Abstract
The present study investigated the phenotype of heterozygous and homozygous neuropeptide S receptor (Npsr) deficient C57BL/6 mice in NPS- and cocaine induced hyperactivity, spontaneous and reactive locomotor activity, elevated plus maze, conditioned fear, and prepulse inhibition of the acoustic startle response. In Npsr-deficient mice, a strong reduction of spontaneous locomotor activity and of the startle magnitude was observed; heterozygous mice had an intermediate phenotype. In the other experiments, Npsr deficiency leads to no or only a very modest phenotype. These results support an important role of neuropeptide S in regulating locomotor activity.
Copyright © 2010. Published by Elsevier B.V.
MeSH terms
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Acoustic Stimulation
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Animals
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Cocaine / administration & dosage
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Cocaine / pharmacology
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Conditioning, Classical / drug effects
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Conditioning, Classical / physiology
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Immobility Response, Tonic / drug effects
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Immobility Response, Tonic / physiology
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Infusions, Intraventricular
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Inhibition, Psychological
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Maze Learning / drug effects
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Maze Learning / physiology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Motor Activity / drug effects
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Motor Activity / genetics*
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Motor Activity / physiology
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Neuropeptides / administration & dosage
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Neuropeptides / pharmacology
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Receptors, G-Protein-Coupled / drug effects
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Receptors, G-Protein-Coupled / genetics
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Receptors, G-Protein-Coupled / physiology*
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Reflex, Startle / drug effects
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Reflex, Startle / genetics*
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Reflex, Startle / physiology
Substances
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NPSR1 protein, mouse
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Neuropeptides
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Receptors, G-Protein-Coupled
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neuropeptide S, mouse
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Cocaine