User:Etienne Robillard/Notebook/THC

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Contents

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

References

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/ [Website2]
    Antidepressant-like effect of Δ9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L

  2. https://www.ncbi.nlm.nih.gov/pubmed/17140265

    [Eubanks-2006]

    A molecular link between the active component of marijuana and Alzheimer's disease pathology.

  3. http://www.nature.com/articles/npjamd201612

    [Website4]

    Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids

  4. https://www.ncbi.nlm.nih.gov/pubmed/19969019

    [Pope-2010]

    Endocannabinoid signaling in neurotoxicity and neuroprotection.

  5. https://www.ncbi.nlm.nih.gov/pubmed/21150911

    [Zoppi-2011]

    Regulatory role of cannabinoid receptor 1 in stress-induced excitotoxicity and neuroinflammation.

  6. https://www.ncbi.nlm.nih.gov/pubmed/16224541

    [Jiang-2005]

    Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.

  7. https://www.ncbi.nlm.nih.gov/pubmed/17828287

    [Campbell-2007]

    Alzheimer's disease; taking the edge off with cannabinoids?

  8. https://www.ncbi.nlm.nih.gov/pubmed/23704915

    [Xapelli-2013]

    Activation of type 1 cannabinoid receptor (CB1R) promotes neurogenesis in murine subventricular zone cell cultures.

See also

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