Dopamine D1 receptor, but not dopamine D2 receptor, is a critical regulator for acute cocaine-enhanced gene expression

2009 ◽  
Vol 31 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Xiaowei Guan ◽  
Jin Tao ◽  
Shengnan Li
Keyword(s):  
Gene Expression ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Dopamine D1 Receptor ◽  
D1 Receptor ◽  
Dopamine D2

D1 and D2 dopaminergic systems in the rat basolateral amygdala are involved in anxiogenic-like effects induced by histamine

2011 ◽  
Vol 26 (4) ◽  
pp. 564-574 ◽  
Author(s):  
Maryam Bananej ◽  
Ahmad Karimi-Sori ◽  
Mohammad Reza Zarrindast ◽  
Shamseddin Ahmadi
Keyword(s):  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Basolateral Amygdala ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Dopamine D1 Receptor ◽  
D1 Receptor ◽  
Dopamine D2 ◽  
D1 And D2 Receptors ◽  
Male Wistar Rats

Involvement of the dopamine receptors in the basolateral amygdala (BLA) in the effects of histamine on anxiety-like behaviors of the elevated plus maze in male Wistar rats was investigated. The results showed that bilateral intra-BLA injections of histamine (2.5, 5 and 7.5 µg/rat) induced an anxiogenic-like effect, revealed by decreases in percentage of open arm time (%OAT) and open arm entries (%OAE). Intra-BLA administration of dopamine D1 receptor agonist, SKF38393 (0.25 µg/rat), and dopamine D2 receptor agonist, quinpirole (0.03 and 0.05 µg/rat), decreased %OAT but not %OAE. Conversely, intra-BLA administration of dopamine D1 receptor antagonist, SCH23390 (0.5 and 1 µg/rat), and dopamine D2 receptor antagonist, sulpiride (0.3 and 0.5 µg/rat), increased %OAT and %OAE, suggesting an anxiolytic-like effect for both drugs. Interestingly, co-administration of a silent dose of SCH23390 or sulpiride prevented anxiogenic-like effects of SKF38393 and quinpirole, respectively. Conjoint administration of a sub-effective dose of SKF38393 (0.125 µg/rat) or quinpirole (0.01 µg/rat) along with lower doses of histamine (1 and 2.5 µg/rat) induced anxiolytic-like effects. On the other hand, intra-BLA pretreatment with a silent dose of SCH23390 (0.25 µg/rat) or sulpiride (0.1 µg/rat) prevented the anxiogenic-like effect of higher doses of histamine (5 and 7.5 µg/rat). No significant change was observed in total closed arm entries, as an index for motor activity of the animals. It can be concluded that the dopamine D1 and D2 receptors in the BLA may be involved in the anxiogenic-like effects induced by histamine.

Genetic variants of dopamine D2 receptor impact heterodimerization with dopamine D1 receptor

2017 ◽  
Vol 69 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Ewa Błasiak ◽  
Sylwia Łukasiewicz ◽  
Kinga Szafran-Pilch ◽  
Marta Dziedzicka-Wasylewska
Keyword(s):  
Genetic Variants ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Dopamine D1 Receptor ◽  
D1 Receptor ◽  
Dopamine D2

scholarly journals Effect of Zishenpingchan Granule on Neurobehavioral Manifestations and the Activity and Gene Expression of Striatal Dopamine D1 and D2 Receptors of Rats with Levodopa-Induced Dyskinesias

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Qing Ye ◽  
Xiao-Lei Yuan ◽  
Jie Zhou ◽  
Can-xing Yuan ◽  
Xu-ming Yang
Keyword(s):  
Gene Expression ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
D2 Receptors ◽  
Striatal Dopamine ◽  
Control Group ◽  
Indirect Pathway ◽  
Dopamine D2 ◽  
D1 And D2 Receptors ◽  
Neurobehavioral Manifestations

This study was performed to observe the effects of Zishenpingchan granule on neurobehavioral manifestations and the activity and gene expression of striatal dopamine D1 and D2 receptors of rats with levodopa-induced dyskinesias (LID). We established normal control group, LID model group, and TCM intervention group. Each group received treatment for 4 weeks. Artificial neural network (ANN) was applied to excavate the main factor influencing variation in neurobehavioral manifestations of rats with LID. The results showed that overactivation in direct pathway mediated by dopamine D1 receptor and overinhibition in indirect pathway mediated by dopamine D2 receptor may be the main mechanism of LID. TCM increased the efficacy time of LD to ameliorate LID symptoms effectively mainly by upregulating dopamine D2 receptor gene expression.

Evidence for the heterotetrameric structure of the adenosine A2A–dopamine D2 receptor complex

2016 ◽  
Vol 44 (2) ◽  
pp. 595-600 ◽  
Author(s):  
Verònica Casadó-Anguera ◽  
Jordi Bonaventura ◽  
Estefanía Moreno ◽  
Gemma Navarro ◽  
Antoni Cortés ◽  
...  
Keyword(s):  
Structural Model ◽  
Dopamine D2 Receptor ◽  
Ex Vivo ◽  
D2 Receptor ◽  
Drug Dosage ◽  
D1 Receptor ◽  
Structural Basis ◽  
Dopamine D2 ◽  
Allosteric Mechanisms ◽  
Adenosine A2a

Heteromers of G-protein-coupled receptors (GPCRs) have emerged as potential novel targets for drug development. Accumulating evidence indicates that GPCRs can form homodimers and heteromers, with homodimers being the predominant species and oligomeric receptors being formed as multiples of dimers. Recently, heterotetrameric structures have been proposed for dopamine D1 receptor (D1R)–dopamine D3 receptor (D3R) and adenosine A2A receptor (A2AR)–dopamine D2 receptor (D2R) heteromers. The structural model proposed for these complexes is a heteromer constituted by two receptor homodimers. The existence of GPCR homodimers and heteromers provides a structural basis for inter-protomer allosteric mechanisms that might account for a multiplicity of unique pharmacological properties. In this review, we focus on the A2AR–D2R heterotetramer as an example of an oligomeric structure that is key in the modulation of striatal neuronal function. We also review the interfaces involved in this and other recently reported heteromers of GPCRs. Furthermore, we discuss several published studies showing the ex vivo expression of A2AR–D2R heteromers. The ability of A2AR agonists to decrease the affinity of D2R agonists has been reported and, on the basis of this interaction, A2AR antagonists have been proposed as potential drugs for the treatment of Parkinson's disease. The heterotetrameric structure of the A2AR–D2R complex offers a novel model that can provide new clues about how to adjust the drug dosage to the expected levels of endogenous adenosine.

Sign in / Sign up

Export Citation Format

Share Document