User:Tkadm30/Notebook/THC

Synopsis

• 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

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/

   Antidepressant-like effect of Δ9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L

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

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

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

   Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids

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

   Endocannabinoid signaling in neurotoxicity and neuroprotection.

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

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

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

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

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

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

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

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

See also

• TRPV1 Notebook
• THCV Notebook
• Cannabinoid
• http://www.thenakedscientists.com/forum/index.php?topic=65952.0