scholarly journals Repeated quinpirole treatment: Locomotor activity, dopamine synthesis, and effects of selective dopamine antagonists

Synapse ◽  
1995 ◽  
Vol 20 (3) ◽  
pp. 209-216 ◽  
Author(s):  
James K. Rowlett ◽  
Bruce A. Mattingly ◽  
Michael T. Bardo
Keyword(s):  
Locomotor Activity ◽  
Dopamine Antagonists ◽  
Dopamine Synthesis ◽  
Selective Dopamine

scholarly journals The incentive amplifying effects of nicotine are reduced by selective and non-selective dopamine antagonists in rats

2014 ◽  
Vol 126 ◽  
pp. 50-62 ◽  
Author(s):  
Matthew I. Palmatier ◽  
Marissa R. Kellicut ◽  
A. Brianna Sheppard ◽  
Russell W. Brown ◽  
Donita L. Robinson
Keyword(s):  
Dopamine Antagonists ◽  
Selective Dopamine

Effects of Dopamine Antagonists on Changes in Spontaneous EEG and Locomotor Activity in Ketamine-Treated Rats

1997 ◽  
Vol 57 (1-2) ◽  
pp. 361-365 ◽  
Author(s):  
M Yamamoto ◽  
Y Mizuki ◽  
M Suetsugi ◽  
Y Ozawa ◽  
M Ooyama ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Dopamine Antagonists

scholarly journals Effects of Selective Dopamine D2 or D3 Receptor Antagonism on Morphine-Induced Locomotion in Mice

2020 ◽  
Author(s):  
Christian A. Botz-Zapp ◽  
Stephanie L. Foster ◽  
Amy H. Newman ◽  
David Weinshenker ◽  
Daniel F. Manvich
Keyword(s):  
Locomotor Activity ◽  
Inhibitory Effect ◽  
Opioid Use Disorder ◽  
Locomotor Sensitization ◽  
Opioid Use ◽  
R And D ◽  
Morphine Administration ◽  
Additional Support ◽  
The Impact ◽  
Selective Dopamine

AbstractRationaleThe dopamine D3 receptor (D3R) has garnered interest as a pharmacotherapeutic target for the treatment of opioid use disorder (OUD). Recent evidence suggests that D2R and D3R antagonism oppositely affect the locomotor-activating effects of cocaine, but whether this pattern extends to opioid-induced hyperactivity remains unresolved.ObjectiveThis study compared the impact of selective D2R vs. D3R antagonists on the locomotor-activating effects of acute and repeated morphine administration in mice. Catalepsy following D2R vs. D3R antagonism alone or in combination with morphine was also assessed.MethodsC57Bl/6J mice were pretreated with either the highly-selective D3R antagonist PG01037 (vehicle, 10.0 mg/kg) or the selective D2R antagonist L-741,626 (vehicle, 10.0 mg/kg) and tested for 1) locomotor activity induced by acute morphine administration (10.0 – 56.0 mg/kg), 2) locomotor sensitization following repeated morphine administration (56.0 mg/kg), or 3) catalepsy after administration of either antagonist alone or in combination with morphine (10.0 – 56.0 mg/kg).ResultsIn locomotion studies, both PG01037 and L-741,626 shifted the acute morphine dose-response function rightward/downward, although the inhibitory effect of L-741,626 pretreatment was more robust. Likewise, PG01037 pretreatment partially attenuated, while L-741,626 pretreatment fully abolished, morphine-induced locomotor sensitization. L-741,626 produced catalepsy that was blunted by morphine, whereas PG01037 did not induce catalepsy under any conditions.ConclusionsD2R or D3R antagonism attenuates morphine-induced locomotor activity and sensitization. D2R antagonism produces a stronger suppression of these effects, but also induced modest cataleptic effects which were not observed following D3R antagonism. The results lend additional support to the investigation of selective D3R antagonists as treatments for OUD.

scholarly journals Mesocorticolimbic circuit mechanisms underlying the effects of ketamine on dopamine: a translational imaging study

2019 ◽  
Author(s):  
Michelle Kokkinou ◽  
Elaine E. Irvine ◽  
David R. Bonsall ◽  
Sridhar Natesan ◽  
Lisa A. Wells ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Molecular Mechanisms ◽  
Imaging Study ◽  
Dopamine Neurons ◽  
Striatal Dopamine ◽  
Pharmacological Intervention ◽  
Dopamine Synthesis ◽  
Midbrain Dopamine ◽  
Midbrain Dopamine Neurons

ABSTRACTPatients with schizophrenia show increased striatal dopamine synthesis capacity in imaging studies. However, the mechanism underlying this is unclear but may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and parvalbumin (PV) neuronal dysfunction leading to disinhibition of mesostriatal dopamine neurons. Here, we test this in a translational mouse imaging study using a ketamine model. Mice were treated with sub-chronic ketamine (30mg/kg) or saline followed by in-vivo positron emission tomography of striatal dopamine synthesis capacity, analogous to measures used in patients. Locomotor activity was measured using the open field test. In-vivo cell-type-specific chemogenetic approaches and pharmacological interventions were used to manipulate neuronal excitability. Immunohistochemistry and RNA sequencing were used to investigate molecular mechanisms. Sub-chronic ketamine increased striatal dopamine synthesis capacity (Cohen’s d=2.5, P<0.001) and locomotor activity. These effects were countered by inhibition of midbrain dopamine neurons, and by activation of cortical and ventral subiculum PV interneurons. Sub-chronic ketamine reduced PV expression in these neurons. Pharmacological intervention with SEP-363856, a novel psychotropic agent with agonism at trace amine receptor 1 (TAAR1), significantly reduced the ketamine-induced increase in dopamine synthesis capacity. These results show that sub-chronic ketamine treatment in mice mimics the dopaminergic alterations in patients with psychosis, and suggest an underlying neurocircuit involving PV interneuron hypofunction in frontal cortex and hippocampus as well as activation of midbrain dopamine neurons. A novel TAAR1 agonist reversed the dopaminergic alterations suggesting a therapeutic mechanism for targeting presynaptic dopamine dysfunction in patients.

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