Brain neuronal Cb2 cannabinoid receptors in drug abuse and depression - Assignment Example

? Brain Neuronal Cb2 Cannabinoid Receptors in Drug Abuse and Depression: From Mice to Human s Brain Neuronal Cb2 Cannabinoid Receptors in Drug Abuse and Depression: From Mice to Human Subjects Background of the Study The stressful events might cause addiction to substances and major depression within the context of mental health problems. Many humans go through high relapse cases and reoccurrence of the cases even after they undergo treatment. Laboratory detecting procedure does not show the presence of cannabinoid CB2 receptors (CB2-Rs) in a healthy brain. The demonstration in rats indicates the presence of CB2-R in microglia and other cells linked to inflammation. The role of neuronal expression by CB2-R is ambiguous and controversies in its role in substance use and depression remain unknown. The methodology of research is to indicate the hypothesis placed in genetic variations of the CB2 gene in relation to the depression experienced by the human population. Alteration of the CB2 gene expression involves the impact of substances which are abusive such as cocaine, opiates and ethanol in rats. In the study, a demonstration of high incidence of polymorphism occurrence in CB2 in Japanese samples showed high levels of the Q63R but not the H316Y. Gene transcripts of CB2-Rs formed in naive mice’s brain remain in modulation as they are exposed to stressors and drugs (Alcamo & Krumhardt, 2004). The mice that preferred alcohol reduced the expression of the CB2 gene expression. The mice were treated with a chronic treatment in JWH015 and a putative CB2-R. The enhanced consumption is increased, but not in the control sample mice. A direct injection of intracerebroventricular was administered into the brain of the mouseby CB2 anti- sense. This reduced the aversions in the plus-maze tests, indicating a functional presence of CB2-Rs in the brain as the behaviors of the brain are modified. The research indicates the use of electron microscopy during the sub cellular localization of the gene on the post- synaptic elements in the brain of the mice. The research data demonstrated a functional indication of CB2-Rs existing in the brain. The effects of cannabinoids in accelerating substance abuse and depression go beyond the neuro-immunocannabinoid activity (Ali & Kuhar, 2008). Introduction Drug dependence and depression are associated with mental problems arising from lifestyle depressions. Many go through a relapse and the effects of the drugs reoccur even after treatment. Depression comes as a result of anhedonia and mood changes. Anhedonia refers to the disinterest in pleasurable things that life provides. The study of anhedonia is through chronic mild stress (CMS) model with rodents as samples. The CMS model recognizes drug addiction as a brain disease (Tenenbaum & Eklund, 2007). Researchers work to uncover the genetics involved in substance abuse and depression. The main rationale in substance abuse included in marijuana in the hypothesis based on self-medication. There is evidence growth between the growth in depression and the use of cannabis. Presentation of comorbid in cannabis abuse and depression has grown among patients. The use of cannabis in adults increases the symptoms of depression but, the existence of depression does not mean that the patient used cannabis. Researchers discovered the use of an endocannabinoid physiological control system (EPCS) enables psychologists to examine the CNS and its effects in mental disorders. This study enables the description of the role of EPCS in neuropsychiatric disorders. During the abuse of marijuana, two receptors are activated. CB1-Rs activate in the brain and its periphery, as the CB2-Rs express in the immune cells of the body. The neuron expression of CB2-Rs in the human brain and its causes in depression of substance remains unknown. Many laboratories are not able to display the presence of CB2- Rs in brains that are healthy but the demonstration expressed CB2-R in rat microglial cells and other inflammation cells located in the brain (Kolcaba & Kolcaba, 1991). Reports indicate the presence of cannabinoid CB2-Rs in mice preferences and for humans, it read as alcoholism. This supports the functioning of neuronal presence in CB2-R2 while maintaining the CNS in mammals. With extensive research of cannabis, the results indicate expression of the brain CB2-Rs in the model of the mouse as depression. This also reveals the effects of abused substances (Sharma, 2009). The research reports and identifies the presence of CB2- Rs in the neurons of the brain and the glial process. The study seeks to improve the understanding of the role of CB2-Rs in the human brain. The hypothesis is that the genetic variants of CB2 gene might associate with depression amongst humans. The alteration of CB2 gene expression involves the impacts of substances that are abused in mice. According to the data, CB2-Rs express in the brain and play a role in stimulating depression and substance usage (Castle, Murray, & D'Souza, 2011). Brain Neuronal CB2 Cannabinoid Receptors in Drug Abuse and Depression Literature provides little information of the role of CB2- Rs in addictive disorders and in depression. The studies in the report provide evidence for the use of CB-Rs in substance abuse and depression. The findings are important as they provide researchers with better approaches of understanding addictive disorders and depression. The report of the research indicates the presence of CB2-Rs in the neuronal process as opposed to the view that the CB2- Rs restricted to predominantly and peripheral tissues in immune cells (Esanu & Uhlir, 2003). The study also indicates modification of CB2 gene expression mostly in the brains of animals treated with substance abuse disorders. Substances such as alcohol, cocaine and morphine help in the application of the CMS model and exposure of the pre-natal capsaicin exposure. While the study was underway, the model mouse presented the CB2 gene in brain after a CMS and CB2- R protein enhanced the prenatal capsaicin exposure. Treatment