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Akito Tanoue - One of the best experts on this subject based on the ideXlab platform.

  • Role of Vasopressin V1a Receptor in ∆^9-tetrahydrocannabinol-induced cataleptic immobilization in mice
    Psychopharmacology, 2017
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Kenichi Mishima, Emi Koushi, Takayuki Myose, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki
    Abstract:

    Rationale Cannabis is a widely used illicit substance. ∆^9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to cause catalepsy in rodents. Recent studies have shown that Vasopressin V1a and V1b Receptors are widely distributed in the central nervous system and are capable of influencing a wide variety of brain functions such as social behavior, emotionality, and learning and memory. Objectives The present study was designed to examine the possible involvement of V1a and V1b Receptors in THC-induced catalepsy-like immobilization. Methods The induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a Receptor knockout (V1aRKO), and V1b Receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine_1A Receptor antagonist WAY100635 (0.1 mg/kg, i.p.) on THC-induced catalepsy was also evaluated in V1aRKO mice. Moreover, the effects of the V1a Receptor antagonist VMAX-357 and the V1b Receptor antagonist ORG-52186 on THC-induced catalepsy were evaluated in ddY mice. Results THC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice. Conclusions These findings suggest that V1a Receptor regulates THC-induced catalepsy-like immobilization.

  • Role of Vasopressin V1a Receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice.
    Psychopharmacology, 2017
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Kenichi Mishima, Emi Koushi, Takayuki Myose, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki
    Abstract:

    Cannabis is a widely used illicit substance. ∆9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to cause catalepsy in rodents. Recent studies have shown that Vasopressin V1a and V1b Receptors are widely distributed in the central nervous system and are capable of influencing a wide variety of brain functions such as social behavior, emotionality, and learning and memory. The present study was designed to examine the possible involvement of V1a and V1b Receptors in THC-induced catalepsy-like immobilization. The induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a Receptor knockout (V1aRKO), and V1b Receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine1A Receptor antagonist WAY100635 (0.1 mg/kg, i.p.) on THC-induced catalepsy was also evaluated in V1aRKO mice. Moreover, the effects of the V1a Receptor antagonist VMAX-357 and the V1b Receptor antagonist ORG-52186 on THC-induced catalepsy were evaluated in ddY mice. THC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice. These findings suggest that V1a Receptor regulates THC-induced catalepsy-like immobilization.

  • The intercalated cells of the mouse kidney OMCD_is are the target of the Vasopressin V1a Receptor axis for urinary acidification
    Clinical and Experimental Nephrology, 2013
    Co-Authors: Yukiko Yasuoka, Akito Tanoue, Mizuka Kobayashi, Yuichi Sato, Hiroshi Nonoguchi, Hirotsugu Okamoto, Ming Zhou, Hiroshi Abe, Katsumasa Kawahara
    Abstract:

    Background Vasopressin V1a Receptor (V1aR) null mice have insufficient acid–base balance, but the target cell for V1aR signaling which results in the urinary acidification has not been identified. Methods By using a quantitative in situ hybridization technique and a double-staining technique with an anti-AQP3 antibody in mice, we investigated the axial distribution and acidosis-induced expression of V1aR mRNA along the nephron. We also investigated the acidosis-induced morphological change in the tubule cells from wild-type and V1aR-null (V1aR^−/−) mice. Results In the normal condition, V1aR mRNA was moderately expressed in the medullary thick ascending limb (MTAL) and highly expressed in the intercalated cell (IC) throughout the collecting duct (CD). However, no expression was observed in the proximal tubule, thin limbs of Henle’s loop, and the principal cell of the CD. Importantly, V1aR mRNA was upregulated significantly both in the TAL and the IC of the CD in the inner stripe of the outer medulla (MTAL_is and IC of OMCD_is, respectively) when mice were treated with NH_4Cl (0.28 mol/L) for 6 days. Acidosis-induced hypertrophy, which was completely attenuated in V1aR^−/− mice, was observed only in the IC of OMCD_is ( P  

