DRD1_MOUSE Drd1 ELISA tesk kit
- Known as:
- DRD1_MOUSE Drd1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16753
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- DRD1_MOUSE Drd1 ELISA tesk kit
Related genes to: DRD1_MOUSE Drd1 ELISA tesk kit
- Gene:
- DRD1 NIH gene
- Name:
- dopamine receptor D1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q35.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-04-27
- Date modifiied:
- 2016-10-05
Related products to: DRD1_MOUSE Drd1 ELISA tesk kit
Related articles to: DRD1_MOUSE Drd1 ELISA tesk kit
- Pathological neovascularization is the leading cause of childhood blindness in retinopathy of prematurity (ROP). Anti-vascular endothelial growth factor agents are commonly used to treat this condition, yet their variable efficacy and off-target effects demand alternative strategies. Here, we investigated the relationship between retinal dopamine (DA) dynamics and pathological angiogenesis in the oxygen-induced retinopathy (OIR) mouse model mimicking ROP pathogenesis. We determined the individual effects of apomorphine (APO), a non-selective DA receptor agonist, and selective agonists or antagonists of dopamine D1 receptor (Drd1) and dopamine D2 receptor (Drd2), on pathological neovascularization. Integrating single-cell RNA sequencing with Müller cell-specific Drd2 knockout OIR mice, we identified that Drd2-mediated signaling in Müller cells orchestrates hypoxia-inducible factor alpha and vascular endothelial growth factor A biosynthesis in Müller cells during the hypoxic-ischemic phase of OIR. Collectively, OIR-induced dopaminergic deficiency and impaired Drd2 activity in Müller cells synergistically exacerbate pathological angiogenesis. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/06/03
Wang QiShi JiajiaOuyang ShuaiZhang TingtingYang HaoranZhu JiadiWang LuyaoLv YuanDong SisiChen RuyiLing XuemeiJiao ShimingDong MengmengYan WenjunYang JingleiYan BiaoChen JiangfanQu JiaZhao FeiZhou Xiangtian - Ciliopathies frequently involve abnormal brain development and affected individuals often present with varying degrees of cognitive impairment and behavioral alterations. In parallel, genetic studies have linked primary cilia to neurodevelopmental disorders such as autism spectrum disorder (ASD). Together, these observations point to a role for primary cilia in cognition, yet their mechanistic contribution to neural function remains unclear. To address this, we define neural computation as the integration of inputs, dynamic thresholding, and routing of outputs, and propose that primary cilia function not as passive sensory antennae, but as dynamic computational microdomains. Within this framework, cilia integrate extrinsic signals and intrinsic cellular states through modular signaling pathways, including GPCR-cAMP-PKA cascades and tightly regulated trafficking mechanisms. These processes are spatially constrained by ciliary gating and transport systems, enabling selective filtering, amplification, and transformation of inputs into context-dependent outputs. During development, these molecular computations scale to shape neural circuit architecture. Ciliary signaling regulates neurogenesis, specifies neuronal identity, and guides neuronal migration and connectivity, thereby embedding computational parameters into the physical structure of the brain. In the mature brain, ciliary GPCRs modulate neuronal and circuit-level dynamics. Receptors such as 5HT6 and SSTR3 influence neuronal excitability and excitation-inhibition balance, while hypothalamic MC4R functions as a rheostat to stabilize state-dependent signaling. In parallel, dynamic trafficking of DRD1 receptors enables flexible regulation of dopaminergic signaling across subcellular compartments. Disruption of ciliary function has been linked to memory impairments, suggesting a role in regulating the stability and competition of memory engrams. These effects may involve multiple plasticity mechanisms, including synaptic tagging and capture, activity-dependent synchronization, and adult neurogenesis. Together, these findings support a unifying view in which primary cilia perform molecular computations that scale across development and adult brain function to influence neural circuits and behavior. Future integration of cilia-targeted molecular tools with systems-level approaches will be essential for disentangling developmental effects from active computational roles in the mature brain. - Source: PubMed