of the mouse with CB2-R on a chronic base with the agonist JWH015 improves alcohol consumption in the stressed mice, but not in the controlled mice. In animals that preferred alcohol, the CB2 gene expressed a low regulation in the midbrain, suggesting the presence of CB2-Rs in the use of drugs as an effect. The structure of CB2 gene is defined poorly with characterization of fewer studies for CNS function. This is different from the CB1 gene. Though many features of the CB2 gene structure, variation and regulation come with the emergence of identification of the neuronal CB2-Rs in CNS, the CB2 gene contains a single exon similar to that of the CB2 structure in the mice (Esanu & Uhlir, 2003). The difference between the mice and the human is that is encodes the transcripts using different first exons. The mice CB2 gene displays conservation in most regions, but in humans, the gene contains glutamines. Rats and mice have arginine instead in the position. Humans experience several polymorphisms in the CB2 including Q63R and H316Y being linked to autoimmune and osteoporosis (Kendall & Alexander, 2009). The present hypothesis that indicates genetic variants of the CB2 gene has significant effects on depression and alcoholism. The hypothesis was tested and it runs under the support of identification of a missense polymorphism at the connector of CB2 cDNA at the 188-89 connection (Tenenbaum & Eklund, 2007). The brains activity comes with abundant CB2-R in the neuronal and glial processes detected in a much lower level than the CB1 receptors report. The report comes with the support of CB2-Rsin the dorsal root, the brain stem, cerebellum, the spinal cord and ganglion. Controversies remain specific to the CB2-R staining because the body contains numerous antibodies capable of restringing non-specific staining (Mail, Ishiguro, & Gong, 2008). The study therefore indicates rigorous controls including: 1. Absorption and incubation of the CB2-R antibody that immunizes peptide forming a CB2 block in the cerebellum of the rat. 2. In the hybrid data, the CB2 gene is seen in the cerebellum of the wild type but not in the CB2 knockout mice. The gene does not exist in the wild mice sample. Absence of CB2 mRNA in the CB2-R deficient in the mice, but exists in the wild type controls. This also demonstrates with the other mice. In previous experiments, the demonstrations indicate two types of antibodies from the CB2 antibodies. The patterns similarly occur in the rat s cerebellum and spleen. The analysis of western blot analyses shows the specific brands used in the identification of CB2 antibodies. They are not absent when the antibodies are absorbed in peptide. The analysis also indicates levels of expression of the CB1 gene using RT-PCR showed an analysis of 100 times more than that experienced in the brain stem. The spleen is the most abundant CB2 gene transcript in comparison to other regions (Kolcaba, 2003). The definitive electronic view under the microscope shows a precise localization of the CB2-Rs. During analysis, the transmission of the data displays in the micrograph data indicates high-resolution of the CB2-R localization the ultra structure location. The electron micrograph in the hippocampus areas indicates black depositions and the mitochondria. In some of the areas in the axon terminals show immune reactive for the CB2-Rs. Presence of the synaptic vesicles is present in the location. The axon terminal makes contact with the dendrite without the immune straining for CB2-Rs (Pearsons, 2007). Conclusion Human beings go through depressions and addiction to mental health problems. This comes as a result of stressful events in life. Laboratory testing may not indicate the presence of CB2 in cannabinoid receptors in brains that are healthy, but expressions of CB2_R indicate in other brains and rat microglia cells. The neuronal expressions in CB2-Rs remain controversial as its role in depression remains unknown. The levels indicating in substance abuse also hold up in hypothesis. The research indicates great generic variation of the CB2 gene in association to depression in human beings. The study gives a clear comparison between the rodents’ analysis and human analysis. The data clearly shows the expression of the genes but provides targets that are novel for the effects of the drug substance beyond disorders. The receptors of drug abuse and depression in the human brain indicate brain neuronal function under the influence of cannabinoid receptors. Rats play an important role in showing the changes between the healthy person and an alcoholic or drug abuser. The indication displays a proper linkage in the genetics displayed in the rats and the humans. The study does help prove factors previously outlined by the experiment (Mail, Ishiguro, & Gong, 2008). References Alcamo, E., & Krumhardt, B., 2004. Anatomy Physiology. London: Adventure Works Press. Ali, S. F., & Kuhar, M. J., 2008. Drug addiction: research frontiers and treatment advances. London: John Wiley & Sons. Castle, D., Murray, R. M., & D'Souza, D. C., 2011. Marijuana and Madness. Cambridge: Cambridge University Press. Esanu, J. M., & Uhlir, P. F., 2003. The Role of Scientific and Technical Data and Information in the Public Domain. London: National Academies Press. Kendall, D. A., & Alexander, S., 2009. Behavioral Neurobiology of the Endocannabinoid System. London: Springer. Kolcaba, K., 2003. Comfort theory and practice: a vision for holistic health care and research. London: Springer Publishing Company. Kolcaba, K., & Kolcaba, R., 1991. An analysis of the concept of comfort. Journal of Advanced Nursing, 16 (11), pp. 1301-1310. Mail, E. S., Ishiguro, H., & Gong, J. P., 2008. Brain Neuronal CB2 Cannabinoid Receptors in Drug Abuse and Depression: From Mice to Human Subjects. London: Sage. Pearsons, 2007. Seeing Anthropology: Cultural Anthropology Through Film (with Ethnographic Film Clips DVD), 4/E [Motion Picture]. Sharma, H. S., 2009. New Concepts of Psychostimulants Induced Neurotoxicity. London: Academic Press. Tenenbaum, G., & Eklund, R. C., 2007. Handbook of Sport Psychology. London: John Wiley & Sons. Read More