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維基專題:神經科學/templatesII

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苯丙胺在多巴胺能神經元的藥物效應動力學
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A pharmacodynamic model of amphetamine and TAAR1
via AADC
圖像頂端包含可點擊的連結
Amphetamine enters the presynaptic neuron across the neuronal membrane or through DAT. Once inside, it binds to TAAR1 or enters synaptic vesicles through VMAT2. When amphetamine enters the synaptic vesicles through VMAT2, dopamine is released into the cytosol (yellow-orange area). When amphetamine binds to TAAR1, it reduces postsynaptic neuron firing rate via potassium channels英語G protein-coupled inwardly-rectifying potassium channel and triggers protein kinase A (PKA) and protein kinase C (PKC) signaling, resulting in DAT phosphorylation. PKA-phosphorylation causes DAT to withdraw into the presynaptic neuron (internalize) and cease transport. PKC-phosphorylated DAT may either operate in reverse or, like PKA-phosphorylated DAT, internalize and cease transport. Amphetamine is also known to increase intracellular calcium, an effect which is associated with DAT phosphorylation through a CAMKIIα英語CAMKIIα-dependent pathway, in turn producing dopamine efflux.

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