  • Decreased expression of aquaporin 2 in the collecting duct of mice lacking the Vasopressin V1a Receptor
    Clinical and Experimental Nephrology, 2013
    Co-Authors: Yukiko Yasuoka, Akito Tanoue, Mizuka Kobayashi, Yuichi Sato, Hiroshi Nonoguchi, Hirotsugu Okamoto, Katsumasa Kawahara
    Abstract:

    Background Vasopressin V1a Receptor null (V1aR^−/−) mice recently showed incomplete urinary concentration due to higher urine volume during control and water diuresis (euhydration), but showed normal response during dehydration (Aoyagi et al., Am J Physiol 295: F100–7, 2008 ). Methods Water balance, plasma Vasopressin, plasma and urine osmolality, and aquaporin 2 (AQP2) expression in the kidney of wild-type (WT) and V1aR^−/− mice were therefore further examined using improved methods of urine collection (urinary bladder urine). Results V1aR^−/− mice demonstrated a lower urine osmolality (3,360 ± 138 vs. 3,610 ± 47 mOsm/kgH_2O) and a higher plasma osmolality (354.3 ± 1.3 vs. 342.5 ± 1.5 mOsm/kgH_2O) after dehydration for 24 h compared to WT mice ( P  

  • The intercalated cells of the mouse kidney OMCD is are the target of the Vasopressin V1a Receptor axis for urinary acidification
    Clinical and experimental nephrology, 2013
    Co-Authors: Yukiko Yasuoka, Akito Tanoue, Mizuka Kobayashi, Yuichi Sato, Hiroshi Nonoguchi, Hirotsugu Okamoto, Ming Zhou, Hiroshi Abe, Katsumasa Kawahara
    Abstract:

    Background Vasopressin V1a Receptor (V1aR) null mice have insufficient acid–base balance, but the target cell for V1aR signaling which results in the urinary acidification has not been identified.

Larry J Young - One of the best experts on this subject based on the ideXlab platform.

  • genetic influences on receptive joint attention in chimpanzees pan troglodytes
    Scientific Reports, 2015
    Co-Authors: William D. Hopkins, Alaine C. Keebaugh, Lisa A Reamer, Jennifer Schaeffer, Steven J Schapiro, Larry J Young
    Abstract:

    Despite their genetic similarity to humans, our understanding of the role of genes on cognitive traits in chimpanzees remains virtually unexplored. Here, we examined the relationship between genetic variation in the arginine Vasopressin V1a Receptor gene (AVPR1A) and social cognition in chimpanzees. Studies have shown that chimpanzees are polymorphic for a deletion in a sequence in the 5′ flanking region of the AVPR1A, DupB, which contains the variable RS3 repetitive element, which has been associated with variation in social behavior in humans. Results revealed that performance on the social cognition task was significantly heritable. Furthermore, males with one DupB+ allele performed significantly better and were more responsive to socio-communicative cues than males homozygous for the DupB- deletion. Performance on a non-social cognition task was not associated with the AVPR1A genotype. The collective findings show that AVPR1A polymorphisms are associated with individual differences in performance on a receptive joint attention task in chimpanzees.

  • Personality in Chimpanzees (Pan troglodytes): Exploring the Hierarchical Structure and Associations with the Vasopressin V1a Receptor Gene
    PloS one, 2014
    Co-Authors: Robert D. Latzman, William D. Hopkins, Alaine C. Keebaugh, Larry J Young
    Abstract:

    One of the major contributions of recent personality psychology is the finding that traits are related to each other in an organized hierarchy. To date, however, researchers have yet to investigate this hierarchy in nonhuman primates. Such investigations are critical in confirming the cross-species nature of trait personality helping to illuminate personality as neurobiologically-based and evolutionarily-derived dimensions of primate disposition. Investigations of potential genetic polymorphisms associated with hierarchical models of personality among nonhuman primates represent a critical first step. The current study examined the hierarchical structure of chimpanzee personality as well as sex-specific associations with a polymorphism in the promoter region of the Vasopressin V1a Receptor gene (AVPR1A), a gene associated with dispositional traits, among 174 chimpanzees. Results confirmed a hierarchical structure of personality across species and, despite differences in early rearing experiences, suggest a sexually dimorphic role of AVPR1A polymorphisms on hierarchical personality profiles at a higher-order level.

