Cocaine's Adverse Effect on Neurochemical Function of the Brain
Cocaine is a tropane diester alkaloid that that when snorted smoked or injected, cocaine enters the bloodstream and then flows to the brain. The feeling of euphoria is caused by a buildup of the neurochemical called dopamine. Dopamine is a catecholamine that acts as a pacesetter for many nerve cells throughout the brain. Dopamine is responsible for keeping cells operating at an appropriate level. Dopamine molecules latch on to receptors on neighboring cells. The part of the limbic system that seems to notice the highest form of cocaine high is called the nucleus accumbens. This often feels the high of cocaine by causing a buildup of dopamine in the nucleus accumbens and yields a very powerful; feeling of euphoria, the feeling is so strong that many would ignore other means like thirst-quenching or sex to instead pursue more cocaine. This feeling of euphoria comes from the increase in productivity of cells that receive dopamine molecules. These dopamine molecules act as a pacesetter for the cells and once activated are stimulated and work at a much faster rate.
Cocaine effects neurochemical function by causing various genes within the nucleus accumbens to be changed or modifies limiting the production of neurotransmitters chemical, glutamate, and the brain’s natural opioid-like compounds. This combats the notion that cocaine is merely a mass flood of dopamine molecules, it is much more severe causing a modification of ΔFosB, a pace making chemical. This chemical does not leave the cell that produces it and stimulates neighboring cells as dopamine does. ΔFosB will remain in its original cell and stimulate genes, these types of chemicals are known as genetic transcription factors. Cocaine has an adverse effect that comes from the mass buildup of this chemical from the standard limited amount of ΔFosB. These molecules last for about six to eight weeks before they undergo a chemical decomposition. This buildup of ΔFosB can accumulate for as many times as cocaine is used for the span of two months reaching incredibly high concentrations. The following reaction occurs and is what causes the transition from use to addiction and abuse. ΔFosB has a role in the genetic machinery that determines the basic properties of many cells, including long-term permanent structures and interfaces with other cells. In experiments with mice, this mass influx of ΔFosB was shown to have a very similar effect on the behavior of mice as human addicts have, and those who has a normal concentration remained acting normal. 
ΔFosB is only found within the nucleus accumbens in normal animals. However, chronic administration and use of cocaine show an increase of ΔFosB in several additional regions in the brain including, the frontal cortex and amygdala. The frontal cortex having a buildup ΔFosB shows control over cocaine urges, however, this has not been provided evidence is a hypothesis. A current study is occurring to identify which specific genes ΔFosB are stimulating to produce this effect. By comparing nucleus accumbens from mice that lack transcription factors that more than one-hundred ΔFosB-mediated changes in gene expression. This work indicates that ΔFosB causes approximately twenty-five percent of all chronic cocaine-induced changes in gene expression, a highlight to the dominant role of this transcription.
However, ΔFosB cannot explain why ex-abusers still feel an addiction and craving for the substance and eventually relapse. Scientists have found some long-lasting neurobiological effects. The key type of cocaine-related change appears within the nerve cells themselves. Cocaine causes the physical structure of nerve cells to be altered within the nucleus accumbens. With chronic cocaine use and exposure, nervous cells extended and sprout offshoots on their dendrites, which are branch-like fibers that grow out of the nerve cell bodies and collects signals from other nerve cells. As more dendrites exist the larger the antenna and will collect a greater volume of nerve signals coming from other regions. This will allow other regions enhanced influence over the nucleus accumbens, which could drive some of the long-lived behavioral changes associated with addiction. An example of this would be how the hippocampus and amygdala having enhanced inputs that could be responsible for intense craving that occurs when drug-associated memories are stimulated. It is still unknown how cocaine triggers the stretching of nerve cells but it seems to involve ΔFosB. One of the genes that are stimulated by ΔFosB is called CDK5, a known regulator of nerve cell growth.
The research can later be applied to advance treatments to understand the neurobiology of cocaine addiction is essential to advance treatments for cocaine addiction. This would allow for more specialized treatments and shift away from the method to bind the cocaine molecules to blood vessels and never allow them to reach the brain. This focuses on the cocaine's initial effect, not long-lasting changes that ΔFosB causes the changes of proteins. It takes a long time for these developments to occur so basic knowledge is required to try and deter those who would use cocaine as a drug so that these effects can be avoided. Although psychological and social factor dominates presentation and diagnosis of addiction, the disease is at its core biological and is explained by the neurochemical application that can be used.
Do the effects that cocaine has on the human body increase in potency as the person ages or does it stay the same?
ReplyDeleteThe actual effect of cocaine on the brain does become slightly more potent as the body ages but this is not as important as how often cocaine is used. If used to often then the effects take root and modify the brain. However, as time goes on the brain becomes more receptive to the effect of the protein ΔFosB and how it can change which genes are caused leading to more damage. Hope this clarified and good question.
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