User:Tkadm30/Notebook/THC: Difference between revisions
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* THC may reduce intraocular pressure (IOP) in retinal ganglion cells (RGCs) through intracellular CB1 receptor activation. | * 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. | ** A potential treatment for glaucoma to prevent optic nerve damage. | ||
====Traumatic brain injury==== | |||
* How do delta9-THC exert a neuroprotective effect on TBI? | |||
** Review: https://www.ncbi.nlm.nih.gov/pubmed/25264643 | |||
====PTSD==== | |||
XXX | |||
===Effects of THC on neurogenesis, synaptogenesis and BDNF signaling=== | ===Effects of THC on neurogenesis, synaptogenesis and BDNF signaling=== | ||
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===Notes=== | ===Notes=== | ||
* 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, delta9-THC, and endogenous cannabinoids (anandamide) ? | * '''Possible cross-talk between dopaminergic vitamin D, delta9-THC, and endogenous cannabinoids (anandamide) ?''' | ||
===Experimental=== | ===Experimental=== | ||
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#Todd-2016 https://www.ncbi.nlm.nih.gov/pubmed/26377899 | #Todd-2016 https://www.ncbi.nlm.nih.gov/pubmed/26377899 | ||
//Neural correlates of interactions between cannabidiol and Δ(9) -tetrahydrocannabinol in mice: implications for medical cannabis. | //Neural correlates of interactions between cannabidiol and Δ(9) -tetrahydrocannabinol in mice: implications for medical cannabis. | ||
#Nguyen-2014 https://www.ncbi.nlm.nih.gov/pubmed/25264643 | |||
//Effect of marijuana use on outcomes in traumatic brain injury. | |||
</biblio> | </biblio> | ||
Revision as of 11:26, 22 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.
Traumatic brain injury
- How do delta9-THC exert a neuroprotective effect on TBI?
PTSD
XXX
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, delta9-THC, 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.
-
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.
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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.
-
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.
-
Low serotonergic tone and elevated risk for substance misuse.
-
Neural correlates of interactions between cannabidiol and Δ(9) -tetrahydrocannabinol in mice: implications for medical cannabis.
-
Cannabinoid potentiation of glycine receptors contributes to cannabis-induced analgesia.
-
A chronic low dose of Δ9-tetrahydrocannabinol (THC) restores cognitive function in old mice.
-
Effect of marijuana use on outcomes in traumatic brain injury.