To understand the steps that THC take to bind and active neurons, it's best to know the parts of the brain that are involved, "Neurons are the cells that process information in the brain.
Chemicals called neurotransmitters allow neurons to communicate with each other. Neurotransmitters fill the gap, or synapse, between two neurons and bind to protein receptors, which allow various functions in the brain and body to be turned on and off. Some neurons have thousands of receptors that are specific to particular neurotransmitters.
Foreign chemicals, like THC, can mimic or block actions of neurotransmitters and interfere with normal functions. Cannabinoids work slightly different from other neurotransmitters; in fact, they work backwards. Neurons work by communicating with each other and the rest of the body by sending chemical messages.
These messages are responsible for regulating our motor and cognitive functions. However, with the endocannabinoid EC system, the message is communicated differently.
They can control what happens next when the cells are activated, allowing it to control how messages are sent, received, and processed but the cell. Scientists have identified the two primary cannabinoid receptors which are CB1 and CB2.
The CB1 receptor is found in the brain and nervous system and is the main receptor for THC and anandamide. The receptor found in the immune system and surrounding structures is CB2, which is responsible for modulating antiinflammatory effects. When "THC gets into the brain rapidly it attaches to cannabinoid receptors. The natural EC system is finely tuned to react appropriately to incoming information. It prevents the natural chemicals from doing their job properly and throws the whole system off balance.
As such strangely some even think THC is a great way to manage some pest control issue too. The following video does a great job of explaining how the brain normally functions without any interference from THC and how it changes once THC in consumed.
Login here. Register Free. They also discuss how modulation of ANA levels through inhibition of enzymatic metabolic pathways could provide a basis for developing new pharmaco-therapeutic tools for the treatment of substance use disorders [ 4 ]. The authors found that systemic administration of AM significantly inhibited intravenous heroin self-administration similar to SRA. These findings suggest that AM or other neutral CB 1 R antagonists may serve as a new class of CB 1 R-based medications for the treatment of opioid addiction without SRA-like side-effects [ 5 ].
They suggest that allosteric CB 1 modulators provide tremendous opportunities to develop CB 1 ligands with novel mechanisms of action; these ligands potentially improve the pharmacological effects and enhance drug safety in treating the disorders by regulating the functions of the CB 1 receptor [ 6 ].
This study challenges the experimental approach that targeting peripheral CB 1 R is desirable for the treatment of metabolic syndromes without adverse neuropsychiatric effects using rodents. The results suggest that none of the tested four polyclonal antibodies are highly mouse CB 2 R-specific.
Non-specific binding may be related to the expression of mutant or truncated CB 2 R-like proteins in those partial CB 2 -KO mice and the use of anti-rat CB 2 antibodies because the epitopes are different between rat and mouse CB 2 Rs [ 8 ]. This work provides an important caution for using CB 2 R antibodies to identify CB 2 R expression in the future study. Xia et al. Authors introduce several novels of CB 2 R radiotracers that have been developed and evaluated to quantify microglial activation.
There are two review articles that discuss the endocannabinoid eCB system. Based on available data they suggest that the interaction between the endocannabinoid and endovanilloid signaling systems can be exploited for therapeutic applications in health and disease. Overall, the present special issue provides an overview and insight on pharmacological mechanisms and therapeutic potentials of cannabis, cannabinoid receptors, and eCB system.
I believe that this special issue will promote further efforts to apply cannabinoid ligands as the therapeutic strategies for treating a variety of diseases.
Although concepts and accumulating lines of evidence have been established, the challenges still remain in the cannabinoid research field and clinical practice. Following four aspects should be addressed in the future research regarding cannabis, cannabinoid receptors, and eCB system.
Heterogeneity: We should fully realize that cannabis, cannabinoid receptors, and eCB system exhibit high heterogeneity, from genes to receptors to intracellular G-protein-coupled signal pathways and membrane ion channels. For example, the same cannabinoid ligand e. Specificity: The most effort in cannabinoid research field is paid for identifying the specificity of cannabinoid effects.
The key question, for instance, is which way is better for desired pharmacology and therapeutics: the specificity or multiple targets. Inducible profile: Cannabinoid receptor, particularly brain CB 2 R, expression displays dynamic and inducible profiles under various pathological conditions. The inducible feature makes brain CB 2 Rs possible as therapeutic targets in the treatment of diseases without interruption of normal brain function.
Cannabidiol does not display drug abuse potential in mice behavior. Acta Pharmacol Sin. Computational systems pharmacology analysis of cannabidiol: a combination of chemogenomics-knowledgebase network analysis and integrated in silico modeling and simulation. GPR6, and GPR12 as novel molecular targets: their biological functions and interaction with cannabidiol. The thalamus showed a distinctive heterogeneous distribution of cannabinoid receptors, with the highest concentration of receptors localized in the mediodorsal nucleus, anterior nuclear complex, and in the midline and intralaminar complex of nuclei, i.
The basal ganglia showed a distinctive heterogeneous pattern of receptor binding, with the very highest concentrations in the globus pallidus internus, moderate concentrations in the globus pallidus externus and ventral pallidum, and moderately low levels of binding throughout the striatal complex. In the midbrain, some of the highest levels of cannabinoid receptor binding sites in the human brain were present in the substantia nigra pars reticulata, with very low levels of labelling in all other midbrain areas.
The highest densities of cannabinoid receptor binding in the hindbrain were localized in the molecular layer of the cerebellar cortex and the dorsal motor nucleus of the vagus, with moderate densities of receptors in the nucleus of the solitary tract. The spinal cord showed very low levels of receptor binding.
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