Template:Amphetamine pharmacodynamics

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Pharmacodynamics of amphetamine in a dopamine neuron
A pharmacodynamic model of amphetamine and TAAR1
via AADC
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Amphetamine enters the presynaptic neuron across the neuronal membrane or through DAT.
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Once inside, it binds to TAAR1 or enters synaptic vesicles through VMAT2.
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When amphetamine enters synaptic vesicles through VMAT2, it collapses the vesicular pH gradient, which in turn causes dopamine to be released into the cytosol (light tan-colored area) through VMAT2.
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When amphetamine binds to TAAR1, it reduces the firing rate of the dopamine neuron via potassium channels and activates protein kinase A (PKA) and protein kinase C (PKC), which subsequently phosphorylate DAT.
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PKA-phosphorylation causes DAT to withdraw into the presynaptic neuron (internalize) and cease transport.
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PKC-phosphorylated DAT may either operate in reverse or, like PKA-phosphorylated DAT, internalize and cease transport.
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Amphetamine is also known to increase intracellular calcium, an effect which is associated with DAT phosphorylation through a CAMKIIα-dependent pathway, in turn producing dopamine efflux.
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