Mutant mice lacking the cholecystokinin2 receptor show a dopamine-dependent hyperactivity and a behavioral sensitization to morphine

Valérie Daugé; Françoise Beslot; Toshimitsu Matsui; Bernard Pierre Roques

doi:10.1016/S0304-3940(01)01867-5

Mutant mice lacking the cholecystokinin₂ receptor show a dopamine-dependent hyperactivity and a behavioral sensitization to morphine

Valérie Daugé, Françoise Beslot, Toshimitsu Matsui, Bernard Pierre Roques

Research output: Contribution to journal › Article › peer-review

22 Scopus citations

Abstract

Cholecystokinin₂ (CCK₂) receptor-deficient mice were used to analyze the in vivo function of CCK₂ receptor and especially the incidence of this gene invalidation on enkephalinergic and dopaminergic systems. Hyperlocomotor activity of CCK₂ receptor-deficient mice was suppressed by a selective D2 antagonist but not by a D1 antagonist. Injection of amphetamine induced a hyperlocomotor activity in both groups of mice while mutant mice were less sensitive to cocaine. Administration of 6 mg/kg of morphine once every 2 days for 5 days significantly (P < 0.05) enhanced motor activity the last day compared to the first day, only in CCK₂ receptor-deficient mice. These results emphasize the role of CCK₂ receptors in counteracting the effects of dopaminergic systems and suggest that CCK₂ receptor invalidation could lead to a slight behavioral sensitization.

Original language	English
Pages (from-to)	41-44
Number of pages	4
Journal	Neuroscience Letters
Volume	306
Issue number	1-2
DOIs	https://doi.org/10.1016/S0304-3940(01)01867-5
State	Published - 22 Jun 2001
Externally published	Yes

Keywords

Amphetamine
Cholecystokinin receptor-deficient mice
Cocaine
Dopamine antagonists
Morphine
Sensitization

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10.1016/S0304-3940(01)01867-5

Cite this

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title = "Mutant mice lacking the cholecystokinin2 receptor show a dopamine-dependent hyperactivity and a behavioral sensitization to morphine",

abstract = "Cholecystokinin2 (CCK2) receptor-deficient mice were used to analyze the in vivo function of CCK2 receptor and especially the incidence of this gene invalidation on enkephalinergic and dopaminergic systems. Hyperlocomotor activity of CCK2 receptor-deficient mice was suppressed by a selective D2 antagonist but not by a D1 antagonist. Injection of amphetamine induced a hyperlocomotor activity in both groups of mice while mutant mice were less sensitive to cocaine. Administration of 6 mg/kg of morphine once every 2 days for 5 days significantly (P < 0.05) enhanced motor activity the last day compared to the first day, only in CCK2 receptor-deficient mice. These results emphasize the role of CCK2 receptors in counteracting the effects of dopaminergic systems and suggest that CCK2 receptor invalidation could lead to a slight behavioral sensitization.",

keywords = "Amphetamine, Cholecystokinin receptor-deficient mice, Cocaine, Dopamine antagonists, Morphine, Sensitization",

author = "Val{\'e}rie Daug{\'e} and Fran{\c c}oise Beslot and Toshimitsu Matsui and Roques, {Bernard Pierre}",

year = "2001",

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T1 - Mutant mice lacking the cholecystokinin2 receptor show a dopamine-dependent hyperactivity and a behavioral sensitization to morphine

AU - Daugé, Valérie

AU - Beslot, Françoise

AU - Matsui, Toshimitsu

AU - Roques, Bernard Pierre

PY - 2001/6/22

Y1 - 2001/6/22

N2 - Cholecystokinin2 (CCK2) receptor-deficient mice were used to analyze the in vivo function of CCK2 receptor and especially the incidence of this gene invalidation on enkephalinergic and dopaminergic systems. Hyperlocomotor activity of CCK2 receptor-deficient mice was suppressed by a selective D2 antagonist but not by a D1 antagonist. Injection of amphetamine induced a hyperlocomotor activity in both groups of mice while mutant mice were less sensitive to cocaine. Administration of 6 mg/kg of morphine once every 2 days for 5 days significantly (P < 0.05) enhanced motor activity the last day compared to the first day, only in CCK2 receptor-deficient mice. These results emphasize the role of CCK2 receptors in counteracting the effects of dopaminergic systems and suggest that CCK2 receptor invalidation could lead to a slight behavioral sensitization.

AB - Cholecystokinin2 (CCK2) receptor-deficient mice were used to analyze the in vivo function of CCK2 receptor and especially the incidence of this gene invalidation on enkephalinergic and dopaminergic systems. Hyperlocomotor activity of CCK2 receptor-deficient mice was suppressed by a selective D2 antagonist but not by a D1 antagonist. Injection of amphetamine induced a hyperlocomotor activity in both groups of mice while mutant mice were less sensitive to cocaine. Administration of 6 mg/kg of morphine once every 2 days for 5 days significantly (P < 0.05) enhanced motor activity the last day compared to the first day, only in CCK2 receptor-deficient mice. These results emphasize the role of CCK2 receptors in counteracting the effects of dopaminergic systems and suggest that CCK2 receptor invalidation could lead to a slight behavioral sensitization.

KW - Amphetamine

KW - Cholecystokinin receptor-deficient mice

KW - Cocaine

KW - Dopamine antagonists

KW - Morphine

KW - Sensitization

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