User:Tkadm30/Notebook/THC: Difference between revisions
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* THC may increase serotonergic tone. <cite>Nutt-2011</cite> | * THC may increase serotonergic tone. <cite>Nutt-2011</cite> | ||
* Possible cross-talk between dopaminergic vitamin D and endogenous cannabinoids (anandamide) ? | |||
===Experimental=== | ===Experimental=== | ||
Revision as of 08:57, 20 May 2017
Synopsis
- Delta9-tetrahydrocannabinol (THC) is the main psychoactive constituent of the 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
Alzheimer
- THC may inhibit acetylcholinesterase-induced intraneuronal amyloid beta aggregation in Alzheimer's disease. [2]
- THC may prevent intracellular amyloid beta proteotoxicity and inflammatory response. [3]
Antipsychotic-induced dopamine supersensitivity
- THC is effective glutamatergic agent for reversing drug-induced neuronal excitotoxicity. [4]
Glaucoma
- THC may reduce intraocular pressure (IOP) in retinal ganglion cells (RGCs) through intracellular CB1 receptor activation.
- A potential treatment for glaucoma to prevent optic nerve damage.
Effects of THC on neurogenesis, synaptogenesis 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.
Notes
- THC may increase serotonergic tone. [9]
- Possible cross-talk between dopaminergic vitamin D and endogenous cannabinoids (anandamide) ?
Experimental
- Endogenous retrograde trafficking may promote hippocampal development (neurogenesis) and synaptogenesis.
- Arachidonic acid/DHA levels affect neural stem/progenitor cells (NSPCs) proliferation in the hippocampus. (Reference needed)
- THC may enhance corticostriatal functional connectivity though increased c-Fos expression. [10]
References
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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.
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Endocannabinoid signaling in neurotoxicity and neuroprotection.
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Regulatory role of cannabinoid receptor 1 in stress-induced excitotoxicity and neuroinflammation.
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Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.
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Alzheimer's disease; taking the edge off with cannabinoids?
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Activation of type 1 cannabinoid receptor (CB1R) promotes neurogenesis in murine subventricular zone cell cultures.
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Low serotonergic tone and elevated risk for substance misuse.
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Neural correlates of interactions between cannabidiol and Δ(9) -tetrahydrocannabinol in mice: implications for medical cannabis.
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Cannabinoid potentiation of glycine receptors contributes to cannabis-induced analgesia.
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A chronic low dose of Δ9-tetrahydrocannabinol (THC) restores cognitive function in old mice.
