Abstract
We demonstrate abnormal dopaminergic neurotransmission in anorexic mice, homozygous for a recessive mutation (anx) causing starvation and motor disturbances. Isolated neurons from anx/anx striatum displayed a markedly increased activity of the Na+,K+-ATPase compared with normal littermates. Dopamine down-regulates Na+,K+-ATPase activity in striatal medium spiny neurons in rat, mouse and guinea pig. However, addition of dopamine in vitro failed to suppress the increased activity in anx/anx striatal neurons. Striatal dopamine and its metabolites, but not norepinephrine, were slightly but significantly lower in anx/anx mice than in normal littermates. We suggest that abnormal dopaminergic transmission may contribute to the anx phenotype.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anorexia / genetics*
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Anorexia / metabolism*
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Anorexia / pathology
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Aromatic-L-Amino-Acid Decarboxylases / metabolism
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Biogenic Monoamines / metabolism
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Corpus Striatum / metabolism*
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Corpus Striatum / pathology
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Dopamine / metabolism*
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Dopamine / pharmacology
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Enzyme Activation / drug effects
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Enzyme Activation / genetics
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Mice
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Mice, Neurologic Mutants
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Neurons / drug effects
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Neurons / metabolism
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Neurons / pathology
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Phenotype
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Sodium-Potassium-Exchanging ATPase / genetics
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Sodium-Potassium-Exchanging ATPase / metabolism
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Synaptic Transmission* / physiology
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Tyrosine 3-Monooxygenase / metabolism
Substances
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Biogenic Monoamines
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Tyrosine 3-Monooxygenase
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Aromatic-L-Amino-Acid Decarboxylases
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Sodium-Potassium-Exchanging ATPase
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Dopamine