Abstract
An electrophysiological study was performed to elucidate the role of nicotinic receptors in the striatal neurons in chloral hydrate-anesthetized rats. The effects of microiontophoretic application of nicotine and other drugs were examined on the caudate nucleus (CN) neurons activated monosynaptically by stimulation of the substantia nigra pars compacta (SN). Application of nicotine facilitated spontaneous firing. The nicotine-induced firing of the CN neurons was inhibited by concomitant application of domperidone or hexamethonium. These findings suggested that nicotine enhances dopamine release from the SN-derived dopaminergic nerve terminals by activating the neurons via D2 receptors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / drug effects
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Animals
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Caudate Nucleus / cytology
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Caudate Nucleus / drug effects
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Caudate Nucleus / metabolism
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Corpus Striatum / cytology
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Corpus Striatum / drug effects*
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Corpus Striatum / metabolism
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Dopamine / metabolism*
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Dopamine Agonists / administration & dosage
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Dopamine Antagonists / administration & dosage
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Electric Stimulation
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Electrodes, Implanted
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Iontophoresis
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Male
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Neurons / cytology
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Neurons / drug effects*
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Neurons / metabolism
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Nicotine / administration & dosage*
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Nicotinic Antagonists / administration & dosage
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Rats
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Rats, Wistar
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Receptors, Nicotinic / metabolism
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Substantia Nigra / physiology*
Substances
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Dopamine Agonists
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Dopamine Antagonists
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Nicotinic Antagonists
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Receptors, Nicotinic
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Nicotine
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Dopamine