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Sweet Marijane,
'''This page has moved [https://www.isotoperesearch.ca/wiki/index.php?title=THC here]'''


Before the dawn of ages you have cured the afflicted from mental oppression,
__TOC__
===Synopsis===
* Delta(9)-tetrahydrocannabinol (THC) is the main psychoactive constituent of the Cannabis sativa L (Marijuana) plant.
* Others marijuana-derived cannabinoids includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), Cannabigerol (CBG), and Tetrahydrocannabivarin (THCV).
* Marijuana-derived cannabinoids are known as phytocannabinoids.
* THCA is the biosynthetic precursor of THC.


We have learned to cultivate you  even you were repressed from repressors of the truth,
===Antidepressant properties of THC===
* THC may stimulate anandamide mobilization(?) by binding to the CB1 receptor, thus producing a antidepressant and neuroprotective effect. <cite>Website2</cite>


We have tried to make you appear as a sickeness for the weaken, but you were our reason for hope and justice,
===Neuroprotective properties of THC===
====Alzheimer====
* THC may inhibit acetylcholinesterase-induced intraneuronal amyloid beta aggregation in Alzheimer's disease. <cite>Eubanks-2006</cite>
* THC may prevent intracellular amyloid beta proteotoxicity and inflammatory response. <cite>Website4</cite>
====Drug-induced dopamine supersensitivity====
* THC is high-affinity dopamine agonist for reversing drug-induced dopamine supersensitivity. <cite>Pope-2010</cite>
====Cognitive aging====
* THC may reverse the cognitive aging process in the brain. (Reference needed)


To prevail on us,
====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.
====Tardive diskinesia====
* [https://www.mrnice.nl/forum/9-patients-forum/15850-cannabinoids-prevention-management-tardive-diskinesia.html Cannabinoids for prevention and management of tardive diskinesia?]


We have ridiculized you as a gateway drug for ridiculous reasons, and you were none of that,
====Traumatic brain injury====
* Do THC exert a neuroprotective effect on TBI?
** Review: https://www.ncbi.nlm.nih.gov/pubmed/25264643


We have guessed on your origins blindly, yet poorly aware of the [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165946/ science] which you draw your benefits and [http://www.ncbi.nlm.nih.gov/pubmed/16728591/ love] for us,
====Posttraumatic stress disorder====
* THC may reduce chronic nightmares frequency and alter dreaming activity?


We try to commit you in illegal prohibition and traffic, but you still growing silently,
====Sleep regulation====
* THC may affect REM-sleep rebound. <cite>Murillo-2003</cite>
* THC may reduce REM-sleep and increase slow wave sleep (SWS).


You were equally refusing to listen to the voices of oppression and resisting to moths,
===Effects of THC on neurogenesis, synaptogenesis and BDNF signaling===
* Hippocampal CB1 receptors regulate stress-induced neuroinflammation in the hippocampus. <cite>Zoppi-2011</cite>
* THC enhance adult hippocampal neurogenesis and BDNF signaling through intracellular CB1 receptor activation. <cite>Jiang-2005</cite><cite>Campbell-2007</cite>
* Intracellular CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. <cite>Xapelli-2013</cite>


And I love you for that,
===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.


My Dear Sweet Marijane,  
===Notes===
* THC may increase serotonergic tone. <cite>Nutt-2011</cite>
* '''Possible cross-talk between dopaminergic vitamin D, delta9-THC, and endogenous cannabinoids (anandamide) ?'''


Let your roots become a source of inspiration for thoses who seek the truth and recomfort in your love!
===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. <cite>Todd-2016</cite>
* Long-term THC administration may depletes melatonin synthesis.


----
===References===
<biblio>
#Eubanks-2006 https://www.ncbi.nlm.nih.gov/pubmed/17140265
//A molecular link between the active component of marijuana and Alzheimer's disease pathology.
#Pope-2010 https://www.ncbi.nlm.nih.gov/pubmed/19969019
//Endocannabinoid signaling in neurotoxicity and neuroprotection.
#Jiang-2005 https://www.ncbi.nlm.nih.gov/pubmed/16224541
//Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.
#Campbell-2007 https://www.ncbi.nlm.nih.gov/pubmed/17828287
//Alzheimer's disease; taking the edge off with cannabinoids?
#Xapelli-2013 https://www.ncbi.nlm.nih.gov/pubmed/23704915
//Activation of type 1 cannabinoid receptor (CB1R) promotes neurogenesis in murine subventricular zone cell cultures.
#Zoppi-2011 https://www.ncbi.nlm.nih.gov/pubmed/21150911
//Regulatory role of cannabinoid receptor 1 in stress-induced excitotoxicity and neuroinflammation.
#Website2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/
//Antidepressant-like effect of Δ9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L.
#Website4 http://www.nature.com/articles/npjamd201612
//Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids.
#Xiong-2011 https://www.ncbi.nlm.nih.gov/pubmed/21460829
//Cannabinoid potentiation of glycine receptors contributes to cannabis-induced analgesia.
#Gorzo-2017 https://www.ncbi.nlm.nih.gov/pubmed/28481360
//A chronic low dose of Δ9-tetrahydrocannabinol (THC) restores cognitive function in old mice.
#Nutt-2011 https://www.ncbi.nlm.nih.gov/pubmed/22045940
//Low serotonergic tone and elevated risk for substance misuse.
#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.
#Nguyen-2014 https://www.ncbi.nlm.nih.gov/pubmed/25264643
//Effect of marijuana use on outcomes in traumatic brain injury.
#Murillo-2003 https://www.ncbi.nlm.nih.gov/pubmed/12895525
//Potential role of the cannabinoid receptor CB1 in rapid eye movement sleep rebound.
</biblio>


