Conditioned locomotion induced by unilateral intrastriatal administration of Apomorphine: D2 receptor activation is critical but not the expression of the unconditioned response

2006 ◽  
Vol 1083 (1) ◽  
pp. 85-95 ◽  
Author(s):  
Flávia Regina Cruz Dias ◽  
Robert J. Carey ◽  
Marinete Pinheiro Carrera
Keyword(s):  
D2 Receptor ◽  
Receptor Activation ◽  
Unconditioned Response ◽  
Conditioned Locomotion ◽  
Intrastriatal Administration

scholarly journals The Adenosine A2A Receptor Activation in Nucleus Accumbens Suppress Cue-Induced Reinstatement of Propofol Self-administration in Rats

2021 ◽  
Author(s):  
Zhanglei Dong ◽  
Bingwu Huang ◽  
Chenchen Jiang ◽  
Jiangfan Chen ◽  
Han Lin ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
D2 Receptor ◽  
Fixed Ratio ◽  
Receptor Activation ◽  
Addictive Behaviors ◽  
Self Administration ◽  
A2a Receptors ◽  
Mediated Effects ◽  
Seeking Behavior ◽  
Adenosine A2a

AbstractPropofol has shown strong addictive properties in rats and humans. Adenosine A2A receptors (A2AR) in the nucleus accumbens (NAc) modulate dopamine signal and addictive behaviors such as cocaine- and amphetamine-induced self-administration. However, whether A2AR can modulate propofol addiction remains unknown. AAV-shA2AR was intra-NAc injected 3 weeks before the propofol self-administration training to test the impacts of NAc A2AR on establishing the self-administration model with fixed ratio 1 (FR1) schedule. Thereafter, the rats were withdrawal from propofol for 14 days and tested cue-induced reinstatement of propofol seeking behavior on day 15. The propofol withdrawal rats received one of the doses of CGS21680 (A2AR agonist, 2.5–10.0 ng/site), MSX-3 (A2AR antagonist, 5.0–20.0 μg/site) or eticlopride (D2 receptor (D2R) antagonist, 0.75–3.0 μg/site) or vehicle via intra-NAc injection before relapse behavior test. The numbers of active and inactive nose-poke response were recorded. Focal knockdown A2AR by shA2AR did not affect the acquisition of propofol self-administration behavior, but enhance cue-induced reinstatement of propofol self-administration compared with the AAV-shCTRLgroup. Pharmacological activation of the A2AR by CGS21680 (≥ 5.0 ng/site) attenuated cue-induced reinstatement of propofol self-administration behavior. Similarly, pharmacological blockade of D2R by eticlopride (0.75–3.0 μg/site) attenuated propofol seeking behavior. These effects were reversed by the administration of MSX-3 (5.0–20.0 μg/site). The A2AR- and D2R-mediated effects on propofol relapse were not confounded by the learning process, and motor activity as the sucrose self-administration and locomotor activity were not affected by all the treatments. This study provides genetic and pharmacological evidence that NAc A2AR activation suppresses cue-induced propofol relapse in rats, possibly by interacting with D2R.

Dose-Dependent Effects of Dopamine (D2) Receptor Activation on Non-Focal Plasticity in Humans

2008 ◽  
Vol 1 (3) ◽  
pp. 282
Author(s):  
K. Monte-Silva ◽  
M. Kuo ◽  
W. Paulus ◽  
M. Nitsche
Keyword(s):  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Receptor Activation ◽  
Dopamine D2 ◽  
Dose Dependent

D2 receptor activation in distinct striatal neurons in comparison with D3 receptors

1996 ◽  
Vol 6 ◽  
pp. 23-24
Author(s):  
M. Sasa ◽  
K. Ishihara ◽  
T. Amano ◽  
H. SasMatsubayashi ◽  
T. Momiyama ◽  
...  
Keyword(s):  
D2 Receptor ◽  
Receptor Activation ◽  
Striatal Neurons ◽  
D3 Receptors

scholarly journals Dopamine receptors mediate strategy abandoning via modulation of a specific prelimbic cortex–nucleus accumbens pathway in mice

