Up-Regulation of Vasopressin and Angiotensin II Receptors in the Thalamus and Brainstem of Inbred Polydipsic Mice

Tribollet, Eliane; Ueta, Yoichi; Heitz, Freddy; Marguerat, Anouk; Koizumi, Kiyomi; Yamashita, Hiroshi

doi:10.1159/000048227

Cited by 16 publications

(15 citation statements)

References 24 publications

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“…We would note that the vast majority of the anatomical literature is from rat, while our pharmacological experiments were performed in mice. Although two studies have systematically compared OTR and V1AR distribution in mouse CNS, one of them focused on forebrain structures (Insel et al, 1991) while the other examined spinal distribution only as caudally as the trigeminal nucleus caudalis (Tribollet et al, 2002). One putative explanation for the V1AR-dependency of OXT-induced analgesia would be a species difference in receptor distribution.…”

Section: Discussionmentioning

confidence: 99%

Oxytocin-Induced Analgesia and Scratching Are Mediated by the Vasopressin-1A Receptor in the Mouse

Schorscher-Petcu¹,

Sotocinal²,

Ciura³

et al. 2010

Journal of Neuroscience

169

146

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The neuropeptides oxytocin (OXT) and arginine vasopressin (AVP) contribute to the regulation of diverse cognitive and physiological functions including nociception. Indeed, OXT has been reported to be analgesic when administered directly into the brain, the spinal cord, or systemically. Here, we characterized the phenotype of oxytocin receptor (OTR) and vasopressin-1A receptor (V1AR) null mutant mice in a battery of pain assays. Surprisingly, OTR knock-out mice displayed a pain phenotype identical to their wild-type littermates. Moreover, systemic administration of OXT dose-dependently produced analgesia in both wild-type and OTR knock-out mice in three different assays, the radiant-heat paw withdrawal test, the von Frey test of mechanical sensitivity, and the formalin test of inflammatory nociception. In contrast, OXT-induced analgesia was completely absent in V1AR knock-out mice.

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Section: Discussionmentioning

confidence: 99%

Oxytocin-Induced Analgesia and Scratching Are Mediated by the Vasopressin-1A Receptor in the Mouse

Schorscher-Petcu¹,

Sotocinal²,

Ciura³

et al. 2010

Journal of Neuroscience

169

146

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“…This suggests potential strain specific sex differences in V1aR in mice, i.e. a sex differences in the mammillary nucleus was found in C57B6 mice (Dubois Dauphin et al, 1996), but not in ICR mice (Tribollet et al, 2002). Although a thorough comparative analysis of the V1aR throughout the brain of commonly used laboratory mice is lacking, findings thus far suggests that mice, in general, may show few sex differences in V1aR binding density in the brain.…”

Section: Sex Differences In Vasopressin and Oxytocin Receptors In mentioning

confidence: 93%

“…For example, female prairie and montane voles showed higher OTR binding densities in the medial prefrontal cortex compared to males (Smeltzer et al, 2006), while male mandarin voles showed higher OTR mRNA expression in the MeA (Cao et al, 2013). It was also found that male ICR mice had lower OTR binding in the VMH than female ICR mice (Tribollet et al, 2002). Male S. xerampelinus singing mice had higher OTR binding in the MeA and hippocampal CA1 compared to females (Campbell et al, 2009).…”

Section: Sex Differences In Vasopressin and Oxytocin Receptors In mentioning

confidence: 95%

“…Likewise, although no sex differences were found in the hippocampal CA1 region, SSc, LS, and VTA of C57B6 mice (Hammock and Levitt, 2012), other brain regions were not tested for sex differences and the number of mice per sex (n=3) is too low to draw any definitive conclusions. In ICR mice, using the 125 I linear V1aR antagonist, males (n=6) and females (n=6) showed a lack of sex differences in all regions analyzed (subfornical organ, LS, PVN, paraventricular thalamus, mammillary complex, parabrachial nucleus, area postrema-nucleus of the solitary tract, and hypoglossal nucleus; Tribollet et al, 2002). This suggests potential strain specific sex differences in V1aR in mice, i.e.…”

Section: Sex Differences In Vasopressin and Oxytocin Receptors In mentioning

confidence: 99%

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Vasopressin and oxytocin receptor systems in the brain: Sex differences and sex-specific regulation of social behavior