  • a polymorphic indel containing the rs3 microsatellite in the 5 flanking region of the Vasopressin V1a Receptor gene is associated with chimpanzee pan troglodytes personality
    Genes Brain and Behavior, 2012
    Co-Authors: William D. Hopkins, Zoe R. Donaldson, Larry J Young
    Abstract:

    Vasopressin is a neuropeptide that has been strongly implicated in the development and evolution of complex social relations and cognition in mammals. Recent studies in voles have shown that polymorphic variation in the promoter region of the arginine Vasopressin V1a Receptor gene (avpr1a) is associated with different dimensions of sociality. In humans, variation in a repetitive sequence element in the 5' flanking region of the AVPR1A, known as RS3, have also been associated with variation in AVPR1a gene expression, brain activity and social behavior. Here, we examined the association of polymorphic variation in this same 5' flanking region of the AVPR1A on subjective ratings of personality in a sample of 83 chimpanzees (Pan troglodytes). Initial analyses indicated that 34 females and 19 males were homozygous for the short allele, which lacks RS3 (DupB(-/-)), while 18 females and 12 males were heterozygous and thus had one copy of the long allele containing RS3 (DupB(+/-)), yielding overall allelic frequencies of 0.82 for the DupB(-) allele and 0.18 for the DupB(+) allele. DupB(+/+) chimpanzees were excluded from the analysis because of the limited number of individuals. Results indicated no significant sex difference in personality between chimpanzees homozygous for the deletion of the RS3-containing DupB region (DupB(-/-)); however, among chimpanzees carrying one allele with the DupB present (DupB(+/-)), males had significantly higher dominance and lower conscientiousness scores than females. These findings are the first evidence showing that the AVPR1A gene plays a role in different aspects of personality in male and female chimpanzees.

  • a polymorphic indel containing the rs3 microsatellite in the 5 flanking region of the Vasopressin V1a Receptor gene is associated with chimpanzee pan troglodytes personality
    Genes Brain and Behavior, 2012
    Co-Authors: William D. Hopkins, Zoe R. Donaldson, Larry J Young
    Abstract:

