Sandbox 420: Difference between revisions
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CB1 is one of two receptors in the human body that recognizes five endocannabinoid compounds as well as exogenous cannabinoids like THC and K2. The CB1 receptor is a G protein-coupled receptor located primarily in the nervous system <ref name="review">PMID: 185848585</ref>. The primary function of the CB1 receptor is to bind endogenous and exogenous ligands to activate signal transduction pathways for the cells in which they are located <ref name = "review"/>. The function of CB1 receptors thus depends on the location of the receptor as well as the type of ligand binding to the receptor. As a result, CB1 receptors are involved in regulating a variety of physiological functions including regulation of neurotransmitters, pain modulation, memory, motor control, control of appetite, and regulation of anxiety. | CB1 is one of two receptors in the human body that recognizes five endocannabinoid compounds as well as exogenous cannabinoids like THC and K2. The CB1 receptor is a G protein-coupled receptor located primarily in the nervous system <ref name="review">PMID: 185848585</ref>. The primary function of the CB1 receptor is to bind endogenous and exogenous ligands to activate signal transduction pathways for the cells in which they are located <ref name = "review"/>. The function of CB1 receptors thus depends on the location of the receptor as well as the type of ligand binding to the receptor. As a result, CB1 receptors are involved in regulating a variety of physiological functions including regulation of neurotransmitters, pain modulation, memory, motor control, control of appetite, and regulation of anxiety. | ||
==Regulation of Neurotransmitters== | ===Regulation of Neurotransmitters=== | ||
The highest concentration of CB1 receptors is found within presynaptic nerve terminals <ref>PMID: 16723537</ref>. When ligands bind to CB1 receptors in presynaptic nerve terminals, calcium channels are inhibited. The release of calcium is a key component of nerve signal transduction pathway that results in the release of neurotransmitters in the synaptic cleft. As a result, activated CB1 receptors are able to regulate the release of neurotransmitters. CB1 receptors have been shown to inhibit the release of glutamate, acetylcholine, and noradrenaline <ref name = "review"/>. | The highest concentration of CB1 receptors is found within presynaptic nerve terminals <ref>PMID: 16723537</ref>. When ligands bind to CB1 receptors in presynaptic nerve terminals, calcium channels are inhibited. The release of calcium is a key component of nerve signal transduction pathway that results in the release of neurotransmitters in the synaptic cleft. As a result, activated CB1 receptors are able to regulate the release of neurotransmitters. CB1 receptors have been shown to inhibit the release of glutamate, acetylcholine, and noradrenaline <ref name = "review"/>. Additionally, activated CB1 receptors suppresses the activity of GABAergic neurons, which control neurons responsible for the release of dopamine <ref name ="g">DOI 10.1073/pnas.1016442108</ref>. By suppressing GABAergic neurons, dopamine levels in the brain are increased. This action of CB1 receptors is responsible for the pleasure associated the THC use and the potential for abuse of exergonic cannabinoids. | ||
===Pain Modulation=== | |||
==Pain Modulation== | |||
CB1 receptors are also highly expressed in areas of the nervous system involved with pain modulation, specifically in the dorsal root ganglia <ref name = "review"/>. This is one of the most well known functions of CB1 receptors and is responsible for the pain reduction effects associated with THC. | CB1 receptors are also highly expressed in areas of the nervous system involved with pain modulation, specifically in the dorsal root ganglia <ref name = "review"/>. This is one of the most well known functions of CB1 receptors and is responsible for the pain reduction effects associated with THC. | ||
==Memory== | ===Memory=== | ||
CB1 receptors are also highly concentrated in the hippocampus. The hippocampus is a region of the brain involved with learning and memory <ref name ="g"/>. The relatively high density of CB1 receptors in the hippocampus is responsible for the memory-altering effects of THC and other cannabinoids <ref> PMID: 22385967 </ref>. | CB1 receptors are also highly concentrated in the hippocampus. The hippocampus is a region of the brain involved with learning and memory <ref name ="g"/>. The relatively high density of CB1 receptors in the hippocampus is responsible for the memory-altering effects of THC and other cannabinoids <ref> PMID: 22385967 </ref>. | ||
==Motor Control== | ===Motor Control=== | ||
CB1 receptors are also located in the basal ganglia, a region of the brain responsible for the coordination of movement <ref name="review"/>. The binding of endocannabinoids has been shown to play a critical role in fine motor control. Specifically, it has been shown that CB1 receptor binding is decreased in patients with neurodegenerative diseases such as Parkinson’s and Huntington’s disease. In contrast, CB1 receptors have a lesser influence on gross motor control due to the lower concentration of receptors in the cerebellum, which is responsible for coordinating gross motor control <ref name="review"/>. | CB1 receptors are also located in the basal ganglia, a region of the brain responsible for the coordination of movement <ref name="review"/>. The binding of endocannabinoids has been shown to play a critical role in fine motor control. Specifically, it has been shown that CB1 receptor binding is decreased in patients with neurodegenerative diseases such as Parkinson’s and Huntington’s disease. In contrast, CB1 receptors have a lesser influence on gross motor control due to the lower concentration of receptors in the cerebellum, which is responsible for coordinating gross motor control <ref name="review"/>. | ||
==Control of Appetite== | ===Control of Appetite=== | ||
CB1 receptors play a significant role in appetite control by regulating food intake, influencing fat accumulation, and altering lipid and glucose metabolism. Activation of CB1, results in the release of hormones that promote hunger and thus stimulate appetite <ref name = "food">PMID: 24933167</ref>. CB1 also interacts with the neuropeptides controlling functions of lipid and glucose metabolism. As a result, the endogenous function of CB1 receptors is key to controlling homeostasis in energy balance <ref name="food"/>. Furthermore, hyperactivity of these functions is associated THC use. This function of CB1 receptors may play a key role in the development of obesity treatments. | CB1 receptors play a significant role in appetite control by regulating food intake, influencing fat accumulation, and altering lipid and glucose metabolism. Activation of CB1, results in the release of hormones that promote hunger and thus stimulate appetite <ref name = "food">PMID: 24933167</ref>. CB1 also interacts with the neuropeptides controlling functions of lipid and glucose metabolism. As a result, the endogenous function of CB1 receptors is key to controlling homeostasis in energy balance <ref name="food"/>. Furthermore, hyperactivity of these functions is associated THC use. This function of CB1 receptors may play a key role in the development of obesity treatments. | ||
==Regulation of Anxiety== | ===Regulation of Anxiety=== | ||
CB1 receptors are responsible for mediating the anti-anxiety effects of cannabinoids, like THC. In low doses, cannabinoids reduce anxiety; however, high doses of cannabinoids act to increase anxiety <ref name="toxic" />. This is one reason why synthetic cannabinoids like K2, an extremely potent synthetic cannabinoid, produces the harmful side effect of extreme anxiety. | CB1 receptors are responsible for mediating the anti-anxiety effects of cannabinoids, like THC. In low doses, cannabinoids reduce anxiety; however, high doses of cannabinoids act to increase anxiety <ref name="toxic" />. This is one reason why synthetic cannabinoids like K2, an extremely potent synthetic cannabinoid, produces the harmful side effect of extreme anxiety. | ||
== References == | == References == | ||
<references/> | <references/> | ||