The nucleus accumbens is the release sight for the neurotransmitter dopamine, a nature chemical in the central nervous system. When released in standard quantities, it assists in critical brain functions. Like most neurotransmitters, dopaminergic signaling entails an equilibrium between dopamine release and the re-uptake by presynaptic nerve terminal. Under specific circumstances, a stimulus will promote the release of dopamine into the synapse. Dopamine transporters will then remove the dopamine from the synapse so that vesicular monoamine transporters can store the neurotransmitter into vesicles, release it, and protect it from oxidation (Riddle et al, 2006). Damages in dopamine transporters or the vesicular monoamine transporters will cause
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Meth activates dopamine (DA) neurotransmitter release from the cytosol to the extracellular space through the process of reverse transport through dopamine transporters (DAT). According to previous knowledge, methamphetamine use has shown evidence of dopamine oxidation within the neuronal cytosol. Dopamine’s reactive structure allows it to oxidize to produce free radicals and reactive quinones, an aromatic compound. Vesicular monoamine transporters (VMAT-2) are responsible for packaging dopamine into vesicles to prepare them for release in the synapse. Methamphetamine interferes with VMAT-2’s ability to prevent dopamine uptake into vesicles. Meth’s disruption of VMAT-2 has shown to lead to nerve terminal damage. Moreover, DAT plays a major role in the regulation of cytoplasmic DA concentrations. Therefore meth induced reduction of DAT in a nerve cell decreases DAT mediated DA efflux, which in affect causes a DA buildup in the …show more content…
A study done by (1) examined the effect of methamphetamine on dopamine terminals in the brain of fifteen detoxified substance abusers an eighteen comparison subjects. It was hypothesized that the use of meth significantly reduces dopamine transporters. To test this hypothesis, they administered a dopamine transporter ligand, [11C] d-threo-methylphenidate, to their subjects and used positron emission tomography scanning to measure transporter levels. Their results show that substance abusers who have been detoxified for at least eleven month have reduced transporters by 27.8% in the caudate and 21.1% in the putamen of the basal ganglia in comparison to non-users (Figure 1). This article successfully explained the effect of methamphetamine on dopamine transporters in users who have been detoxified for at least eleven months. However, it did not go in detail about the rate of regeneration with abstinence. In article (2) five meth users were examined after approximately 1.6 months of abstinence and again after nine months. Their results showed that there was no differences between short and protracted abstinence in the cerebellum, caudate or putamen of meth abusers who were evaluated twice. However, binding of [11C] d-threo-methylphenidate in striatum showed a significant increase
Meth activates dopamine (DA) neurotransmitter release from the cytosol to the extracellular space through the process of reverse transport through dopamine transporters (DAT). According to previous knowledge, methamphetamine use has shown evidence of dopamine oxidation within the neuronal cytosol. Dopamine’s reactive structure allows it to oxidize to produce free radicals and reactive quinones, an aromatic compound. Vesicular monoamine transporters (VMAT-2) are responsible for packaging dopamine into vesicles to prepare them for release in the synapse. Methamphetamine interferes with VMAT-2’s ability to prevent dopamine uptake into vesicles. Meth’s disruption of VMAT-2 has shown to lead to nerve terminal damage. Moreover, DAT plays a major role in the regulation of cytoplasmic DA concentrations. Therefore meth induced reduction of DAT in a nerve cell decreases DAT mediated DA efflux, which in affect causes a DA buildup in the …show more content…
A study done by (1) examined the effect of methamphetamine on dopamine terminals in the brain of fifteen detoxified substance abusers an eighteen comparison subjects. It was hypothesized that the use of meth significantly reduces dopamine transporters. To test this hypothesis, they administered a dopamine transporter ligand, [11C] d-threo-methylphenidate, to their subjects and used positron emission tomography scanning to measure transporter levels. Their results show that substance abusers who have been detoxified for at least eleven month have reduced transporters by 27.8% in the caudate and 21.1% in the putamen of the basal ganglia in comparison to non-users (Figure 1). This article successfully explained the effect of methamphetamine on dopamine transporters in users who have been detoxified for at least eleven months. However, it did not go in detail about the rate of regeneration with abstinence. In article (2) five meth users were examined after approximately 1.6 months of abstinence and again after nine months. Their results showed that there was no differences between short and protracted abstinence in the cerebellum, caudate or putamen of meth abusers who were evaluated twice. However, binding of [11C] d-threo-methylphenidate in striatum showed a significant increase