DCE1_BOVIN GAD1 ELISA tesk kit
- Known as:
- DCE1_BOVIN GAD1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16212
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- DCE1_BOVIN GAD1 ELISA tesk kit
Related genes to: DCE1_BOVIN GAD1 ELISA tesk kit
- Gene:
- GAD1 NIH gene
- Name:
- glutamate decarboxylase 1
- Previous symbol:
- GAD
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
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- The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg - Memory processes are susceptible to impairment induced by excessive consumption of hypercaloric diets, particularly those rich in saturated fats and fructose. Such dietary patterns have been linked to disrupted neurotransmission in the prefrontal cortex (PFC), where the balance between excitation and inhibition depends on efficient glucose metabolism and the synthesis of neuroactive amino acids. However, the molecular mechanisms underlying these effects remain poorly understood. Here, male C57BL/6 mice were fed for 10 weeks with a control diet, a high-fat diet (HFD), a high-fructose diet (HFrD), or a combined high-fat/high-fructose diet (HFFrD). Their body weight gain and visceral adiposity were primarily driven by saturated fat intake, whereas hyperglycemia was observed across all diets. Also, we assessed metabolic outcomes, recognition memory, and PFC molecular profiles, including neuroactive amino acids (GABA, glutamate, glutamine, aspartate, alanine, glycine, and taurine) and the expression of genes related to glucose metabolism (Slc2a1, Pcx, G6pd, Gck, Pck1, Irs2) and the glutamate/GABA-glutamine cycle (Glul, Glud1, Gad1, Gad2). Behaviorally, HFFrD reduced locomotor activity and caused the most significant impairment in recognition memory. In the PFC, diet composition generated distinct amino acid profiles, revealing vulnerability of the glutamine-glutamate-GABA cycle to hypercaloric intake. Transcriptional responses were diet-specific, with consistent Gad1 upregulation and broader induction of glucose metabolism-related genes. Together, these findings demonstrate diet-dependent metabolic and neurochemical remodeling in the PFC and support a link between excessive fat and/or fructose intake with disrupted glutamine-glutamate homeostasis and memory deficits. - Source: PubMed
Publication date: 2026/06/02
Martínez-Orozco HumbertoReyes-Castro Luis AntonioLomas-Soria ConsueloSolís-Ortíz SilviaDiaz-Miranda Sofía Yolanda - Empathy, ranging from emotional contagion to consolation, is central to social cognition. While neural mechanisms of observed pain are well studied, how witnessing trauma affects empathy-related behaviors remains unclear. Using an observational social defeat (OSD) model, we find that OSD-exposed mice display enhanced allogrooming toward defeated conspecifics, indicating increased consolation behavior. Whole-brain cFos mapping and fiber photometry reveal selective activation of medial amygdala (MeA) GABAergic neurons during empathic allogrooming. NG2 glia modulate this behavior via GABA signaling; their specific ablation in the MeA reduces inhibitory synaptic transmission, disinhibiting neighboring GABAergic neurons and increasing allogrooming. Single-cell RNA analysis reveals that GABA signaling originates from Gad1-expressing NG2 glia. Genetic knockout of Gad1 in NG2 glia recapitulates the phenotype. This mechanism requires elevated corticosterone induced by social defeat. Our findings highlight the role of NG2 glia-GABA neuron interactions in promoting prosocial empathy and suggest targeting GABA signaling in NG2 glia as a potential therapeutic strategy for vicarious trauma. - Source: PubMed
Publication date: 2026/05/25
Jian YujinJin ShengyuLiu PengZheng XiaoliHong XiaoqiHan YongSemyanov AlexeyDuan ShuminTong Xiaoping - Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and synaptic dysfunction. Among the earliest regions affected is the retrosplenial cortex (RSC), where parvalbumin-expressing (PV + ) interneurons are particularly susceptible to AD-related pathology. To understand the molecular alterations within these vulnerable neurons we employed a dual-platform spatial transcriptomics approach, integrating GeoMx Digital Spatial Profiler (DSP) and Xenium In Situ. We analyzed the transcriptomic profiles of PV+ and NeuN+ neurons in the RSC of female 5xFAD mice. We leveraged the individual strengths of each platform to generate a robust and comprehensive dataset. Using non-negative matrix factorization and k-means clustering, we identified disease-associated metagenes and examined their spatial distribution. Our analysis revealed distinct transcriptional subpopulations within PV+ interneurons, with specific metagenes differentially expressed in RSC. Dner, Gad1, and Pvalb exhibited significant down-regulation in TG mice, suggesting impairments in PV+ interneuron function and GABAergic signalling. Cross-validation between GeoMx DSP and Xenium In Situ as well as RNAscope and immunohistochemistry confirmed the reproducibility and robustness of these findings. This study provides insights into the heterogeneity and molecular vulnerabilities of PV+ interneurons in AD and demonstrates the power of integrating spatial transcriptomic platforms to uncover disease-associated neuronal subtypes and molecular markers. - Source: PubMed
Publication date: 2026/05/20
Seo HeewonTerstege Dylan JRen YiLiu ShiyingGoring Kimberly-Ann RuthAhn Bo YoungEpp Jonathan R - 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