https://transhumanist.ru/index.php?action=history&feed=atom&title=AVPR1A 2026-06-21T11:56:28Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=AVPR1A&diff=5963&oldid=prev 2021-05-12T15:02:46Z

<p>Новая страница: «Vasopressin V1a receptor (V1aR) (AVPR V1a) (Antidiuretic hormone receptor 1a) (Vascular/hepatic-type arginine vasopressin receptor) [AVPR1] ==Publications== {{m...»</p> <p><b>Новая страница</b></p><div>Vasopressin V1a receptor (V1aR) (AVPR V1a) (Antidiuretic hormone receptor 1a) (Vascular/hepatic-type arginine vasopressin receptor) [AVPR1]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Introduction of the human [[AVPR1A]] gene substantially alters brain receptor expression patterns and enhances aspects of social behavior in transgenic mice.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24924430<br /> |abstract=Central arginine vasopressin receptor 1A ([[AVPR1A]]) modulates a wide range of behaviors, including stress management and territorial aggression, as well as social bonding and recognition. Inter- and intra-species variations in the expression pattern of [[AVPR1A]] in the brain and downstream differential behavioral phenotypes have been attributed to differences in the non-coding regions of the [[AVPR1A]] gene, including polymorphic elements within upstream regulatory areas. Gene association studies have suggested a link between [[AVPR1A]] polymorphisms and autism, and [[AVPR1A]] has emerged as a potential pharmacological target for treatment of social cognitive impairments and mood and anxiety disorders. To further investigate the genetic mechanism giving rise to species differences in [[AVPR1A]] expression patterns and associated social behaviors, and to create a preclinical mouse model useful for screening drugs targeting [[AVPR1A]], we engineered and extensively characterized bacterial artificial chromosome (BAC) transgenic mice harboring the entire human [[AVPR1A]] locus with the surrounding regulatory elements. Compared with wild-type animals, the humanized mice displayed a more widely distributed ligand-[[AVPR1A]] binding pattern, which overlapped with that of primates. Furthermore, humanized [[AVPR1A]] mice displayed increased reciprocal social interactions compared with wild-type animals, but no differences in social approach and preference for social novelty were observed. Aspects of learning and memory, specifically novel object recognition and spatial relocation recognition, were unaffected. The biological alterations in humanized [[AVPR1A]] mice resulted in the rescue of the prepulse inhibition impairments that were observed in knockout mice, indicating conserved functionality. Although further behavioral paradigms and additional cohorts need to be examined in humanized [[AVPR1A]] mice, the results demonstrate that species-specific variations in the genomic content of regulatory regions surrounding the [[AVPR1A]] locus are responsible for differential receptor protein expression patterns across species and that they are likely to contribute to species-specific behavioral variation. The humanized [[AVPR1A]] mouse is a potential preclinical model for further understanding the regulation of receptor gene expression and the impact of variation in receptor expression on behaviors, and should be useful for screening drugs targeting human [[AVPR1A]], taking advantage of the expression of human [[AVPR1A]] in human-relevant brain regions. <br /> |mesh-terms=* Aging<br /> * Animals<br /> * Brain<br /> * Chromosomes, Artificial, Bacterial<br /> * Humans<br /> * Mice, Transgenic<br /> * Organ Specificity<br /> * Prepulse Inhibition<br /> * Receptors, Vasopressin<br /> * Reflex, Startle<br /> * Sensory Gating<br /> * Social Behavior<br /> * Task Performance and Analysis<br /> |keywords=* AVPR1A<br /> * Autism<br /> * Humanized mouse<br /> * Microsatellite<br /> * Social behavior<br /> * Species-specific<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107330<br /> }}</div>

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