Polyclonal Rabbit ADRA2A Antibody
- Known as:
- Polyclonal Rabbit ADRA2A Antibody
- Catalog number:
- KA0122
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ADRA2A Antibody
Related genes to: Polyclonal Rabbit ADRA2A Antibody
- Gene:
- ADRA2A NIH gene
- Name:
- adrenoceptor alpha 2A
- Previous symbol:
- ADRA2, ADRA2R
- Synonyms:
- ADRAR
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-03-22
Related products to: Polyclonal Rabbit ADRA2A Antibody
Related articles to: Polyclonal Rabbit ADRA2A Antibody
- Stress is known to play a critical role in relapse to drug use as well as in food craving. Craving itself is a key determinant of relapse, and cue-induced drug craving has been shown to increase, or 'incubate', over time for certain drugs such as cocaine and nicotine, though this effect is less consistent for others such as opiates. However, the modulations of stress-related biochemical systems after early or protracted withdrawal that could contribute to this incubation phenomenon have not yet been systematically examined in animal models, nor has the specificity of these mechanisms been tested across different drug classes or reinforcers. To address this gap, we analysed brains from male Lewis rats that self-administered cocaine (0.75 mg/kg, i.v.), heroin (0.075 mg/kg, i.v.), or saline, and subsequently assessed changes in plasma corticosterone, ornithine and other stress-related amines, alongside central gene and protein expression CRH, CRH2 receptor, and α- and β-adrenergic receptor subunits -Adra1, Adra2a and Adrb1) in cortico-striato-amygdalar nodes (after 1 or 30 days of withdrawal). A parallel experiment was conducted using sucrose as a reinforcer. Our findings indicate that although most effects were reinforcer-specific, convergent adaptations were also observed, particularly within noradrenergic systems and the basolateral amygdala, expanding our knowledge about the neurochemical rearrangements occurring during withdrawal. - Source: PubMed
Publication date: 2026/04/16
Roura-Martínez DavidUcha MarcosMoreno-Fernández MarioCastillo Carlos AlbertoBallesteros-Yánez InmaculadaMarcos AlbertoAmbrosio EmilioHiguera-Matas Alejandro - Raynaud's phenomenon (RP) is the first noticeable symptom of systemic sclerosis (SSc), appearing even years before other signs. Vascular and immune pathways, hallmarks in SSc pathogenesis, are implicated in primary RP. Hence, we aimed to define the shared genetic architecture between these conditions to explore pathogenic mechanisms and whether pleiotropic loci could help identify primary RP patients at increased genetic risk of developing SSc. - Source: PubMed
Publication date: 2026/04/08
Rangel-Peláez CarlosRodriguez-Martin InmaculadaRosa-Baez CarlosKerick MartinDel-Castillo Alfredo Guillen-Simeón-Aznar Carmen PCallejas José LDistler OliverProudman Susanna MNikpour MandanaHunzelmann NicolasMoroncini Gianlucade Vries-Bouwstra Jeska KHerrick Ariane LAllanore YannickAlarcón-Riquelme Marta EBeretta LorenzoMayes Maureen DDenton Christopher PAssassi ShervinMartín JavierAcosta-Herrera MarialbertOrtiz-Fernández Lourdes - Norepinephrine is a key neuromodulator of hypothalamic circuits that regulate energy balance. Previous studies suggested that norepinephrine inhibits proopiomelanocortin (POMC) neurons of the arcuate nucleus via α2a-adrenoceptors (ADRA2A), but the underlying mechanisms and physiological relevance of this pathway were not assessed. We therefore investigated how ADRA2 activation regulates POMC neuron activity and whether Adra2a expressed in POMC neurons contributes to energy and glucose homeostasis in vivo. We used whole-cell patch clamp electrophysiology in male and female mice to evaluate the impact of norepinephrine and the ADRA2 agonist UK 14,304 on definitive POMC neurons in the arcuate nucleus. We also generated and validated a novel Adra2a-flox mouse line, which was crossed with Pomc-CreERT2 mice to produce inducible POMC-specific Adra2a knockout mice (POMC). These mice were used for both electrophysiological analyses and in vivo assessment of energy and glucose homeostasis. Multiplex RNAscope confirmed that Adra2a was highly expressed in ~50% of POMC neurons, with significantly higher expression in females. Norepinephrine and the selective ADRA2 agonist UK 14,304 robustly inhibited POMC neurons in hypothalamic slices, producing hyperpolarization, reduced firing, and decreased input resistance independent of sex. These effects were mediated in part by activation of multiple potassium conductances, as blockade of K and K channels attenuated the response. They were also partly indirect, as blockade of synaptic transmission reduced the proportion of neurons that were inhibited. Deletion of Adra2a in definitive POMC neurons had little effect on body weight, food intake, or adiposity, but modestly impaired glucose tolerance in males. Electrophysiological studies revealed that loss of Adra2a in POMC neurons prevented UK 14,304-induced inhibition in approximately half of POMC neurons, supporting the involvement of both direct and indirect effects of UK 14,304 on POMC neuron activity. In conclusion, ADRA2A robustly inhibits hypothalamic POMC neurons through both direct and indirect mechanisms. However, Adra2a expression in POMC neurons is largely dispensable for the regulation of energy balance. These findings suggest that noradrenergic inhibition of POMC neuron activity involves additional cellular targets or network-level pathways beyond POMC neurons themselves. - Source: PubMed
Lavoie OlivierTurmel AudreyKhouma AxelleMinbashi Moeini MoeinLiu ChenMichael Natalie JCaron Alexandre - Comprehending sex differences in stress vulnerability and the associated neurocircuitry has been elusive until the development of a method for investigating social defeat in female mice. - Source: PubMed
Publication date: 2026/03/15
Yaeger Jazmine D WJohn Megan MLedesma Leighton JGreschke Trent LGale J JMeyer Lauren SBrummels Renée AKorzan Wayne JWaters R ParrishSummers Cliff H - Genetic factors are thought to play an important role in antipsychotic-induced weight gain (AIWG). Polygenic risk scores (PRS) could provide a measure of genetic predisposition to antipsychotic drug induced weight gain (AIWG).We conducted a study to examine how a PRS, generated using SNPs, identified from a recent meta-analysis, related to weight-change over time in people with first episode-psychosis. - Source: PubMed
Heald AdrianIllangasekera YasithaLoureiro Camila MarcelinoShakespeare MarkJameson AdamPhillipson AdrianReynolds Gavin PDalton Caroline