Dumais

Veenema

2016

Frontiers in Neuroendocrinology

432

350

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The neuropeptides vasopressin (VP) and oxytocin (OT) and their receptors in the brain are involved in the regulation of various social behaviors and have emerged as drug targets for the treatment of social dysfunction in several sex-biased neuropsychiatric disorders. Sex differences in the VP and OT systems may therefore be implicated in sex-specific regulation of healthy as well as impaired social behaviors. We begin this review by highlighting the sex differences, or lack of sex differences, in VP and OT synthesis in the brain. We then discuss the evidence showing the presence or absence of sex differences in VP and OT receptors in rodents and humans, as well as showing new data of sexually dimorphic V1a receptor binding in the rat brain. Importantly, we find that there is lack of comprehensive analysis of sex differences in these systems in common laboratory species, and we find that, when sex differences are present, they are highly brain region- and species- specific. Interestingly, VP system parameters (VP and V1aR) are typically higher in males, while sex differences in the OT system are not always in the same direction, often showing higher OT expression in females, but higher OT receptor expression in males. Furthermore, VP and OT receptor systems show distinct and largely non-overlapping expression in the rodent brain, which may cause these receptors to have either complementary or opposing functional roles in the sex-specific regulation of social behavior. Though still in need of further research, we close by discussing how manipulations of the VP and OT systems have given important insights into the involvement of these neuropeptide systems in the sex-specific regulation of social behavior in rodents and humans.

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“…Investigation of polydipsia stemming from diabetes insipidus in humans indicates that dysregulation or mutation of the type-2 vasopressin receptor is a common cause (Moeller et al, 2013). Consistent with this notion, the STR/N inbred mouse strain, which exhibits a spontaneous water polydipsia, had 7- to 10-fold greater arginine vasopressin (AVP) binding in the thalamic paraventricular nucleus, and binding was absent in the hypothalamic paraventricular nucleus when compared to non-polydipsic control mice (Tribollet et al, 2002). Taken in conjunction with recent work demonstrating the role of AVP and type 1B receptors in the modulation of HPA axis function and the transition from excessive ethanol intake to dependence in rats (Edwards, Guerrero, Ghomeim, Roberts, & Koob, 2012), the potential role of AVP signaling in ethanol SIP deserves further attention.…”

Section: Steps Toward Enhancing the Utility Of Sip In The Study Omentioning

confidence: 77%

Applications of schedule-induced polydipsia in rodents for the study of an excessive ethanol intake phenotype

Ford

2014

Alcohol

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Schedule-induced polydipsia (SIP) is generated by subjecting a highly motivated animal to a sub-optimal rate of food reinforcement while also providing access to a fluid. SIP is one of several adjunctive (or displacement) behaviors that are expressed in an exaggerated form that is deemed ‘excessive’. This feature makes SIP an attractive model for studying an excessive ethanol drinking phenotype in rodents. Multiple experimental variables are crucial for the full manifestation of adjunctive drinking, including the degree of food deprivation, the inter-pellet interval selected, and the size of the food reward offered. Although these variables were extensively studied and optimized for water polydipsia in rats, a similarly customized approach to ethanol SIP and application of the procedure in mice have largely been curtailed in favor of the default variable values historically used for water SIP in rats. Further, ethanol SIP also requires careful consideration of variables such as taste and ethanol concentration. Investigation of the stress axis and neurochemical systems such as dopamine and serotonin in mediating adjunctive drinking stemmed from two leading hypotheses regarding the underlying mechanisms of SIP generation: 1) SIP as a coping strategy to mitigate stress associated with the aversive environmental condition, and 2) SIP as a displacement of reward in a highly motivated animal. Ethanol SIP is a powerful model of excessive intake because it can generate an ethanol-dependent state and sustain frequent and intoxicating levels of blood ethanol with voluntary oral consumption. The required food deprivation and the loss of the excessive drinking phenotype following removal of the generator schedule are the two main limitations of the model. Future utility of ethanol SIP will be enhanced by more fully dissecting the underlying hormonal and neurochemical mechanisms and optimizing experimental variables for ethanol SIP on a per species and strain basis.

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Up-Regulation of Vasopressin and Angiotensin II Receptors in the Thalamus and Brainstem of Inbred Polydipsic Mice

Cited by 16 publications

References 24 publications

Oxytocin-Induced Analgesia and Scratching Are Mediated by the Vasopressin-1A Receptor in the Mouse

Oxytocin-Induced Analgesia and Scratching Are Mediated by the Vasopressin-1A Receptor in the Mouse

Vasopressin and oxytocin receptor systems in the brain: Sex differences and sex-specific regulation of social behavior

Applications of schedule-induced polydipsia in rodents for the study of an excessive ethanol intake phenotype

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