Publication date: 2026/06/02
Teoh AndrewArinjay MishraGiri DwaipayanPhua Siew Cheng - Brain-derived neurotrophic factor (BDNF) is a master regulator of neuronal differentiation and inhibitory circuit maturation in the mammalian brain. Yet, its downstream mediators in distinct neuronal populations remain incompletely defined. Here, we identify mitogen- and stress-activated kinase 1 (MSK1) as a critical mediator of BDNF signalling during postnatal striatal development. MSK1 expression predominates in GABAergic neurons across the cortex and striatum, with region-specific dynamics: MSK1 expression in cortical GABAergic interneurons declines from postnatal day 5 (P5) to day 30 (P30), while expression in striatal GABAergic medium spiny neurons (MSNs) persists into adulthood. Using a novel Msk1 KO mouse model, generated by deleting exon IV of Msk1, we find that striatal volume and MSN dendritic complexity decrease by P60, without cortical neuron alterations, underscoring MSK1´s striatal-specific role. Mechanistically, MSK1 drives BDNF-induced MeCP2 phosphorylation at serine 421 in MSNs via MAPK/ERK, independently of CaMKII, forming a nuclear complex with MeCP2, thus amplifying MSK1´s role in transcriptional regulation. This MSK1-MeCP2 signalling is also involved in BDNF-dependent and independent morphological developmental processes of cultured striatal neurons. Accordingly, Msk1 KO striatum shows dysregulated GABAergic (Gad1, Gabrg3) and dopaminergic (Drd1, Drd2, Drd3) gene expression, mirroring profiles in MeCP2 deficient models. Behaviourally, Msk1 KO mice display hypersociability, impaired nest-building, and increased depressive-like behaviour in the forced swimming test, contributing to striatal circuit dysfunction. These findings link MSK1-mediated molecular disruptions to inhibitory circuit imbalances and behaviours reminiscent of psychiatric disorders, positioning MSK1 as a potential therapeutic target for neurodevelopmental and psychiatric disorders, including those associated with MeCP2 dysfunction. - Source: PubMed
Publication date: 2026/05/18
Varela-Andrés NataliaHernández-Del Caño CarlosCebrián-León AlejandroBlanco AdriánLos Arcos-López de Pariza IzaskunFernández Del Campo Inés SGarcía-Losada SandraArévalo Juan CarlosSánchez-Martín ManuelBajo-Grañeras RaquelMartín RicardoSánchez-Aguilera AlbertoMerchán Miguel ADeogracias Rubén - Ketamine triggers cellular pyroptosis through an NOD-like receptor protein 3 (NLRP3)/caspase-1 pathway, leading to neurotoxicity and cognitive deficits. Dopamine receptor D1 (DRD1) activation, however, suppresses NLRP3 inflammasome activation, thereby curbing inflammation. We hypothesized that ketamine induces pyroptosis through the NLRP3/caspase-1 pathway, resulting in neurotoxicity and cognitive dysfunction, and that DRD1 activation could counteract these effects. - Source: PubMed
Pan YingZhang Jia-YuLi AngZhu Xiu-MeiLv PengZhang Feng-TongBai YangLi YangWei Jia-YiYao Jun - Stress can cause or exacerbate psychiatric illness, and effects on the transcription factor CREB within the nucleus accumbens (NAc) are critically involved. In rodents, stress-induced activation of NAc CREB produces elevations in dynorphin (DYN), an endogenous opioid expressed in dopamine D1-receptor (D1R)-expressing medium spiny neurons (MSNs). In turn, elevated DYN signaling produces features of mood and anxiety disorders via actions at kappa-opioid receptors (KORs). Although individual differences in stress sensitivity have been described-with some appearing susceptible and others resilient-the contribution of NAc DYN to these phenotypes is unclear. Here we examined relationships between social behavior and DYN in D1R-expressing MSNs in mice exposed to chronic social defeat stress (CSDS). We used quantitative (q)RNAscope to assess co-expression of genes encoding CREB ( ), D1Rs ( ), and DYN ( ) within the NAc. To leverage individual variability, we performed regression analyses across all mice, revealing negative correlations between social interaction behavior and expression of and , linking higher social avoidance with higher expression of these genes. There was no correlation with , suggesting stress-induced elevations in depend on CREB activation (phosphorylation). These findings suggest that stress-induced elevations in D1R-associated DYN signaling within the NAc is a biomarker of susceptibility. - Source: PubMed
Publication date: 2026/04/24
Burek DominikaCarlezon William A