Impaired social interaction and reduced anxiety-related behavior in vasopressin V1a receptor knockout mice

Egashira, Nobuaki; Tanoue, Akito; Matsuda, Tomomi; Koushi, Emi; Harada, Satoko; Takáno, Yukio; Tsujimoto, Gozoh; Mishima, Kenichi; Iwasaki, Katsunori; Fujiwara, Michihiro

doi:10.1016/j.bbr.2006.12.009

Cited by 168 publications

(128 citation statements)

References 31 publications

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“…The MB test was performed as a modified version (Li et al, 2006) of the test originally described for testing mice (Broekkamp et al, 1986, Njung'e and Handley, 1991, Borsini et al, 2002, Nicolas et al, 2006, Egashira et al, 2007. The rats were placed individually in a plexiglass cage (41.3cm x 26 cm x 29.8 cm high, Ferplast, Geo Maxi, Italy) with a 5 cm deep layer of bedding holding 15 marbles on its surface (25 mm diameter; arranged in a 3 x 5 pattern; space between two marbles ~ 4.5 cm).…”

Section: 5 Marble Buryingmentioning

confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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Short title:Stress-related behavior in Brattleboro rat after DDAVP treatment You created this PDF from an application that is not licensed to print to novaPDF printer (http://www.novapdf.com) Balázsfi et al. 2Highlights  The effect of AVP on affective and memory symptoms is due to its central role  DDAVP treatment compensated the peripheral effects of congenital AVP absence  DDAVP did not significantly alter the behavior of KO animals in the paradigms tested  AVP signaling in the medial amygdala contributes to the behavioral effect measured in FS AbstractBeside its hormonal function in salt and water homeostasis, vasopressin -released into distinct brain areas -plays a crucial role in stress-related behavior resulting in the enhancement of an anxious/depressive-like state.We aimed to investigate whether correction of the peripheral symptoms of congenital absence of AVP also corrects the behavioral alterations in AVP-deficient Brattleboro rats. Wild type (WT) and vasopressin-deficient (KO) male Brattleboro rats were tested.Half of the KO animals were treated by desmopressin (V2-receptor agonist) via osmotic minipump (subcutaneous) to eliminate the peripheral symptoms of vasopressin-deficiency. Anxiety was studied by elevated plus maze (EPM), defensive withdrawal (DW) and marble burying (MB) tests, while depressive-like changes were monitored in forced swimming (FS) and anhedonia by sucrose preference test. Cell activity was examined in septum and amygdala by c-Fos immunohistochemistry after 10min FS.

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Section: 5 Marble Buryingmentioning

confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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“…V1aR antagonist has been shown to block aggressive behavior (Ferris et al, 2006). In addition, V1aR Ϫ/Ϫ mice display an impairment of social interaction (Bielsky et al, 2005) and reduced anxiety-related behavior (Egashira et al, 2007), suggesting that AVP and oxytocin may be involved in excitatory inputs from the amygdala to orexin neurons.…”

Section: Physiological Significance Of Avp and Oxytocin-mediated Actimentioning

confidence: 99%

“…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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“…Oxytocin knockout mice revealed the role of oxytocin in mediating social recognition, social memory, aggression, maternal behaviors, and ultrasonic vocalizations by pups separated from the nest [5,10,29,39,42,57]. Vasopressin receptor subtype V1a (Avpr1a) knockout mice displayed impaired social recognition and low anxiety-like behaviors [4,5,12], and reduced responses to social olfactory cues [51]. Higher levels of the…”

Section: Introductionmentioning

confidence: 99%

Reduced ultrasonic vocalizations in vasopressin 1b knockout mice

Scattoni¹,

McFarlane²,

Zhodzishsky³

et al. 2008

Behavioural Brain Research

130

119

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The neuropeptides oxytocin and vasopressin have been implicated in rodent social and affiliative behaviors, including social bonding, parental care, social recognition, social memory, vocalizations, territoriality, and aggression, as well as components of human social behaviors and the etiology of autism. Previous investigations of mice with various manipulations of the oxytocin and vasopressin systems reported unusual levels of ultrasonic vocalizations in social settings. We employed a vasopressin 1b receptor (Avpr1b) knockout mouse to evaluate the role of the vasopressin 1b receptor subtype in the emission of ultrasonic vocalizations in adult and infant mice. Avpr1b null mutant female mice emitted fewer ultrasonic vocalizations, and their vocalizations were generally at lower frequencies, during a resident-intruder test. Avpr1b null mutant pups emitted ultrasonic vocalizations similar to heterozygote and wildtype littermates when separated from the nest on postnatal days 3, 6, 9, and 12. However, maternal potentiation of ultrasonic vocalizations in Avpr1b null and heterozygote mutants was absent, when tested at postnatal day 9. These results indicate that Avpr1b null mutant mice are impaired in the modulation of ultrasonic vocalizations within different social contexts at infant and adult ages.

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Impaired social interaction and reduced anxiety-related behavior in vasopressin V1a receptor knockout mice

Cited by 168 publications

References 31 publications

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

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

Reduced ultrasonic vocalizations in vasopressin 1b knockout mice

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