Abstract
Tyrosine hydroxylase activity was measured in the brain of rats treated chronically with saline or cocaine (10 mg/kg, 2 x day, for 7 days). Tyrosine hydroxylase activity was significantly increased in the ventral tegmental area 1, 6 and 12 weeks after the last treatment with cocaine. The increase in tyrosine hydroxylase activity at 6 weeks after the last cocaine injection was prevented by the prior administration of MK-801, haloperidol or clozapine but not by the D1 receptor antagonist, SCH-23390. SCH-23390 produced a significant increase in tyrosine hydroxylase activity when administered with saline. These data indicate that glutaminergic and dopaminergic D2-receptor mediated mechanisms are important in regulating the effect of cocaine on the ventral tegmental area.
MeSH terms
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Animals
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Benzazepines / pharmacology
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Cocaine / pharmacology*
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Dizocilpine Maleate / pharmacology
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Dopamine Antagonists / pharmacology
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Dopamine Uptake Inhibitors / pharmacology*
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Excitatory Amino Acid Antagonists / pharmacology
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Haloperidol / pharmacology
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Male
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Rats
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Rats, Sprague-Dawley
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Receptors, Dopamine D1 / antagonists & inhibitors
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Receptors, Dopamine D2 / drug effects
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Receptors, Dopamine D2 / metabolism*
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Receptors, Glutamate / drug effects
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Receptors, Glutamate / metabolism*
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Tyrosine 3-Monooxygenase / metabolism*
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Ventral Tegmental Area / drug effects
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Ventral Tegmental Area / enzymology*
Substances
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Benzazepines
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Dopamine Antagonists
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Dopamine Uptake Inhibitors
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Excitatory Amino Acid Antagonists
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Receptors, Dopamine D1
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Receptors, Dopamine D2
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Receptors, Glutamate
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Dizocilpine Maleate
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Tyrosine 3-Monooxygenase
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Cocaine
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Haloperidol