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Queen's University
Pharmacology and Toxicology
PHAR 100
Hisham Elbatarny

Cannabis Introduction • Cannabis Sativa • History ◦ 2700 BC to 1800’s Hemp used to make rope.Also a drug. ◦ 1920-30 Outlawed marijuana. ◦ 1960’s-1970’s Increased use of marijuana. ▪ 60% of young adults in USA; similar in Canada smoked pot ◦ 1978 U.S.A. sponsored a spraying project to kill marijuana plants ▪ paraquat caused lung damage: when harvested dying plants it found its way onto market • 1980’s Use began to stabilize That is no further increase in rate of smoking. • 1990’s Increase in use of marijuana. Fourth most widely used drug in the world. • 1996 Arizona and California voters approved the use of marijuana for medical use. • 1997 Ont Court allows epileptic to use Marijuana • 1999 Health Canada announces clinical trials on cannabis. Health Canada to provide a standardized product. ◦ ~ 40 thousand people are legally allowed to use marijuana • 1964 THC discovered: tetrahydrol canabinol • Adenylyl cyclase inhibition • 1988 Receptor binding Studies • 1990 CB cl1ned and mapped: target for drug • 1992 Anandamide: endogenous compound that uses the canaboid receptrors → putative neurotransmitter • 1994 First receptor antagonist synthesized • 1995 Precipitated withdrawal to cannabis use • 1999 Abstinence syndrome descrived • 2003 Link between CB (on 2erkal cells?) receptors and inflammation • 2006 Inhaled form of THC: in puffer, approved for neuropathic pain • 2012 Vote to legalize recreational use in one US state.Another votes to legalize for medical use. ◦ Canada: approved to treat nausea associated w/ cancer chemotherapy Classification • Legal – Narcotic • Pharmacological – CNS depressant ◦ Euphoriant ◦ Hallucinogen Pharmacology • Active ingredients – Cannabinoids, • e.g. tetrahydrocannabinol ▪ other cannabinoids in marijuana • Receptors for THC in: ◦ Cerebral cortex ◦ Cerebellum ◦ Hippocampus ◦ Hypothalamus ◦ And other areas ▪ more cannabanoid receptors in the nervous system then any other system • Inhibit release of other transmitters: inhibits inhibatory pathways ◦ can inhibit GABA responses that are inhibiting dopaminergic responses: increase in dopaminergic responses • CB1 in the above areas • CB2 in the periphery • is CB3 but unknown Anandamide THC Mechanism of Action • Binds to CB1 receptors in CNS causing disinhibition of dopaminergic neurons. ◦ (Inhibit GABAand glutamate release) ◦ Reward system (dopamine increased as GABArelease inhibited) ◦ Large number of cannabinoid receptors in CNS Immunosuppression • CB2 Receptor on lymphocytes ◦ Inhibits the action of these cells ◦ May be involved in inflammation • CB3 Function unknown Absorption • From lung – very rapid ◦ duration 3 to 4 hours maximum (max effect 1 -2 hours) • Orally absorption slow and incomplete ◦ Effect orally is less than smoked, at least less euphoria • Metabolism ◦ Slow – half-life 30 hours ( 2 pools) ◦ Stored in fat and this pool slowly excreted ◦ Users test positive weeks after stopping as it is the metabolites that are measured in drug test Medical Uses • Sedative and hypnotic – old use ◦ benzodiazepines are better for this • Nausea and vomiting (cancer chemotherapy) ◦ approved use, but efficacy less than new drugs. ▪ 35-40% response from patients ▪ new drugs: 85-90% response • Anorexia (HIV- drugs cause loss of appetite): activatin
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