dopamine, serotonin, norepinephrine and glutamate.

Glutamate and acetylcholine are stimulant of neurogenesis witch its very nice when moving in a enriched environment. You can metamorphose unbelievably fast with adaptagen and nootropics.

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sativa

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Posts: 372

#4 [url]

Feb 8 10 6:09 AM

You can use it once every 72 hours without becoming a pothead.
SWIM did this experiment for a couple weeks and it was successful.

-toastus

My intention is to take something resembling this mix after having smoked, i don't smoke often...but anything i can do to remedy any non-positive effects from cannabis!

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toastus

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#5 [url]

Feb 8 10 6:12 AM

It also appears that the CB1 receptor inhibits production of cyclic adenosine monophosphate (cAMP). I am currently putting together a new topic which deals with cAMP and PDE4 inhibitors (inhibiting PDE4 leads to increased levels of cAMP)

-sativa

You gotta understand that cAMP is just an intracellular messenger, not an intercellular messenger. It controls things inside a certain cell, not between cells. cAMP in one type of neuron will not affect other neurons. For example, the beta-adrenergic receptors and the D1 receptor both stimulate cAMP, but they have very different effects. All cAMP means is that the cell turns on.

More cAMP is good because it means the cell's energy gets put to use and it does what it needs to do. More cAMP = less aging and less mitochondrial breakdown, according to the Secret Life of Mitochondria whose link I am too lazy to find right now. cAMP in itself isn't really a neuromodulator, more like a total cellular modulator.

Also I just found out D3 is a receptor that lowers cAMP. WOW, I thought it would raise cAMP. That's really interesting. So D3 shuts down dopamine neurons to cause waving purple visuals? Weird.

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toastus

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#6 [url]

Feb 8 10 6:19 AM


My intention is to take something resembling this mix after having smoked, i don't smoke often...but anything i can do to remedy any non-positive effects from cannabis!

-sativa

lol, while I do agree with you and do not want to be like that permanently it is sometimes good to take a mental break from life, which I think is what this plant was designed for in chronic use.

Occasional use: it becomes a super entheogen with God-contact.

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sativa

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#7 [url]

Feb 8 10 6:29 AM


You gotta understand that cAMP is just an intracellular messenger, not an intercellular messenger.

-toastus



I've been reading about cAMP since yesterday, i know!! :)


lol, while I do agree with you and do not want to be like that permanently it is sometimes good to take a mental break from life, which I think is what this plant was designed for in chronic use.


-toastus


I never (consciously) saw it that way!

cAMP and D1:


Phosphodiesterase 4 inhibition enhances the dopamine D1 receptor/PKA/DARPP-32 signaling cascade in frontal cortex.

RATIONALE:

Alteration of dopamine neurotransmission in the prefrontal cortex, especially hypofunction of dopamine D1 receptors, contributes to psychotic symptoms and cognitive deficit in schizophrenia. D1 receptors signal through the cAMP/PKA second messenger cascade, which is modulated by phosphodiesterase (PDE) enzymes that hydrolyze and inactivate cyclic nucleotides. Though several PDEs are expressed in cortical neurons, the PDE4 enzyme family (PDE4A-D) has been implicated in the control of cognitive function. The best studied isoform, PDE4B, interacts with a schizophrenia susceptibility factor, disrupted in schizophrenia 1 (DISC1).

OBJECTIVES:

We explore the control of mouse frontal cortex dopamine D1 receptor signaling and associated behavior by PDE4.

RESULTS:

Inhibition of PDE4 by rolipram induced activation of cAMP/PKA signaling in cortical slices and in vivo, leading to the phosphorylation of DARPP-32 and other postsynaptic and presynaptic PKA-substrates. Rolipram also enhanced DARPP-32 phosphorylation invoked by D1 receptor activation. Immunohistochemical studies demonstrated PDE4A, PDE4B, and PDE4D expression in DARPP-32-positive neurons in layer VI of frontal cortex, most likely in D1 receptor-positive, glutamatergic corticothalamic pyramidal neurons. Furthermore, the ability of rolipram treatment to improve the performance of mice in a sensorimotor gating test was DARPP-32-dependent.

CONCLUSIONS:

PDE4, which is co-expressed with DARPP-32 in D1 receptor-positive cortical pyramidal neurons in layer VI, modulates the level of D1 receptor signaling and DARPP-32 phosphorylation in the frontal cortex, likely influencing cognitive function. These biochemical and behavioral actions of PDE4 inhibitors may contribute to the hypothesized antipsychotic actions of this class of compounds.

