How cocaine effect dopamine in the brain?

Dopamine is generally a neurotransmitter, or a substance synthesized in the brain by certain neurons that are responsible, for pleasure and motivation among other functions. After synthesis, the substance is stored in special little bags, referred to as synaptic vesicle (Giuliano, & Allard, 2002). With the arrival of an electric impulse at the nerve terminal tip, the respective vesicles move directly into the presynaptic membrane that of the neuron discharging their dopamine contents into the synaptic gap. The dopamine molecules pass through this gap attaching themselves to particular receptors situated right in the outer surface that of the brain’s cell membrane. This provokes several reactions in the respective neuron, for instance the outflow and inflow of ions, and the inhibition or release of some important enzymes in the brain receptors. After the release from the receptors, the dopamine molecules move up again through the presynaptic button, through dopamine transport sites. Therefore, in argument, dopamine plays a very crucial role in the human brain (Vanderbilt University, 2008).

Cocaine in the brain compromises the whole process and develops huge effects on the dopamine in the brain. It affects the brain reward system blocking the dopamine transport sites that have the responsibility of taking the dopamine in dopaminergic synapses. Therefore, due to the cocaine effect, dopamine does not move from the synaptic gap remaining free there and increasing in amounts (Giuliano & Allard, 2002). There is a tendency of successive nervous stimuli continuing and their arrival releases more dopamine, which compromises the functioning of the brain. The abnormally presence of substance dopamine in the human brain causes pleasure effects and compromises the body functions leading to a complication in the normality of the victim. A prolonged cocaine use is even worse because it adapts to the synthesis and in the long term, it compromises the natural dopamine synthesis through a decrease in brain neurons (Vanderbilt University, 2008).



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