Locomotor bias produced by intra-accumbens injection of dopamine agonists and antagonists

Messier, Claude; Mrabet, Oulaya; Destrade, Claude

doi:10.1016/0091-3057(92)90079-u

Cited by 20 publications

(6 citation statements)

References 39 publications

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“…The same lesions disrupted sensorimotor gating processes (impaired prepulse inhibition of the acoustic startle response), an effect reversed by the DA antagonist haloperidol. Both the amphetamine hyper-responsiveness and sensorimotor gating deficits are consistent with proposed roles of intraaccumbens DA (Messier et al, 1992;Swerdlow et al, 1990).…”

Section: Introductionsupporting

confidence: 74%

Cholinergic depletion in nucleus accumbens impairs mesocortical dopamine activation and cognitive function in rats

et al. 2012

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Section: Introductionsupporting

confidence: 74%

Cholinergic depletion in nucleus accumbens impairs mesocortical dopamine activation and cognitive function in rats

et al. 2012

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“…The pharmacologic blockade of the D2 receptors inhibits the effects of psychostimulants on motor activity 55 and local injection of D2 antagonists in the NAcc attenuates the increase in locomotor activity induced by a peripheral Amph challenge. 56,57 Interestingly, the specific inhibition of D2 expression in the NAcc did not significantly reduce the locomotor effects of Amph either in the saline-or in the PCP-treated rats as compared with their respective controls. However, the D2 KD blunted the hyperlocomotive effect of Amph in the PCP-treated rats.…”

Section: Discussionmentioning

confidence: 87%

Local inactivation of Gpr88 in the nucleus accumbens attenuates behavioral deficits elicited by the neonatal administration of phencyclidine in rats

et al. 2014

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Gpr88, an orphan G-protein-coupled receptor, is highly and almost exclusively expressed in the medium spiny projection neurons of the striatum, and may thus participate in the control of motor functions and cognitive processing that are impaired in neuropsychiatric disorders such as Parkinson's disease or schizophrenia (SZ). This study investigated the relevance of Gpr88 to SZ-associated behavior by knocking down Gpr88 gene expression in the ventral striatum (nucleus accumbens) in a neurodevelopmental rat model of SZ, generated by neonatal treatment with phencyclidine (PCP). In this model, we compared the effects of the local inactivation in the adult animal of the expression of Gpr88 and of Drd2, a gene strongly implicated in the etiology of SZ and coding for the dopamine receptor type 2 (D2). To inactivate specifically Gpr88 and D2 expression, we used the lentiviral vector-mediated microRNA silencing strategy. The neonatal PCP treatment induced in the adult rat hyperlocomotion in response to amphetamine (Amph) and social novelty discrimination (SND) deficits. The inactivation of D2 did not modify the locomotor response to Amph or the cognitive deficits induced by PCP, whereas the silencing of Gpr88 inhibited the Amph-induced hyperlocomotion and reduced the impairment of SND elicited by neonatal exposure to PCP. These observations suggest a role for Gpr88 in the regulation of cognitive and motor functions, and support its relevance to the pathophysiology and treatment of SZ and other disorders involving dysfunction of the accumbens-striatal complex.

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“…Thus, the haloperidol-specific induction of c-fos in the shell of the NAc, calculated as the ratio of c-fos positive cells in the haloperidol-treated mice with respect to saline-treated mice, was lower by 48% in Rxrg À/À mice as compared to their WT controls (Figure 5D). To validate these findings functionally we tested the locomotor effects of low, non-cataleptic doses of haloperidol, which have been proposed to involve post-synaptic dopamine D2 receptors in the nucleus accumbens (Messier et al, 1992;Millan et al, 2004;Pijnenburg et al, 1976). All mice treated with haloperidol displayed reduction of locomotor activity in the novel environment of the open field, although such reduction was different depending on the genotype (significant genotype 3 treatment interaction, F[4,68] = 2.7; p < 0.05).…”

Section: Neuronmentioning

confidence: 99%

Retinoid X Receptor Gamma Control of Affective Behaviors Involves Dopaminergic Signaling in Mice

Krzyżosiak

Szyszka-Niagolov

Wietrzych

et al. 2010

Neuron

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Abnormal signaling by retinoids or n-3 polyunsaturated fatty acids has been implicated in clinical depression. The converging point in activities of these two classes of molecules is transcriptional activation of retinoid X receptors (Rxr). We show here that ablation of Rxrgamma in mice leads to depressive-like behaviors including increased despair and anhedonia, which were accompanied by reduced expression of dopamine D2 receptor in the shell of nucleus accumbens (NAc) and altered serotonin signaling. While abnormal serotonin signaling is not sufficient to generate the depressive behaviors, increasing D2r expression by chronic fluoxetine (Prozac) treatment or adenoassociated virus type2 (AAV2) mediated expression of Rxrgamma or D2r in the NAc of Rxrgamma(-/-) mice normalizes depressive-like behaviors in Rxrgamma(-/-) animals. Conversely, NAc infusion of raclopride, a D2r antagonist prevents AAV2-Rxrgamma-mediated rescue of despair behaviors in Rxrgamma(-/-) mice. Combined, our data argue that control of NAc D2r expression is critical for Rxrgamma-mediated modulation of affective behaviors.

show abstract

Locomotor bias produced by intra-accumbens injection of dopamine agonists and antagonists

Cited by 20 publications

References 39 publications

Cholinergic depletion in nucleus accumbens impairs mesocortical dopamine activation and cognitive function in rats

Cholinergic depletion in nucleus accumbens impairs mesocortical dopamine activation and cognitive function in rats

Local inactivation of Gpr88 in the nucleus accumbens attenuates behavioral deficits elicited by the neonatal administration of phencyclidine in rats

Retinoid X Receptor Gamma Control of Affective Behaviors Involves Dopaminergic Signaling in Mice

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