The recent identification of cannabinoid receptors and their endogenous lipid ligands has triggered an exponential growth of studies exploring the endocannabinoid system and its regulatory functions in health and disease. Such studies have been greatly facilitated by the introduction of selective cannabinoid receptor antagonists and inhibitors of endocannabinoid metabolism and transport, as well as mice deficient in cannabinoid receptors or the endocannabinoid-degrading enzyme fatty acid amidohydrolase. In the past decade, the endocannabinoid system has been implicated in a growing number of physiological functions, both in the central and peripheral nervous systems and in peripheral organs. More importantly, modulating the activity of the endocannabinoid system turned out to hold therapeutic promise in a wide range of disparate diseases and pathological conditions, ranging from mood and anxiety disorders, movement disorders such as Parkinson9s and Huntington9s disease, neuropathic pain, multiple sclerosis and spinal cord injury, to cancer, atherosclerosis, myocardial infarction, stroke, hypertension, glaucoma, obesity/metabolic syndrome, and osteoporosis, to name just a few. An impediment to the development of cannabinoid medications has been the socially unacceptable psychoactive properties of plant-derived or synthetic agonists, mediated by CB 1 receptors. However, this problem does not arise when the therapeutic aim is achieved by treatment with a CB 1 receptor antagonist, such as in obesity, and may also be absent when the action of endocannabinoids is enhanced indirectly through blocking their metabolism or transport. The use of selective CB 2 receptor agonists, which lack psychoactive properties, could represent another promising avenue for certain conditions. The abuse potential of plant-derived cannabinoids may also be limited through the use of preparations with controlled composition and the careful selection of dose and route of administration. The growing number of preclinical studies and clinical trials with compounds that modulate the endocannabinoid system will probably result in novel therapeutic approaches in a number of diseases for which current treatments do not fully address the patients9 need. Here, we provide a comprehensive overview on the current state of knowledge of the endocannabinoid system as a target of pharmacotherapy.

http://www.phytecs.com/wp-content/uploads/2015/02/Pharmacol-Rev-2006-Pacher-389-462.pdf

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

http://www.student.oulu.fi/~taneliha/15min_Vertailevan_Endokrinologian_opiskelijaesitelma_Endokannabinoidit/Suurin%20osa%20k%E4ytetyist%E4%20artikkeleista/Cannabinoid%20physiology%20and%20pharmacology%2030%20years%20of%20progress.pdf

Cannabinoid physiology and pharmacology: 30 years of progress

Cannabis: effects on memory and the cholinergic limbic system.

Marijuana intoxication and brain activation in marijuana smokers

Cannabinoids and the brain , Cannabinoids and the brain , کتابخانه مرکزی دانشگاه علوم پزشکی تهران

http://psychstudent.persiangig.com/books/Cannabinoids%20and%20the%20Brain.pdf

Cannabinoids and the brain

Δ9-tetrahydrocannabinol alters flow of blood to subcortical areas of the conscious rat brain

In an attempt to define the nature of the involvement of Δ9-tetrahydrocannabinol (THC) with central cholinergic neurotransmission, the effects of THC on direct cholinergic stimulation of the rat brain were investigated. THC, in doses of 3 mg/kg and 6 mg/kg, administered intraperitoneally (i.p.), potentiated the effects of carbachol injection into the lateral septal nucleus, as manifested by enhancement of the drinking response elicited by the septal carbachol injection and by potentiation of the tendency of this carbachol injection to induce abnormal motor responses. Although atropine (10 mg/kg, i.p.) completely blocked the carbachol induced drinking, the atropine did not completely block the drinking response when THC was given with carbachol. The results indicate an apparent sensitization, by THC, of a limbic cholinergic system.

Rose Dagirmanjian

Papers

Δ9-tetrahydrocannabinol alters flow of blood to subcortical areas of the conscious rat brain

Delta 9-tetrahydrocannabinol sensitization of the rat brain to direct cholinergic stimulation.