    Vasopressin is a neuropeptide with multiple physiological functions that has been strongly implicated in the development and evolution of complex social relations and cognition in mammals (Donaldson & Young, 2008, Goodson & Bass, 2001). Studies in several species have shown that one of three known AVP Receptors, arginine Vasopressin V1a Receptor (AVPR1A), is expressed in the brain and plays a prominent role in producing diversity in social behavior, in addition to its role in regulation of vasoconstriction. For example, meadow and prairie voles, which differ dramatically in their pair bonding behavior, show pronounced differences in AVPR1A expression patterns in the brain (Lim et al., 2005, Lim et al., 2004). More recently, several studies in voles have examined variation in behavior and AVPR1A expression in relation to microsatellite length in the promoter region of the V1a Receptor gene (avpr1a). There are both individual and species differences in avpr1a expression and these have been associated with variation in pair bonding and other dimensions of social behavior in voles (Hammock et al., 2005, Hammock & Young, 2005, Hammock & Young, 2006, Young & Wang, 2004). Variation in this polymorphic microsatellite have also been shown to affect avpr1a gene transcription in cell transcription from in vitro reporter assays (Hammock & Young, 2004). In primates, less is known about the functional role of AVPR1A in social behavior but recent studies have shown considerable polymorphic variation in the AVPR1A gene analogous to that seen in voles, suggesting that individual and species differences in sociality may be associated with this gene (Babb et al., 2010, Donaldson et al., 2008, Rosso et al., 2008). In human AVPR1A, variation in repetitive microsatellite element RS3 (see Figure 1) located in the 5’ flanking region of the gene has been linked to variation in social behavior, including altruistic behavior, and pair bonding related behavior in males (Donaldson et al., 2008, Meyer-Lindenberg et al., 2011, Walum et al., 2008). It has also been suggested that AVPR1A may be a candidate susceptibility gene for autism, a spectrum of neurodevelopmental disorders marked by problems in the development of normal social relationships and socio-cognitive abilities (Melke, 2008). Likewise, AVPR1A variation in RS3 is related to activation of the amygdala during a face recognition task (Meyer-Lindenberg et al., 2008). Finally, variation in the length of RS3 has been associated with variation in AVPR1A gene expression in the human brain (Knafo et al., 2008) and in transcription reporter assays in cell culture (Tansey et al., 2011). Thus, our understanding of variation in sociality and cognitive processes as they relate to social cues and processes might benefit from further studies on the AVPR1A gene. Figure 1 Schemative of the polymorphic microsatellite elements in the primate AVPR1A locus. Two repeat motifs (DupA and DupB) in tandem containing repetitive microsatellite elements (STR1 and RS3) are found in the 5’ flanking region of the human AVPR1A ... In this study, we examined the association of an indel containing RS3 upstream of the AVPR1A gene with individual differences in personality in captive chimpanzees (Pan troglodytes). Chimpanzees are an excellent model to explore the functional role of the RS3 polymorphism in the AVPR1A gene because there is a common indel resulting in a complete deletion of the RS3 sequence in 80% of the chimpanzee alleles (Donaldson et al., 2008). Within humans, the RS3 repeat region is housed within a larger, ~350 bp tandem duplicated region. The first of these duplicated regions, DupA, spans -3730 to -4074 bp relative to the transcription start site and contains a GT20-26 microsatellite, known as STR1. The second block, DupB, spans -3382 to -3729 bp and contains the complex microsatellite, RS3 ((CT)6–14(GT)8–24) (Figure 1). Chimpanzees are polymorphic for the presence of the RS3-containing DupB region, leading to a 357 bp difference between the DupB+ and Dup- alleles (Donaldson et al., 2008). The deletion of RS3 in some individuals makes this species ideal for assessing the potential role of the AVPR1a gene, and more specifically RS3, on sociality and related processes (i.e., social cognition). To assess the association between the RS3 DupB indel and personality in the chimpanzees, we compared a sample of individuals who were either homozygous for the deletion (DupB−/−) or were heterozygous and had one DupB containing allele (DupB+/−) on subjective personality ratings. Previous studies have shown that chimpanzees, like humans, have different personalities, which include what has been described as the five-factor model (Digman, 1990) or “Big 5” personality dimensions in humans (extraversion, agreeableness, conscientiousness, neuroticism, & openness). In addition, chimpanzees have a sixth personality dimension, dominance, which is seemingly related to competitive prowess (King & Figueredo, 1997). Despite the recent comparative interest in personality among nonhuman animals (Freeman & Gosling, 2010, Gosling, 2001), to date the majority of studies have focused on the description and construction of personality factors in nonhuman animals (Gosling, 2001) whereas very few studies have examined the potential role of genetic factors on individual differences in personality. In the only study in chimpanzees, Hong et al. (2011) found that polymorphic variation in a gene that encodes tryptophan hydroxylase 2 (TPH2), an enzyme involved in the production of serotonin, was linked to variation in neuroticism. In the current study, we sought to examine whether variation in personality was associated with the AVPR1A 5’ flanking region polymorphism, given its reported important role in sociality. This was accomplished by combining recently published data on personality in a sample of chimpanzees housed at the Yerkes National Primate Center (Weiss et al., 2007) with the Vasopressin genotype data that was reported in a subsample of these same individuals (Donaldson et al., 2008). Thus, we combined the genetic data with the extant personality ratings to assess whether differences in personality were related to the presence or absence of the RS3-containing DupB element in the AVPR1A 5’ flanking region. If the AVPR1A 5’ flanking region plays a role in personality in chimpanzees, then significant differences should be evident in one or more of the traits in chimpanzees with different genotypes.

  • A polymorphic indel containing the RS3 microsatellite in the 5′ flanking region of the Vasopressin V1a Receptor gene is associated with chimpanzee (Pan troglodytes) personality
    Genes brain and behavior, 2012
    Co-Authors: William D. Hopkins, Zoe R. Donaldson, Larry J Young
    Abstract:

