Cholecystokinin 2 receptor-deficient mice display altered function of brain dopaminergic system

Kõks, Sulev; Volke, Vallo; Veraksitš, Alar; Rünkorg, Kertu; Sillat, Tarvo; Abramov, Urho; Bourin, Michel; Huotari, Marko; Männistö, Pekka T.; Matsui, Toshimistu; Vasar, Eero

doi:10.1007/s002130100855

Cited by 31 publications

(20 citation statements)

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“…Results from studies using KO mice were dose-dependent and present somewhat complicated results with regard to interpretation. Mice lacking functional CCK 2 receptors were less stimulated by 3 mg/kg amphetamine compared to WT mice, but more stimulated by 6 mg/kg amphetamine; a 1 mg/kg dose did not induce stimulation in either genotype (Koks et al, 2001;2003;Runkorg et al, 2006). L-365,260 has been shown to alter the development of behavioral sensitization to amphetamine; low doses increased sensitization while higher doses attenuated amphetamine-induced locomotor sensitization (Wunderlich et al, 2000).…”

Section: Cell Support and Signaling Proteins: Amphetamine And Methamphementioning

confidence: 97%

Behavioral genetic contributions to the study of addiction-related amphetamine effects

Phillips

Kamens

Wheeler

2008

Neuroscience & Biobehavioral Reviews

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Amphetamines, including methamphetamine, pose a significant cost to society due to significant numbers of amphetamine-abusing individuals who suffer major health-related consequences. In addition, methamphetamine use is associated with heightened rates of violent and property-related crimes. The current paper reviews the existing literature addressing genetic differences in mice that impact behavioral responses thought to be relevant to the abuse of amphetamine and amphetaminelike drugs. Summarized are studies that used inbred strains, selected lines, single gene knockouts and transgenics, and quantitative trait locus (QTL) mapping populations. Acute sensitivity, neuroadaptive responses, rewarding and conditioned effects are among those reviewed. Some gene mapping work has been accomplished, and although no amphetamine-related complex trait genes have been definitively identified, translational work leading from results in the mouse to studies performed in humans is beginning to emerge. The majority of genetic investigations has utilized single-gene knockout mice and has concentrated on dopamine-and glutamate-related genes. Genes that code for cell support and signaling molecules are also well-represented. There is a large behavioral genetic literature on responsiveness to amphetamines, but a considerably smaller literature focused on genes that influence the development and acceleration of amphetamine use, withdrawal, relapse, and behavioral toxicity. Also missing are genetic investigations into the effects of amphetamines on social behaviors. This information might help to identify at-risk individuals and in the future to develop treatments that take advantage of individualized genetic information.

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Section: Cell Support and Signaling Proteins: Amphetamine And Methamphementioning

confidence: 97%

Behavioral genetic contributions to the study of addiction-related amphetamine effects

Phillips

Kamens

Wheeler

2008

Neuroscience & Biobehavioral Reviews

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“…Animals without CCK 2 receptors display disturbances in the development of gastric mucosa (Nagata et al 1996) and in learning abilities (Sebret et al 1999). The activity of the dopaminergic system is also affected in mice with non-functional CCK 2 receptors because of increased sensitivity of dopamine D 2 receptors (DaugØ et al 2001a;Kðks et al 2001). Recent evidence suggests altered function of the endogenous opioid system in mice without CCK 2 receptors.…”

Section: Introductionmentioning

confidence: 98%

Targeted mutation of CCK2 receptor gene modifies the behavioural effects of diazepam in female mice

et al. 2003

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Female mice lacking CCK2 receptors are less anxious than their wild-type (+/+) littermates. The reduced anxiety in homozygous (-/-) mice probably explains why the administration of a higher dose of diazepam is necessary to induce an anxiolytic-like action in these animals. The highest dose of diazepam (3 mg/kg) induced significantly stronger suppression of locomotor activity and impairment of motor co-ordination in the homozygous (-/-) mice compared to the wild-type (+/+) littermates. The increase in the action of diazepam is probably related to the elevated density of benzodiazepine receptors in the cerebellum of homozygous (-/-) mice. The present study seems to be in favour of increased tone of the GABAergic system in mice without CCK2 receptors.

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“…Finally, studies in transgenic mice further support the idea that CCK modulates psychostimulant-induced, dopaminergic dependant SPA. In contrast to Otsuka-Long-Evans rats, which naturally lack CCK-A receptors and display reduced AMPH-induced hyperactivity compared to the lean rats [229], mice lacking CCK-B receptors exhibit a greater increase in AMPH-induced SPA, a suppression of apomorphine-induced SPA [230, 231] and increased density of dopamine-2 receptors as compared to wild types [231]. Taken together, these data demonstrate that the CCK-dopamine interactions within VTA-NAcc circuits are important to the control of SPA, and in particular psychostimulant-induced SPA.…”

Section: Dopaminergic Brain Pathways Mediating Spa and Neatmentioning

confidence: 99%

Neuropeptidergic Mediators of Spontaneous Physical Activity and Non-Exercise Activity Thermogenesis

Teske¹,

Billington

Kotz³

2007

Neuroendocrinology

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Lean individuals have high levels of spontaneous physical activity (SPA) and the energy expenditure derived from that activity, termed non-exercise activity thermogenesis or NEAT, appears to protect them from obesity. Conversely, obesity in different human populations is characterized by low levels of SPA and NEAT. Like in humans, elevated SPA in rats appears to protect against obesity: obesity-resistant rats have significantly greater SPA and NEAT than obesity-prone rats. We review the literature on brain mechanisms important in mediating SPA and NEAT. The focus is on neuropeptides, including cholecystokinin, corticotropin-releasing hormone (also known as corticotropin-releasing factor), neuromedin U, neuropeptide Y, leptin, agouti-related protein, orexin-A (also known as hypocretin-1), and ghrelin. We also review information regarding interactions between these neuropeptides and dopamine, a neurotransmitter important in mediating motor function. Finally, we present evidence that elevated signaling of pathways mediating SPA and NEAT may protect against weight gain and obesity.

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Cholecystokinin 2 receptor-deficient mice display altered function of brain dopaminergic system

Cited by 31 publications

References 0 publications

Behavioral genetic contributions to the study of addiction-related amphetamine effects

Behavioral genetic contributions to the study of addiction-related amphetamine effects

Targeted mutation of CCK2 receptor gene modifies the behavioural effects of diazepam in female mice

Neuropeptidergic Mediators of Spontaneous Physical Activity and Non-Exercise Activity Thermogenesis

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