Abstract
Drugs of abuse cause activation of the cyclic AMP response element binding protein (CREB) in the nucleus accumbens (NAc). Expression of active CREB in rat NAc medium spiny neurons (MSNs) increased their excitability, whereas dominant-negative CREB had the opposite effect. Decreasing excitability of NAc MSNs in vivo by overexpression of potassium channels enhanced locomotor responses to cocaine, suggesting that the increased NAc MSN excitability caused by CREB helped to limit behavioral sensitivity to cocaine.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Calcium Channel Blockers / metabolism
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Cocaine / pharmacology
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Cyclic AMP Response Element-Binding Protein / genetics
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Cyclic AMP Response Element-Binding Protein / metabolism*
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Dopamine Uptake Inhibitors / pharmacology
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Motor Activity / drug effects
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Motor Activity / physiology
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Neurons / cytology
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Neurons / drug effects
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Neurons / physiology*
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Nucleus Accumbens / cytology*
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Nucleus Accumbens / drug effects
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Nucleus Accumbens / physiology
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Patch-Clamp Techniques
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Potassium Channel Blockers / metabolism
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Potassium Channels, Inwardly Rectifying / genetics
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Potassium Channels, Inwardly Rectifying / metabolism*
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Rats
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Sodium Channel Blockers / metabolism
Substances
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Calcium Channel Blockers
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Cyclic AMP Response Element-Binding Protein
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Dopamine Uptake Inhibitors
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Kir2.1 channel
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Potassium Channel Blockers
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Potassium Channels, Inwardly Rectifying
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Sodium Channel Blockers
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Cocaine