    Vasopressin is a neuropeptide that has been strongly implicated in the development and evolution of complex social relations and cognition in mammals. Recent studies in voles have shown that polymorphic variation in the promoter region of the arginine Vasopressin V1a Receptor gene (avpr1a) is associated with different dimensions of sociality. In humans, variation in a repetitive sequence element in the 5' flanking region of the AVPR1A, known as RS3, have also been associated with variation in AVPR1a gene expression, brain activity and social behavior. Here, we examined the association of polymorphic variation in this same 5' flanking region of the AVPR1A on subjective ratings of personality in a sample of 83 chimpanzees (Pan troglodytes). Initial analyses indicated that 34 females and 19 males were homozygous for the short allele, which lacks RS3 (DupB(-/-)), while 18 females and 12 males were heterozygous and thus had one copy of the long allele containing RS3 (DupB(+/-)), yielding overall allelic frequencies of 0.82 for the DupB(-) allele and 0.18 for the DupB(+) allele. DupB(+/+) chimpanzees were excluded from the analysis because of the limited number of individuals. Results indicated no significant sex difference in personality between chimpanzees homozygous for the deletion of the RS3-containing DupB region (DupB(-/-)); however, among chimpanzees carrying one allele with the DupB present (DupB(+/-)), males had significantly higher dominance and lower conscientiousness scores than females. These findings are the first evidence showing that the AVPR1A gene plays a role in different aspects of personality in male and female chimpanzees.

Katsunori Iwasaki - One of the best experts on this subject based on the ideXlab platform.

  • Role of Vasopressin V1a Receptor in ∆^9-tetrahydrocannabinol-induced cataleptic immobilization in mice
    Psychopharmacology, 2017
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Kenichi Mishima, Emi Koushi, Takayuki Myose, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki
    Abstract:

    Rationale Cannabis is a widely used illicit substance. ∆^9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to cause catalepsy in rodents. Recent studies have shown that Vasopressin V1a and V1b Receptors are widely distributed in the central nervous system and are capable of influencing a wide variety of brain functions such as social behavior, emotionality, and learning and memory. Objectives The present study was designed to examine the possible involvement of V1a and V1b Receptors in THC-induced catalepsy-like immobilization. Methods The induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a Receptor knockout (V1aRKO), and V1b Receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine_1A Receptor antagonist WAY100635 (0.1 mg/kg, i.p.) on THC-induced catalepsy was also evaluated in V1aRKO mice. Moreover, the effects of the V1a Receptor antagonist VMAX-357 and the V1b Receptor antagonist ORG-52186 on THC-induced catalepsy were evaluated in ddY mice. Results THC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice. Conclusions These findings suggest that V1a Receptor regulates THC-induced catalepsy-like immobilization.

  • Role of Vasopressin V1a Receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice.
    Psychopharmacology, 2017
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Kenichi Mishima, Emi Koushi, Takayuki Myose, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki
    Abstract:

    Cannabis is a widely used illicit substance. ∆9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to cause catalepsy in rodents. Recent studies have shown that Vasopressin V1a and V1b Receptors are widely distributed in the central nervous system and are capable of influencing a wide variety of brain functions such as social behavior, emotionality, and learning and memory. The present study was designed to examine the possible involvement of V1a and V1b Receptors in THC-induced catalepsy-like immobilization. The induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a Receptor knockout (V1aRKO), and V1b Receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine1A Receptor antagonist WAY100635 (0.1 mg/kg, i.p.) on THC-induced catalepsy was also evaluated in V1aRKO mice. Moreover, the effects of the V1a Receptor antagonist VMAX-357 and the V1b Receptor antagonist ORG-52186 on THC-induced catalepsy were evaluated in ddY mice. THC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice. These findings suggest that V1a Receptor regulates THC-induced catalepsy-like immobilization.

  • impaired social interaction and reduced anxiety related behavior in Vasopressin V1a Receptor knockout mice
    Behavioural Brain Research, 2007
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Gozoh Tsujimoto, Kenichi Mishima, Yukio Takano, Katsunori Iwasaki, Emi Koushi, Tomomi Matsuda, Satoko Harada, Michihiro Fujiwara
    Abstract:

    The arginine Vasopressin (AVP) system plays an important role in social behavior. Autism, with its hallmark disturbances in social behavior, has been associated with the V1a Receptor (V1aR) gene. Furthermore, impairments of social function are often observed in symptoms of schizophrenia. Subchronic phencyclidine (PCP) produces behaviors relating to certain aspects of schizophrenic symptoms such as impairing social interaction in animals and it reduces the density of V1aR binding sites in several brain regions. Here, we report that V1aR knockout (KO) mice exhibited impairment of social behavior in a social interaction test, and showed reduced anxiety-related behavior in elevated plus-maze and marble-burying behavior tests. Given the current findings, the V1aR may be involved in the regulation of social interaction, and V1aR KO mice could be used as an animal model of psychiatric disorders associated with social behavior deficits, such as autism and schizophrenia.

