Elevated dopamine alters consummatory pattern generation and increases behavioral variability during learning

Rossi, Mark A.; Yin, Henry H.

doi:10.3389/fnint.2015.00037

Cited by 26 publications

(27 citation statements)

References 55 publications

(67 reference statements)

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“…DAT-KO mice with a two-bottle choice had stronger preference toward sucrose solution, than WT mice (Costa et al, 2007). Furthermore, DAT-KO animals have an altered licking pattern – they had slower licking frequency and longer licking durations when drinking sucrose solution and were much more sensitive to feedback function, with no difference in licking pattern with water solution (Rossi & Yin, 2015). For aversive stimuli (quinine water) there was decreased licking rate for WT, but not for KO animals (Costa et al, 2007).…”

Section: Dat Knockout (Dat-ko) Micementioning

confidence: 99%

Dopamine transporter mutant animals: a translational perspective

Efimova

Gainetdinov

Budygin

et al. 2016

Journal of Neurogenetics

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The dopamine transporter (DAT) plays an important homeostatic role in the control of both the extracellular and intraneuronal concentrations of dopamine, thereby providing effective control over activity of dopaminergic transmission. Since brain dopamine is known to be involved in numerous neuropsychiatric disorders, investigations using mice with genetically altered DAT function and thus intensity of dopamine-mediated signaling have provided numerous insights into the pathology of these disorders and highlight novel pathological mechanisms that could be targeted to provide new therapeutic approaches for these disorders. In this brief overview we discuss recent investigations involving animals with genetically altered DAT function, particularly focusing on translational studies providing new insights into pathology and pharmacology of dopamine-related disorders. Perspective applications of these and newly developed models of DAT dysfunction are also discussed.

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Section: Dat Knockout (Dat-ko) Micementioning

confidence: 99%

Dopamine transporter mutant animals: a translational perspective

Efimova

Gainetdinov

Budygin

et al. 2016

Journal of Neurogenetics

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“…This behavior in rodents has been linked to dopaminergic hyperactivity in the basal ganglia, striatum, and nucleus accumbens (NAc) (Rossi and Yin, 2015).…”

Section: Introductionmentioning

confidence: 99%

Effect of ketamine administration, alone and in combination with E-6837, on climbing behavior

Briones-Aranda

Suárez-Santiago

Picazo

et al. 2016

Behavioural Pharmacology

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Some types of schizophrenia have been associated with repetitive movements lacking specific purpose, also known as stereotyped behavior. Dopamine agonists (D2) and noncompetitive N-methyl-D-aspartate receptor antagonists (e.g. ketamine) have been administered in rodent models to induce stereotyped behavior that resembles some motor symptoms of schizophrenia. Recently, a relationship has been found between 5-HT6 receptors (5-HT6Rs) and dopaminergic activity. The present study evaluates the effect of ketamine (5 and 10 mg/kg), alone and in combination with the 5-HT6R agonist E-6837, on the climbing behavior of male mice. Ketamine was administered with an acute (1 day) and subchronic (5 day) scheme. Later, these doses and schemes were combined with an acute scheme of E-6837 (5 and 10 mg/kg). With both the acute and the subchronic schemes, ketamine increased climbing behavior at a dose of 10 mg/kg, and this effect was reversed by E-6837 (at 5 and 10 mg/kg). The present results suggest that there is an interaction between N-methyl-D-aspartate and 5-HT6 receptors in the regulation of climbing behavior. Further research is necessary to provide more evidence on this interaction.

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“…The changes in locomotive behaviors have been attributed to the activation of dopamine D1-like and D2-like receptors (Janhunen et al 2013). With regard to feeding, dopamine (DA) has been shown to play an important role (Costa et al 2007;Rossi and Yin 2015). For example, alteration of dopamine levels (outside of their physiological range), such as a systemic increases or decreases, impede feeding behavior (Szczypka et al 1999).…”

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confidence: 99%

D1 and D2 antagonists reverse the effects of appetite suppressants on weight loss, food intake, locomotion, and rebalance spiking inhibition in the rat NAc shell

Kalyanasundar

Pérez

Luna

et al. 2015

Journal of Neurophysiology

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R. D1 and D2 antagonists reverse the effects of appetite suppressants on weight loss, food intake, locomotion, and rebalance spiking inhibition in the rat NAc shell. J Neurophysiol 114: 585-607, 2015. First published May 13, 2015 doi:10.1152/jn.00012.2015.-Obesity is a worldwide health problem that has reached epidemic proportions. To ameliorate this problem, one approach is the use of appetite suppressants. These compounds are frequently amphetamine congeners such as diethylpropion (DEP), phentermine (PHEN), and bupropion (BUP), whose effects are mediated through serotonin, norepinephrine, and dopaminergic pathways. The nucleus accumbens (NAc) shell receives dopaminergic inputs and is involved in feeding and motor activity. However, little is known about how appetite suppressants modulate its activity. Therefore, we characterized behavioral and neuronal NAc shell responses to shortterm treatments of DEP, PHEN, and BUP. These compounds caused a transient decrease in weight and food intake while increasing locomotion, stereotypy, and insomnia. They evoked a large inhibitory imbalance in NAc shell spiking activity that correlated with the onset of locomotion and stereotypy. Analysis of the local field potentials (LFPs) showed that all three drugs modulated beta, theta, and delta oscillations. These oscillations do not reflect an aversive-malaise brain state, as ascertained from taste aversion experiments, but tracked both the initial decrease in weight and food intake and the subsequent tolerance to these drugs. Importantly, the appetite suppressant-induced weight loss and locomotion were markedly reduced by intragastric (and intra-NAc shell) infusions of dopamine antagonists SCH-23390 (D1 receptor) or raclopride (D2 receptor). Furthermore, both antagonists attenuated appetite suppressant-induced LFP oscillations and partially restored the imbalance in NAc shell activity. These data reveal that appetite suppressant-induced behavioral and neuronal activity recorded in the NAc shell depend, to various extents, on dopaminergic activation and thus point to an important role for D1/D2-like receptors (in the NAc shell) in the mechanism of action for these anorexic compounds.

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Elevated dopamine alters consummatory pattern generation and increases behavioral variability during learning

Cited by 26 publications

References 55 publications

Dopamine transporter mutant animals: a translational perspective

Dopamine transporter mutant animals: a translational perspective

Effect of ketamine administration, alone and in combination with E-6837, on climbing behavior

D1 and D2 antagonists reverse the effects of appetite suppressants on weight loss, food intake, locomotion, and rebalance spiking inhibition in the rat NAc shell

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