Abstract
Many psychostimulants alter plasmalemmal monoaminergic transporter function. Some, such as cocaine, prevent the reuptake of newly released dopamine, serotonin or norepinephrine into their associated neurons. Others, such as the amphetamines, facilitate release of these transmitters into the extraneuronal space by causing a reversal of function of these carrier proteins. An understanding of how psychostimulants regulate the function of not only plasmalemmal, but also vesicular monoamine transporter function is important to appreciate the pharmacological and sometimes neurotoxic consequences of administering these drugs, as well as the physiological regulation of these carrier proteins. Hence, this review will describe recent ex vivo studies investigating the rapid and differential affects of several stimulants on both plasmalemmal and vesicular monoamine transporter function.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Carrier Proteins / drug effects*
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Carrier Proteins / physiology
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Central Nervous System Stimulants / pharmacology*
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Dopamine Plasma Membrane Transport Proteins
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Humans
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Membrane Glycoproteins / drug effects*
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Membrane Glycoproteins / physiology
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Membrane Transport Proteins*
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Methamphetamine / pharmacology
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Nerve Tissue Proteins*
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Nervous System / drug effects
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Nervous System / pathology
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Neuropeptides*
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Norepinephrine Plasma Membrane Transport Proteins
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Serotonin Plasma Membrane Transport Proteins
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Symporters*
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Vesicular Biogenic Amine Transport Proteins
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Vesicular Monoamine Transport Proteins
Substances
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Carrier Proteins
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Central Nervous System Stimulants
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Dopamine Plasma Membrane Transport Proteins
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Membrane Glycoproteins
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Membrane Transport Proteins
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Nerve Tissue Proteins
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Neuropeptides
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Norepinephrine Plasma Membrane Transport Proteins
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SLC6A2 protein, human
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SLC6A4 protein, human
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Serotonin Plasma Membrane Transport Proteins
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Symporters
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Vesicular Biogenic Amine Transport Proteins
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Vesicular Monoamine Transport Proteins
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Methamphetamine