-http://www.ncbi.nlm.nih.gov/pubmed/21833500




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toastus

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#8 [url]

Feb 8 10 6:39 AM

HELLO, D1 is present in the prefrontal cortex.

We should make a map of the brain with the function of each section and the known receptors in each section. That would be a great thread.

So this means caffeine would potentiate D1 and D5 agonists and would antagonize D2, D3, and Dfour agonists.

D1 and D5 activate cells, while D2, 3, and four inactivate cells...

This may change my understanding of dopamine's waving breathing visuals. If D3 shuts down cells, what cells is it present on? Acetylcholine neurons? How does D3 cause breathing visuals? THIS IS IN THE TOTALLY WRONG THREAD, MY BAD.

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#9 [url]

Feb 8 10 2:26 PM

   
You gotta understand that cAMP is just an intracellular messenger, not an intercellular messenger. It controls things inside a certain cell, not between cells. cAMP in one type of neuron will not affect other neurons. For example, the beta-adrenergic receptors and the D1 receptor both stimulate cAMP, but they have very different effects. All cAMP means is that the cell turns on.More cAMP is good because it means the cell's energy gets put to use and it does what it needs to do. More cAMP = less aging and less mitochondrial breakdown, according to the Secret Life of Mitochondria whose link I am too lazy to find right now. cAMP in itself isn't really a neuromodulator, more like a total cellular modulator.
Also I just found out D3 is a receptor that lowers cAMP. WOW, I thought it would raise cAMP. That's really interesting. So D3 shuts down dopamine neurons to cause waving purple visuals? Weird.

-toastus

To raise cAMP or not to raise cAMP?
http://www.sciencedaily.com/releases/2007/04/070420143324.htm

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sativa

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#11 [url]

Feb 11 10 1:12 AM

Does this mean that a GABA(A) antagonist (which would upregulate GABA(A)?) would reverse the effect that CB1 receptor activation has on the GABA(A) receptor?


Prolonged cannabinoid exposure alters GABA(A) receptor mediated synaptic function in cultured hippocampal neurons.


Abstract

Developing cannabinoid-based medication along with marijuana's recreational use makes it important to investigate molecular adaptations the endocannabinoid system undergoes following prolonged use and withdrawal. Repeated cannabinoid administration results in development of tolerance and produces withdrawal symptoms that may include seizures. Here we employed electrophysiological and immunochemical techniques to investigate the effects of prolonged CB1 receptor agonist exposure on cultured hippocampal neurons. Approximately 60% of CB1 receptors colocalize to GABAergic terminals in hippocampal cultures. Prolonged treatment with the cannabinamimetic WIN 55,212-2 (+WIN, 1 μM, 24 h) caused profound CB1 receptor downregulation accompanied by neuronal hyperexcitability. Furthermore, prolonged +WIN treatment resulted in increased GABA release as indicated by increased mIPSC frequency, a diminished GABAergic inhibition as indicated by reduction in mIPSC amplitude and a reduction in GABA(A) channel number. Additionally, surface staining for the GABA(A) β(2/3) receptor subunits was decreased, while no changes in staining for the presynaptic vesicular GABA transporter were observed, indicating that GABAergic terminals remained intact. These findings demonstrate that agonist-induced downregulation of the CB1 receptor in hippocampal cultures results in neuronal hyperexcitability that may be attributed, in part, to alterations in both presynaptic GABA release mechanisms and postsynaptic GABA(A) receptor function demonstrating a novel role for cannabinoid-dependent presynaptic control of neuronal transmission.




Δ9-THC-induced cognitive deficits in mice are reversed by the GABAA antagonist bicuculline


Rationale

The results of recent in vitro studies have underscored the important role that activation of CB1 receptors has on GABAergic activity in brain areas associated with memory.

Objectives

The primary purpose of this study was to test the hypothesis that the memory disruptive effects of Δ9-tetrahydrocannabinol (Δ9-THC) in vivo are mediated through GABAergic systems. Conversely, we also evaluated whether blocking CB1 receptor signaling would alter memory deficits elicited by GABA agonists.

Methods

The GABAA antagonist bicuculline and GABAB antagonist CGP 36742 were evaluated for their ability to ameliorate ?9-THC-induced deficits in a mouse working memory Morris water maze task. Mice were also assessed in a T-maze task, as well as non-cognitive behavioral assays. Additionally, the effects of GABAA and GABAB agonists were assessed in either CB1 (-/-) mice or wild type mice treated with the CB1 antagonist SR 141716.

