User:Tkadm30/Notebook/THC: Difference between revisions
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===Synopsis=== | ===Synopsis=== | ||
* | * Delta9-tetrahydrocannabinol (THC) is the main psychoactive constituent of Cannabis sativa L (Marijuana) plant. | ||
* Other | * Other marijuana-derived cannabinoids includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), Cannabigerol (CBG), Tetrahydrocannabivarin (THCV). | ||
* | * Marijuana-derived cannabinoids are known as phytocannabinoids. | ||
===Antidepressant properties of THC=== | ===Antidepressant properties of THC=== | ||
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===Neuropsychology of THC tolerance=== | ===Neuropsychology of THC tolerance=== | ||
* CB1 receptor sensitization can be restored by taking breaks of oral THC administration | * CB1 receptor sensitization can be restored by taking breaks of oral THC administration. (Reference needed) | ||
* Alcohol increase THC levels in blood. | * Alcohol increase THC levels in blood. (Reference needed) | ||
* THC tolerance is genetic and regulated by the AKT1 gene. | |||
===Experimental=== | ===Experimental=== | ||
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#Zoppi-2011 https://www.ncbi.nlm.nih.gov/pubmed/21150911 | #Zoppi-2011 https://www.ncbi.nlm.nih.gov/pubmed/21150911 | ||
//Regulatory role of cannabinoid receptor 1 in stress-induced excitotoxicity and neuroinflammation. | //Regulatory role of cannabinoid receptor 1 in stress-induced excitotoxicity and neuroinflammation. | ||
#Website2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/ | #Website2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/ | ||
//Antidepressant-like effect of Δ9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L | //Antidepressant-like effect of Δ9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L | ||
#Website4 http://www.nature.com/articles/npjamd201612 | #Website4 http://www.nature.com/articles/npjamd201612 | ||
//Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids | //Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids | ||
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===See also=== | ===See also=== | ||
* [[User:Etienne_Robillard/Notebook/AKT1|AKT1 Notebook]] | |||
* [[User:Etienne_Robillard/Notebook/TRPV1|TRPV1 Notebook]] | * [[User:Etienne_Robillard/Notebook/TRPV1|TRPV1 Notebook]] | ||
* [[User:Etienne_Robillard/Notebook/THCV|THCV Notebook]] | |||
* [https://en.wikipedia.org/wiki/Cannabinoid Cannabinoid] | |||
* [https://en.wikipedia.org/wiki/Tetrahydrocannabinol Tetrahydrocannabinol] | |||
* https://www.thenakedscientists.com/forum/index.php?topic=65952.0 | |||
Revision as of 03:54, 19 February 2017
Synopsis
- Delta9-tetrahydrocannabinol (THC) is the main psychoactive constituent of Cannabis sativa L (Marijuana) plant.
- Other marijuana-derived cannabinoids includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), Cannabigerol (CBG), Tetrahydrocannabivarin (THCV).
- Marijuana-derived cannabinoids are known as phytocannabinoids.
Antidepressant properties of THC
- THC stimulate anandamide biosynthesis by binding to the CB1 receptor, thus producing a antidepressant and neuroprotective effect. [1]
Neuroprotective properties of THC
- THC inhibit acetylcholinesterase (AChE)-induced intraneuronal amyloid beta aggregation in Alzheimer's disease: [2]
- THC prevent intracellular amyloid beta proteotoxicity and inflammatory response: [3]
- THC is effective as antiglutamatergic therapy for NMDA-induced excitotoxicity. [4]
- Unlike THC, caffeine is a noncompetitive reversible inhibitor of AChE.
- THC reduce intraocular pressure (IOP) in retinal ganglion cells (RGCs) through intracellular CB1 receptor activation; A potential treatment for glaucoma to prevent optic nerve damage.
Proneurogenic effects of THC on neurogenesis and BDNF signaling
- Hippocampal CB1 receptors regulate stress-induced neuroinflammation in the hippocampus. [5]
- THC enhance adult hippocampal neurogenesis and BDNF signaling through intracellular CB1 receptor activation. [6][7]
- Intracellular CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. [8]
Neuropsychology of THC tolerance
- CB1 receptor sensitization can be restored by taking breaks of oral THC administration. (Reference needed)
- Alcohol increase THC levels in blood. (Reference needed)
- THC tolerance is genetic and regulated by the AKT1 gene.
Experimental
- Synaptogenic effect of THC/DHA promote hippocampal development (neurogenesis) and synaptogenesis.
- THC/DHA affect neural stem/progenitor cells (NS/PC) proliferation in the hippocampus.
- THC enhance corticostriatal functional connectivity though increased c-Fos expression.
References
-
Antidepressant-like effect of Δ9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L
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A molecular link between the active component of marijuana and Alzheimer's disease pathology.
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Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids
-
Endocannabinoid signaling in neurotoxicity and neuroprotection.
-
Regulatory role of cannabinoid receptor 1 in stress-induced excitotoxicity and neuroinflammation.
-
Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.
-
Alzheimer's disease; taking the edge off with cannabinoids?
-
Activation of type 1 cannabinoid receptor (CB1R) promotes neurogenesis in murine subventricular zone cell cultures.
