User:Tkadm30/Notebook/THC: Difference between revisions
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===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), and Cannabigerol (CBG). | * Other Marijuana compounds includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), and Cannabigerol (CBG). | ||
* Cannabis-derived cannabinoids are known as phytocannabinoids. | * Cannabis-derived cannabinoids are known as phytocannabinoids. | ||
* THC stimulate anandamide | * THC stimulate anandamide biosynthesis by binding to the CB1 receptor, thus producing a antidepressant and neuroprotective effect. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/ PMID] [https://www.ncbi.nlm.nih.gov/pubmed/7702643 PMID] | ||
=== THC effect on | |||
===Anticholinergic properties of THC=== | |||
* THC inhibit anticholinesterase (AChE) induced beta-amyloid aggregation in Alzheimer's disease: [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562334/ PMID] | |||
* THC as antiglutamatergic therapy for AChE induced neurotoxicity: [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2891218/ PMID] [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366364/ PMID] [https://www.ncbi.nlm.nih.gov/pubmed/18680758 PMID] | |||
* Unlike THC, caffeine is a noncompetitive reversible inhibitor of AChE | |||
===Proneurogenic effect of THC on neurogenesis=== | |||
* Regulation of stress-induced neuroinflammation in the hippocampus. | * Regulation of stress-induced neuroinflammation in the hippocampus. | ||
* Hippocampal neurogenesis is enhanced. [ | * Hippocampal neurogenesis is enhanced. [https://www.ncbi.nlm.nih.gov/pubmed/16224541/ PMID] [https://www.ncbi.nlm.nih.gov/pubmed/17828287 PMID] | ||
* CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. [https://www.ncbi.nlm.nih.gov/pubmed/23704915 PMID] | |||
===Experimental=== | |||
* Synaptogenic effect of Δ9-THC/DHEA ligands promote hippocampal development. | * Synaptogenic effect of Δ9-THC/DHEA ligands promote hippocampal development. | ||
* Δ9-THC/DHEA ligands (synaptamide) affect neural stem/progenitor cells (NS/PC) proliferation in the hippocampus. | * Δ9-THC/DHEA ligands (synaptamide) affect neural stem/progenitor cells (NS/PC) proliferation in the hippocampus. | ||
=== References === | ===References=== | ||
# https://en.wikipedia.org/wiki/Cannabinoid | |||
===See also=== | |||
* [[User:Etienne_Robillard/Notebook/TRPV1|TRPV1 Notebook]] | |||
Revision as of 05:05, 20 August 2015
Synopsis
- Tetrahydrocannabinol (THC) is the main psychoactive constituent of Cannabis sativa L (Marijuana) plant.
- Other Marijuana compounds includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), and Cannabigerol (CBG).
- Cannabis-derived cannabinoids are known as phytocannabinoids.
- THC stimulate anandamide biosynthesis by binding to the CB1 receptor, thus producing a antidepressant and neuroprotective effect. PMID PMID
Anticholinergic properties of THC
- THC inhibit anticholinesterase (AChE) induced beta-amyloid aggregation in Alzheimer's disease: PMID
- THC as antiglutamatergic therapy for AChE induced neurotoxicity: PMID PMID PMID
- Unlike THC, caffeine is a noncompetitive reversible inhibitor of AChE
Proneurogenic effect of THC on neurogenesis
- Regulation of stress-induced neuroinflammation in the hippocampus.
- Hippocampal neurogenesis is enhanced. PMID PMID
- CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. PMID
Experimental
- Synaptogenic effect of Δ9-THC/DHEA ligands promote hippocampal development.
- Δ9-THC/DHEA ligands (synaptamide) affect neural stem/progenitor cells (NS/PC) proliferation in the hippocampus.
