Hypermetabolism of Fat in V1a Vasopressin Receptor Knockout Mice

Hiroyama, Masami; Aoyagi, Toshinori; Fujiwara, Yoko; Birumachi, Jun-ichi; Shigematsu, Yosuke; Kiwaki, Kohji; Tasaki, Ryuji; Endo, Fumio; Tanoue, Akito

doi:10.1210/me.2006-0069

Cited by 77 publications

(78 citation statements)

References 39 publications

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“…A different KO line of the Avpr1a demonstrates a lower basal blood pressure (Egashira et al, 2004;Koshimizu et al, 2006) and impaired lipid metabolism and glucose homeostasis Hiroyama et al, 2007). Both lines have changes in behavior as discussed below.…”

Section: Gene Inactivation In Micementioning

confidence: 99%

Vasopressin: Behavioral roles of an “original” neuropeptide

Caldwell

Lee

Macbeth

et al. 2008

Progress in Neurobiology

427

416

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Vasopressin (Avp) is mainly synthesized in the magnocellular cells of the hypothalamic supraoptic (SON) and paraventricular nuclei (PVN) whose axons project to the posterior pituitary. Avp is then released into the blood stream upon appropriate stimulation (e.g., hemorrhage or dehydration) to act at the kidneys and blood vessels. The brain also contains several populations of smaller, parvocellular neurons whose projections remain within the brain. These populations are located within the PVN, bed nucleus of the stria terminalis (BNST), medial amygdala (MeA) and suprachiasmatic nucleus (SCN).Since the 1950's, research examining the roles of Avp in the brain and periphery has intensified. The development of specific agonists and antagonists for Avp receptors has allowed for a better elucidation of its contributions to physiology and behavior. Anatomical, pharmacological and transgenic, including "knockout," animal studies, have implicated Avp in the regulation of various social behaviors across species.Avp plays a prominent role in the regulation of aggression, generally of facilitating or promoting it. Affiliation and certain aspects of pair-bonding are also influenced by Avp. Memory, one of the first brain functions of Avp that was investigated, has been implicated especially strongly in social recognition. The roles of Avp in stress, anxiety, and depressive states are areas of active exploration. In this review, we concentrate on the scientific progress that has been made on understanding the role of Avp in regulating of these and other behaviors across species, as well as discuss the implications for human behavior.

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Section: Gene Inactivation In Micementioning

confidence: 99%

Vasopressin: Behavioral roles of an “original” neuropeptide

Caldwell

Lee

Macbeth

et al. 2008

Progress in Neurobiology

427

416

View full text Add to dashboard Cite

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“…Recent studies using knock-out mice have begun to reveal the physiological role of AVP and oxytocin in the CNS. V1a receptor knock-out (V1aR Ϫ/Ϫ ) mice showed abnormalities in spatial memory (Egashira et al, 2004), social interaction and anxiety (Bielsky et al, 2005;Egashira et al, 2007), and metabolism (Hiroyama et al, 2007). Oxytocin knock-out mice revealed that oxytocin plays an important role in social cognition and social, sexual, and maternal behavior (Winslow and Insel, 2002).…”

Section: Introductionmentioning

confidence: 99%

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Tsunematsu¹,

Fu²,

Yamanaka³

et al. 2008

J. Neurosci.

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Water homeostasis is a critical challenge to survival for land mammals. Mice display increased locomotor activity when dehydrated, a behavior that improves the likelihood of locating new sources of water and simultaneously places additional demands on compromised hydration levels. The neurophysiology underlying this well known behavior has not been previously elucidated. We report that the anti-diuretic hormone arginine-vasopressin (AVP) is involved in this response. AVP and oxytocin directly induced depolarization and an inward current in orexin/hypocretin neurons. AVP-induced activation of orexin neurons was inhibited by a V1a receptor (V1aR)-selective antagonist and was not observed in V1aR knock-out mice, suggesting an involvement of V1aR. Subsequently activation of phospholipase C␤ triggers an increase in intracellular calcium by both calcium influx through nonselective cation channels and calcium release from calcium stores in orexin neurons. Intracerebroventricular injection of AVP or water deprivation increased locomotor activity in wild-type mice, but not in transgenic mice lacking orexin neurons. V1aR knock-out mice were less active than wild-type mice. These results suggest that the activation of orexin neurons by AVP or oxytocin has an important role in the regulation of spontaneous locomotor activity in mice. This system appears to play a key role in water deprivation-induced hyperlocomotor activity, a response to dehydration that increases the chance of locating water in nature.

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“…The V1a receptor (V1aR) is widely expressed, while the V1bR and V2R are predominantly expressed in the anterior pituitary gland and the kidney, respectively (7,13,17,20). V1aR mediates vascular contraction, cellular proliferation, platelet aggregation, glycogenolysis, lipid metabolism, and glucose tolerance (1,8,10). The V2R is expressed in the thick ascending limbs of Henle's loop (TAL) and the collecting ducts in the kidney (37).…”

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confidence: 99%