Abstract
Neuroplasticity serves an important role for normal striatal function and in disease states. One route to neuroplasticity involves activation of the transcription factor cyclic 3', 5'-adenosine monophosphate (cyclic AMP) response element binding protein (CREB) by phosphorylation of the amino acid 133Ser. Dopamine and glutamate, the two predominant neurotransmitters in the striatum, induce CREB phosphorylation in primary cultures of rat striatum through cyclic AMP and Ca2+ pathways. Here we present the role of N-methyl-D-aspartate receptors and Ca2+ in cyclic AMP-mediated CREB phosphorylation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Benzazepines / pharmacology
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Calcium / physiology
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Colforsin / pharmacology
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Corpus Striatum / physiology*
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Culture Techniques
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Cyclic AMP / metabolism*
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Cyclic AMP Response Element-Binding Protein / metabolism
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Dizocilpine Maleate / pharmacology
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Dopamine / pharmacology
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Dopamine Agonists / pharmacology
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Excitatory Amino Acid Antagonists / pharmacology
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Neuronal Plasticity / physiology*
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Phosphorylation / drug effects
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Rats / embryology
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / physiology
Substances
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Benzazepines
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Cyclic AMP Response Element-Binding Protein
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Dopamine Agonists
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Excitatory Amino Acid Antagonists
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Receptors, N-Methyl-D-Aspartate
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Colforsin
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Dizocilpine Maleate
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SK&F 82958
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Cyclic AMP
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Calcium
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Dopamine