Naked Science Forum
Life Sciences => Physiology & Medicine => Topic started by: smart on 01/12/2016 20:49:29
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How does cannabinoids (THC) induce dopamine D2 receptor agonism and selective binding to aripiprazole?
Does THC administration potent aripiprazole affinity by fine-tuning dopamine receptors?
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The idea that smoking dope "fine tunes" anything is only likely to make sense when smoking dope.
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The idea that smoking dope "fine tunes" anything is only likely to make sense when smoking dope
If your insinuation relates to THC/CBD-consumption being incapable of enhancing cognitive and/or locomotive skills.... you'd be mistaken.
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Dopamine receptors - IUPHAR Review 13.
Beaulieu JM, Espinoza S, Gainetdinov RR.
Abstract
The variety of physiological functions controlled by dopamine in the brain and periphery is mediated by the D1, D2, D3, D4 and D5 dopamine GPCRs. Drugs acting on dopamine receptors are significant tools for the management of several neuropsychiatric disorders including schizophrenia, bipolar disorder, depression and Parkinson's disease. Recent investigations of dopamine receptor signalling have shown that dopamine receptors, apart from their canonical action on cAMP-mediated signalling, can regulate a myriad of cellular responses to fine-tune the expression of dopamine-associated behaviours and functions. Such signalling mechanisms may involve alternate G protein coupling or non-G protein mechanisms involving ion channels, receptor tyrosine kinases or proteins such as β-arrestins that are classically involved in GPCR desensitization. Another level of complexity is the growing appreciation of the physiological roles played by dopamine receptor heteromers. Applications of new in vivo techniques have significantly furthered the understanding of the physiological functions played by dopamine receptors. Here we provide an update of the current knowledge regarding the complex biology, signalling, physiology and pharmacology of dopamine receptors.
THC-induced dopamine agonism and selective binding to aripiprazole may fine-tune the expression of D2 activity.
So my guess is that increased corticostriatal D2 connectivity is neuroprotective and activate glutamatergic (NMDA) pathways.
https://www.ncbi.nlm.nih.gov/pubmed/25671228
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Heteromeric CB1-adenosine (A2A) receptor antagonism appears to decrease dopamine-mediated akathisia induced by aripiprazole:
https://www.ncbi.nlm.nih.gov/pubmed/24211858
https://www.ncbi.nlm.nih.gov/pubmed/25296982
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Aripiprazole may be a potent endocannabinoid enhancer and selective FAAH inhibitor.
See: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704579/ (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704579/)
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Debilify the tranquilizer only serves to ensure your tolerance to the real medicine- benzos stays low enough to work when needed as a last resort
Abilify costs 24usd per pill, benzos cost 00.02usd, the only problem with benzos is they work too well- they allow unhappy people to finally pull the plug without anxiety and usually without a fuss
Tranquilizers known to cause heart attacks and other muscle disorders need to be the last resort while benzos should be available in every convenience store
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If anandamide is really a substrate for aripiprazole, I'll love this drug more.
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Mixing abilify and cannabis?
Do you talk to your medical professional about your self-medication with cannabis?
If not, why not?
Your medical professional is in the best position to discuss the interactions and the effects they may be having on you.
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Where is exothermic when you need him?
evan: I'll keep this in mind and ask her my question when I'll see her.