2018 ◽  
Vol 115 (21) ◽  
pp. E4890-E4899 ◽  
Author(s):  
Qiaoling Cui ◽  
Qian Li ◽  
Hongyan Geng ◽  
Lei Chen ◽  
Nancy Y. Ip ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Dopamine Receptors ◽  
Cortical Neurons ◽  
Critical Role ◽  
D2 Receptor ◽  
Receptor Activation ◽  
Prelimbic Cortex ◽  
Dopamine Depletion ◽  
Dopaminergic Tone ◽  
Type Receptor

The ability to abandon old strategies and adopt new ones is essential for survival in a constantly changing environment. While previous studies suggest the importance of the prefrontal cortex and some subcortical areas in the generation of strategy-switching flexibility, the fine neural circuitry and receptor mechanisms involved are not fully understood. In this study, we showed that optogenetic excitation and inhibition of the prelimbic cortex–nucleus accumbens (NAc) pathway in the mouse respectively enhances and suppresses strategy-switching ability in a cross-modal spatial-egocentric task. This ability is dependent on an intact dopaminergic tone in the NAc, as local dopamine denervation impaired the performance of the animal in the switching of tasks. In addition, based on a brain-slice preparation obtained from Drd2-EGFP BAC transgenic mice, we demonstrated direct innervation of D2 receptor-expressing medium spiny neurons (D2-MSNs) in the NAc by prelimbic cortical neurons, which is under the regulation by presynaptic dopamine receptors. While presynaptic D1-type receptor activation enhances the glutamatergic transmission from the prelimbic cortex to D2-MSNs, D2-type receptor activation suppresses this synaptic connection. Furthermore, manipulation of this pathway by optogenetic activation or administration of a D1-type agonist or a D2-type antagonist could restore impaired task-switching flexibility in mice with local NAc dopamine depletion; this restoration is consistent with the effects of knocking down the expression of specific dopamine receptors in the pathway. Our results point to a critical role of a specific prelimbic cortex–NAc subpathway in mediating strategy abandoning, allowing the switching from one strategy to another in problem solving.

scholarly journals Intracerebroventricular injection of ouabain causes mania-like behavior in mice through D2 receptor activation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Alexander Lopachev ◽  
Anna Volnova ◽  
Anna Evdokimenko ◽  
Denis Abaimov ◽  
Yulia Timoshina ◽  
...  
Keyword(s):  
Mouse Model ◽  
Histological Analysis ◽  
Dopaminergic System ◽  
D2 Receptor ◽  
Brain Structures ◽  
Receptor Activation ◽  
Intracerebroventricular Injection ◽  
Fast Scan Cyclic Voltammetry ◽  
The Central Nervous System ◽  
Brain Ventricle

Abstract Intracerebroventricular (ICV) administration of ouabain, an inhibitor of the Na, K-ATPase, is an approach used to study the physiological functions of the Na, K-ATPase and cardiotonic steroids in the central nervous system, known to cause mania-like hyperactivity in rats. We describe a mouse model of ouabain-induced mania-like behavior. ICV administration of 0.5 µl of 50 µM (25 pmol, 14.6 ng) ouabain into each lateral brain ventricle results in increased locomotor activity, stereotypical behavior, and decreased anxiety level an hour at minimum. Fast-scan cyclic voltammetry showed that administration of 50 µM ouabain causes a drastic drop in dopamine uptake rate, confirmed by elevated concentrations of dopamine metabolites detected in the striatum 1 h after administration. Ouabain administration also caused activation of Akt, deactivation of GSK3β and activation of ERK1/2 in the striatum of ouabain-treated mice. All of the abovementioned effects are attenuated by haloperidol (70 µg/kg intraperitoneally). Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in brain structures were demonstrated by histological analysis. This newly developed mouse model of ouabain-induced mania-like behavior could provide a perspective tool for studying the interactions between the Na,K-ATPase and the dopaminergic system.

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