AVPR1B Antibody
- Known as:
- AVPR1B Antibody
- Catalog number:
- AF1129b
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AVPR1B Antibody
Ask about this productRelated genes to: AVPR1B Antibody
- Gene:
- AVPR1B NIH gene
- Name:
- arginine vasopressin receptor 1B
- Previous symbol:
- AVPR3
- Synonyms:
- -
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-07-06
- Date modifiied:
- 2016-10-05
Related products to: AVPR1B Antibody
Related articles to: AVPR1B Antibody
- To investigate the interaction between HPA-axis gene polymorphisms (FKBP5, NR3C1, AVPR1B, SLC1A3, SKA2) and brain functional alterations in adolescent depression. - Source: PubMed
Publication date: 2026/04/02
Tian SusuLiang QingqingZhou WeiHu XinyiLiu YuxuanTian JiayiLuo YunjiaoFang HaiyanWang Wei - Although several approaches have identified individual genes that contribute to autism spectrum disorder (ASD), more research is needed to establish whether these single nucleotide polymorphisms are associated with a lower risk. Studies have found that the oxytocin receptor (OXTR) and arginine-vasopressin receptors (AVPR) genes have an essential role as neuromodulators or neurotransmitters in ASD. Most of these studies have been primarily carried out in the United States, Western Europe, and Australasia, and there is divergence in the conclusions. - Source: PubMed
Publication date: 2026/01/24
González Cortés TaniaSida Godoy CristinaCruz Jorge Haro SantaRosales González Claudia CeciliaMárquez Ríos Mayra Minerva GuadalupeGutiérrez Contreras ElizabethEspino Silva Perla KarinaRuiz Flores Pablo - Omega-3 polyunsaturated fatty acids (PUFAs) are essential for brain development and function, affecting inflammation, neurotransmission, and neuroplasticity. These nutrients are associated with benefits in managing stress, sleep disorders, anxiety, and mild cognitive impairment. This study investigated the effects of chronic exposure to varying omega-3 PUFA levels, from gestation to adulthood, on behavioral and molecular aspects related to memory, anxiety, and depression in male mice. Dams received one of three diets: Control (soybean oil, 7 %), omega-3 Deficient (sunflower oil, 7 %), or omega-3 Enriched (4.2 % cod liver oil +2.8 % soybean oil). After weaning, the offspring continued on their respective diets until adulthood. The omega-3 Deficient diet led to increased locomotor activity, anxiety-like behavior, and a trend toward greater immobility time in the tail suspension test. It also upregulated the expression of Avp and its receptor Avpr1b within the hypothalamic-pituitary axis, suggesting a potential mechanistic link between omega-3 deficiency and mood disorders. In contrast, the Enriched group exhibited reduced locomotor activity and anxiolytic-like behavior in the elevated plus maze. At the molecular level, the Deficient diet downregulated Grin1, while the Enriched diet upregulated Creb1 in the hippocampus, providing insight into how omega-3 PUFAs influence cognitive processes. Chronic insufficient omega-3 consumption throughout development and adulthood may negatively affect anxiety- and depression-related responses, while high omega-3 intake may play a protective role in anxiety regulation. These findings deepen our understanding of the role of omega-3 PUFAs in affective and cognitive regulation, highlighting the significance of balanced intake to support mental health. - Source: PubMed
Publication date: 2025/12/09
Bianconi SantiagoCantarelli Verónica IRobledo Almonacid Juan EZingerling EmilioWeigandt Diego MBaez María Del CarmenPonzio Marina FWilliams Michael JSchiöth Helgi BSantillán María EStutz GracielaCarlini Valeria P - Milk ejection is the final process in maternal milk transfer from mothers to offspring and is regulated by oxytocin (OT) released from the neurohypophysis in response to the milk ejection reflex. Arginine vasopressin (AVP), another neurohypophyseal hormone well known for its antidiuretic and vasoconstrictive effects, shares structural similarity with OT, and intravenous AVP injection can also induce milk ejection. Nonetheless, AVP has also been reported to inhibit OT-induced milk ejection in rabbits. In this study, we examined the roles of OT and AVP receptors in these opposing effects of AVP on milk ejection using an in vivo assay model in mice. AVP induced milk ejection, and this effect was inhibited by an OT receptor antagonist. Intravenous pretreatment with AVP suppressed the following transient milk ejection induced by intravenous OT injection. Furthermore, AVP treatment interrupted the continuous milk ejection induced by intraperitoneal OT. These inhibitory effects of AVP were ameliorated by pretreatment with a selective Avpr1a antagonist. We further examined the role of AVP receptors using Avpr1a and Avpr1b knockout mice. The AVP-dependent inhibition of OT-induced milk ejection was abolished in Avpr1a knockout mice, but not in Avpr1b knockout mice. Our findings suggest that AVP induces milk ejection through the OT receptor while inhibiting OT-induced milk ejection via Avpr1a. This duality might reflect a physiological mechanism for restricting milk transfer under severe stress or hyperosmotic conditions and could provide insights into breastfeeding difficulties in humans, including the perception of insufficient milk and infant failure to thrive. - Source: PubMed
Kamikawa Akihiro - The neuropeptide arginine-vasopressin (AVP) has been repeatedly associated with the autism spectrum disorder (ASD) but the underlying mechanisms remain unclear. As Shank3B male mice, a model of ASD, exhibit deficits in sociability and social aggression, we focused on the lateral septum (LS), a brain region involved in the regulation of motivated behaviors and observed reduced AVP inputs from the bed nucleus of the stria terminalis (BNST) to LS. Manipulating AVP release from the BNST to LS of wild-type male mice, we found that AVP promotes both sociability and social aggression. Blocking the vasopressin receptor 1a (AVPR1a) in LS impaired sociability, while blocking the receptor 1b (AVPR1b) disrupted social aggression. Consequently, selective activation of AVPR1a or AVPR1b rescued the respective behavioral deficits in Shank3B male mice. These findings reveal that AVP release in LS modulates two distinct social behaviors via different receptors and highlight a possible strategy to rescue sociability during ASD. - Source: PubMed
Publication date: 2025/07/23
Bortolozzo-Gleich Maria HelenaBouisset GuillaumeGeng LanPino Antonia RuizNomura YukiHan ShutingLi YulongLeroy Félix