Results

Memory deficits resulting from 10 mg/kg Δ9-THC in the Morris water maze were completely reversed by bicuculline, though unaffected by CGP 36742. Bicuculline also blocked the disruptive effects of ?9-THC in the T-maze, but failed to alter non-mnemonic effects of Δ9-THC. Although CB1 (-/-) mice exhibited supersensitivity to muscimol-induced water maze deficits compared with wild type control mice, muscimol elicited virtually identical effects in SR 141716-treated and vehicle-treated wild type mice.

Conclusions

This is the first demonstration of which we are aware showing that GABAA receptors may play a necessary role in Δ9-THC-induced memory impairment in whole animals.




Dihydromyricetin Extract

     A natural proven intoxication blocker. Studies show this type of chemical diminishes all memory impairments caused by THC. Contains a chemical called ampelopsin that influences GABA(a) receptors in an inhibitory fashion. This compound not only reverses memory effects caused by GABA, it also prevents long term anxiety caused by THC.


Delta9-tetrahydrocannabinol is a full agonist at CB1 receptors on GABA neuron axon terminals in the hippocampus.


Abstract

Marijuana impairs learning and memory through actions of its psychoactive constituent, delta-9-tetrahydrocannabinol (Delta(9)-THC), in the hippocampus, through activation of cannabinoid CB1 receptors (CB1R). CB1Rs are found on glutamate and GABA neuron axon terminals in the hippocampus where they control neurotransmitter release. Previous studies suggest that Delta(9)-THC is a partial agonist of CB1Rs on glutamate axon terminals in the hippocampus, whereas its effects on GABA terminals have not been described. Using whole-cell electrophysiology in brain slices from C57BL6/J mice, we examined Delta(9)-THC effects on synaptic GABA IPSCs and postsynaptic GABA currents elicited by laser-induced photo-uncaging (photolysis) of alpha-carboxy-2-nitrobenzyl (CNB) caged GABA. Despite robust inhibition of synaptic IPSCs in wildtype mice by the full synthetic agonist WIN55,212-2, using a Tween-80 and DMSO vehicle, Delta(9)-THC had no effects on IPSCs in this, or in a low concentration of another vehicle, randomly-methylated beta-cyclodextrin (RAMEB, 0.023%). However, IPSCs were inhibited by Delta(9)-THC in 0.1% RAMEB, but not in neurons from CB1R knockout mice. Whereas Delta(9)-THC did not affect photolysis-evoked GABA currents, these responses were prolonged by a GABA uptake inhibitor. Concentration-response curves revealed that the maximal effects of Delta(9)-THC and WIN55,212-2 were similar, indicating that Delta(9)-THC is a full agonist at CB1Rs on GABA axon terminals. These results suggest that Delta(9)-THC inhibits GABA release, but does not directly alter GABA(A) receptors or GABA uptake in the hippocampus. Furthermore, full agonist effects of Delta(9)-THC on IPSCs likely result from a much higher expression of CB1Rs on GABA versus glutamate axon terminals in the hippocampus.


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#12 [url]

Feb 11 10 2:48 AM

I am a little confused. It seems that GABA-A antagonists are supposed to prevent the memory loss caused by THC. Both Bicuculine and Dihydromyricetin antagonize GABA-A and prevent the amnesic effects of THC. So the memory impairments of THC and other CB1 agonists are supposed to be caused by GABA-A stimulation right?

But in the last study that you posted it says that THC inhibits GABA release while the first study says that CB1 agonism leads to increased GABA release. It makes more sense that CB1 agonism would increase GABA release leading to increased memory impairment.

But the first study says that GABA release was induced by chronic CB1 agonism. So maybe THC does inhibit GABA release under normal circumstances. But what then causes the GABA-A stimulation that causes the memory impairment induced by CB1 agonism.

All hail King Neptune and his water breathers!!!! maayyonaaaze!

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#13 [url]

Dec 14 12 4:28 PM

Gaba Negative Allosteric Modulators or Antagonists

-Muira Puama
-Thujone
-Bicucilline
-Picrotoxin
-Zinc
-Oroxylin A (Scutellaria baicalensis)
-Amentoflavone
-Kudzu
-ALCAR
-Trigonelline
-Caffeine
-Arecoline and Betel nut
-Dihydromyricetin extract(Hovenia dulcis) ANTI-HANGOVER also
-Strychinine (Nux Vomica)

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#14 [url]

Dec 18 12 5:23 AM

COX-2 inhibithors prevent memory-loss from Cannabis S. working via inderctly GABA and Glutamate.

Most potent natural:

Curcuma
Ginger
Cloves
Rosemary
Sage
Garlic
Black cumin
Passionflower
Hops
Resveratrol
Hemp seed protein

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