All of these mechanisms have potential implications for both amphetamine- and methamphetamine-induced neurotoxicity, as well as dopaminergic neurodegenerative diseases. The drug amphetamine which is mainly used to treat nerve related problems it will start its action by converting themselves into monoamines and they will cross the neural barrier at the presynaptic level. The mechanism of action will also reveal the information regarding the sites that are concentrate to show its effect. Additionally, amphetamine analogs may affect monoamine transporters through phosphorylation, transporter trafficking, and the production of reactive oxygen and nitrogen species. The mechanism of action of any drug will let you know about the complete information regarding how it works and how much time it takes to show its action on the body. These mechanisms include amphetamine-induced exchange diffusion, reverse transport, and channel-like transport phenomena as well as the weak base properties of amphetamine. This review focuses on new insights, obtained from both in vivo and in vitro studies, into the molecular mechanisms whereby amphetamine, and the closely related compounds methamphetamine and methylenedioxymethamphetamine, cause monoamine, and particularly dopamine, release. Plasmalemmal and vesicular monoamine transporters, such as the neuronal dopamine transporter and the vesicular monoamine transporter-2, are two of its principal targets. This creates a sharp mental focus, a state of wakefulness, and increased. With each drug dose, amphetamines force the release of neurotransmitter chemicals, norepinephrine and dopamine, from certain key brain cell receptor sites. Amphetamines cause a buildup of neurotransmitters at synapses within the brain. AbstractAmphetamine is a psychostimulant commonly used to treat several disorders, including attention deficit, narcolepsy, and obesity. Amphetamine’s mechanism of action starts in the brain and travels throughout the body’s central nervous system.
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