User:Tkadm30/Notebook/THC: Difference between revisions
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===Synopsis=== | ===Synopsis=== | ||
* Tetrahydrocannabinol (THC) is the main psychoactive constituent of Cannabis sativa L (Marijuana) plant. | * Tetrahydrocannabinol (THC) is the main psychoactive constituent of Cannabis sativa L (Marijuana) plant. | ||
* Other Marijuana compounds includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), | * Other Marijuana compounds includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), Cannabigerol (CBG), Tetrahydrocannabivarin (THCV). | ||
* Cannabis-derived cannabinoids are known as phytocannabinoids. | * Cannabis-derived cannabinoids are known as phytocannabinoids. | ||
===Antidepressant properties of THC=== | ===Antidepressant properties of THC=== | ||
| Line 9: | Line 9: | ||
===Neuroprotective properties of THC=== | ===Neuroprotective properties of THC=== | ||
* THC inhibit acetylcholinesterase (AChE)-induced beta | * THC inhibit acetylcholinesterase (AChE)-induced intraneuronal amyloid beta aggregation in Alzheimer's disease: <cite>Eubanks-2006</cite> | ||
* THC as antiglutamatergic therapy for | ** THC prevent intracellular amyloid beta proteotoxicity and inflammatory response: <cite>Website4</cite> | ||
* THC is effective as antiglutamatergic therapy for NMDA-induced excitotoxicity. <cite>Pope-2010</cite> | |||
* Unlike THC, caffeine is a noncompetitive reversible inhibitor of AChE. | * 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. | * 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 | ===Proneurogenic effects of THC on neurogenesis and BDNF signaling=== | ||
* Hippocampal CB1 receptors regulate stress-induced neuroinflammation in the hippocampus. <cite>Zoppi-2011</cite> | * Hippocampal CB1 receptors regulate stress-induced neuroinflammation in the hippocampus. <cite>Zoppi-2011</cite> | ||
* THC enhance adult hippocampal neurogenesis through intracellular CB1 receptor activation. <cite>Jiang-2005</cite><cite>Campbell-2007</cite> | * THC enhance adult hippocampal neurogenesis and BDNF signaling through intracellular CB1 receptor activation. <cite>Jiang-2005</cite><cite>Campbell-2007</cite> | ||
* CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. <cite>Xapelli-2013</cite> | * Intracellular CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. <cite>Xapelli-2013</cite> | ||
===Neuropsychology of THC tolerance=== | ===Neuropsychology of THC tolerance=== | ||
* CB1 receptor sensitization can be restored by taking breaks of oral THC administration, which stimulates endocannabinoid production. | * CB1 receptor sensitization can be restored by taking breaks of oral THC administration, which stimulates endocannabinoid production. <cite>Website3</cite> | ||
* Alcohol increase THC levels in blood. | |||
===Experimental=== | ===Experimental=== | ||
* Synaptogenic effect of THC/DHA promote hippocampal development (neurogenesis) and synaptogenesis. | * 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/DHA affect neural stem/progenitor cells (NS/PC) proliferation in the hippocampus. | ||
* [https://www.ncbi.nlm.nih.gov/pubmed/26377899 THC enhance corticostriatal functional connectivity though increased c-Fos expression.] | |||
===References=== | ===References=== | ||
<biblio> | <biblio> | ||
#Eubanks-2006 | #Eubanks-2006 https://www.ncbi.nlm.nih.gov/pubmed/17140265 | ||
//A molecular link between the active component of marijuana and Alzheimer's disease pathology. | //A molecular link between the active component of marijuana and Alzheimer's disease pathology. | ||
#Pope-2010 | #Pope-2010 https://www.ncbi.nlm.nih.gov/pubmed/19969019 | ||
//Endocannabinoid signaling in neurotoxicity and neuroprotection. | //Endocannabinoid signaling in neurotoxicity and neuroprotection. | ||
#Jiang-2005 | #Jiang-2005 https://www.ncbi.nlm.nih.gov/pubmed/16224541 | ||
//Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects. | //Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects. | ||
#Campbell-2007 | #Campbell-2007 https://www.ncbi.nlm.nih.gov/pubmed/17828287 | ||
//Alzheimer's disease; taking the edge off with cannabinoids? | //Alzheimer's disease; taking the edge off with cannabinoids? | ||
#Xapelli-2013 | #Xapelli-2013 https://www.ncbi.nlm.nih.gov/pubmed/23704915 | ||
//Activation of type 1 cannabinoid receptor (CB1R) promotes neurogenesis in murine subventricular zone cell cultures. | //Activation of type 1 cannabinoid receptor (CB1R) promotes neurogenesis in murine subventricular zone cell cultures. | ||
#Zoppi-2011 | #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. | ||
#Website1 https://en.wikipedia.org/wiki/Cannabinoid | #Website1 https://en.wikipedia.org/wiki/Cannabinoid | ||
#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 | ||
#Website3 http://www.thenakedscientists.com/forum/index.php?topic=65952.0 | |||
#Website4 http://www.nature.com/articles/npjamd201612 | |||
//Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids | |||
</biblio> | </biblio> | ||
===See also=== | ===See also=== | ||
* [[User:Etienne_Robillard/Notebook/TRPV1|TRPV1 Notebook]] | * [[User:Etienne_Robillard/Notebook/TRPV1|TRPV1 Notebook]] | ||
Revision as of 07:55, 11 December 2016
Synopsis
- Tetrahydrocannabinol (THC) is the main psychoactive constituent of Cannabis sativa L (Marijuana) plant.
- Other Marijuana compounds includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), Cannabigerol (CBG), Tetrahydrocannabivarin (THCV).
- Cannabis-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, which stimulates endocannabinoid production. [9]
- Alcohol increase THC levels in blood.
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
-
A molecular link between the active component of marijuana and Alzheimer's disease pathology.
-
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.