[[User:Etienne Robillard|Etienne Robillard]] 11:58, 28 January 2013 (EST)
===See also===
* [[User:Etienne_Robillard/Notebook/AKT1|AKT1 Notebook]]
* [[User:Etienne_Robillard/Notebook/TRPV1|TRPV1 Notebook]]
* [[User:Etienne_Robillard/Notebook/THCV|THCV Notebook]]
* [[User:Etienne_Robillard/Notebook/Endocannabinoids|Endocannabinoids Notebook]]
* [https://en.wikipedia.org/wiki/Cannabinoid Cannabinoid]
* [https://en.wikipedia.org/wiki/Tetrahydrocannabinol Tetrahydrocannabinol]
* [https://en.wikipedia.org/wiki/Tetrahydrocannabinolic_acid THCA]
* [https://www.thenakedscientists.com/forum/index.php?topic=65952.0 What are the effects of THC tolerance?]

Latest revision as of 14:58, 2 October 2018

This page has moved here

Synopsis

  • Delta(9)-tetrahydrocannabinol (THC) is the main psychoactive constituent of the Cannabis sativa L (Marijuana) plant.
  • Others marijuana-derived cannabinoids includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), Cannabigerol (CBG), and Tetrahydrocannabivarin (THCV).
  • Marijuana-derived cannabinoids are known as phytocannabinoids.
  • THCA is the biosynthetic precursor of THC.

Antidepressant properties of THC

  • THC may stimulate anandamide mobilization(?) 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]

Drug-induced dopamine supersensitivity

  • THC is high-affinity dopamine agonist for reversing drug-induced dopamine supersensitivity. [4]

Cognitive aging

  • THC may reverse the cognitive aging process in the brain. (Reference needed)

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.

Tardive diskinesia

Traumatic brain injury

Posttraumatic stress disorder

  • THC may reduce chronic nightmares frequency and alter dreaming activity?

Sleep regulation

  • THC may affect REM-sleep rebound. [5]
  • THC may reduce REM-sleep and increase slow wave sleep (SWS).

Effects of THC on neurogenesis, synaptogenesis and BDNF signaling

  • Hippocampal CB1 receptors regulate stress-induced neuroinflammation in the hippocampus. [6]
  • THC enhance adult hippocampal neurogenesis and BDNF signaling through intracellular CB1 receptor activation. [7][8]
  • Intracellular CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. [9]

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. [10]
  • 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. [11]
  • Long-term THC administration may depletes melatonin synthesis.

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/12895525

    [Murillo-2003]

    Potential role of the cannabinoid receptor CB1 in rapid eye movement sleep rebound.

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

    [Zoppi-2011]

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

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

    [Jiang-2005]

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

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

    [Campbell-2007]

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

  9. 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.

  10. https://www.ncbi.nlm.nih.gov/pubmed/22045940

    [Nutt-2011]

    Low serotonergic tone and elevated risk for substance misuse.

  11. https://www.ncbi.nlm.nih.gov/pubmed/26377899

    [Todd-2016]

    Neural correlates of interactions between cannabidiol and Δ(9) -tetrahydrocannabinol in mice: implications for medical cannabis.

  12. https://www.ncbi.nlm.nih.gov/pubmed/21460829

    [Xiong-2011]

    Cannabinoid potentiation of glycine receptors contributes to cannabis-induced analgesia.

  13. https://www.ncbi.nlm.nih.gov/pubmed/28481360

    [Gorzo-2017]

    A chronic low dose of Δ9-tetrahydrocannabinol (THC) restores cognitive function in old mice.

  14. https://www.ncbi.nlm.nih.gov/pubmed/25264643

    [Nguyen-2014]

    Effect of marijuana use on outcomes in traumatic brain injury.

See also

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