  • V1a Receptor knockout mice exhibit impairment of spatial memory in an eight arm radial maze
    Neuroscience Letters, 2004
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Gozoh Tsujimoto, Fuminori Higashihara, Kenichi Mishima, Yoshihiko Fukue, Yukio Takano, Katsunori Iwasaki, Michihiro Fujiwara
    Abstract:

    Abstract In this study, we examined the performance of Vasopressin V1a Receptor (V1aR) and Vasopressin V1b Receptor (V1bR) knockout (KO) mice compared to wild-type (WT) mice in an eight-arm radial maze. V1aR KO mice exhibited an impairment of spatial memory in comparison to WT mice. By contrast, we did not observe any significant differences between the V1bR KO mice and the WT mice in the eight-arm radial maze. Moreover, OPC-21268, a selective V1aR antagonist, impaired spatial memory in the eight-arm radial maze in WT mice characterized by an increased number of errors. These results suggest that the V1aR controls spatial memory in mice.

Nobuaki Egashira - One of the best experts on this subject based on the ideXlab platform.

  • Role of Vasopressin V1a Receptor in ∆^9-tetrahydrocannabinol-induced cataleptic immobilization in mice
    Psychopharmacology, 2017
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Kenichi Mishima, Emi Koushi, Takayuki Myose, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki
    Abstract:

    Rationale Cannabis is a widely used illicit substance. ∆^9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to cause catalepsy in rodents. Recent studies have shown that Vasopressin V1a and V1b Receptors are widely distributed in the central nervous system and are capable of influencing a wide variety of brain functions such as social behavior, emotionality, and learning and memory. Objectives The present study was designed to examine the possible involvement of V1a and V1b Receptors in THC-induced catalepsy-like immobilization. Methods The induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a Receptor knockout (V1aRKO), and V1b Receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine_1A Receptor antagonist WAY100635 (0.1 mg/kg, i.p.) on THC-induced catalepsy was also evaluated in V1aRKO mice. Moreover, the effects of the V1a Receptor antagonist VMAX-357 and the V1b Receptor antagonist ORG-52186 on THC-induced catalepsy were evaluated in ddY mice. Results THC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice. Conclusions These findings suggest that V1a Receptor regulates THC-induced catalepsy-like immobilization.

  • Role of Vasopressin V1a Receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice.
    Psychopharmacology, 2017
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Kenichi Mishima, Emi Koushi, Takayuki Myose, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki
    Abstract:

    Cannabis is a widely used illicit substance. ∆9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to cause catalepsy in rodents. Recent studies have shown that Vasopressin V1a and V1b Receptors are widely distributed in the central nervous system and are capable of influencing a wide variety of brain functions such as social behavior, emotionality, and learning and memory. The present study was designed to examine the possible involvement of V1a and V1b Receptors in THC-induced catalepsy-like immobilization. The induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a Receptor knockout (V1aRKO), and V1b Receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine1A Receptor antagonist WAY100635 (0.1 mg/kg, i.p.) on THC-induced catalepsy was also evaluated in V1aRKO mice. Moreover, the effects of the V1a Receptor antagonist VMAX-357 and the V1b Receptor antagonist ORG-52186 on THC-induced catalepsy were evaluated in ddY mice. THC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice. These findings suggest that V1a Receptor regulates THC-induced catalepsy-like immobilization.

  • impaired social interaction and reduced anxiety related behavior in Vasopressin V1a Receptor knockout mice
    Behavioural Brain Research, 2007
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Gozoh Tsujimoto, Kenichi Mishima, Yukio Takano, Katsunori Iwasaki, Emi Koushi, Tomomi Matsuda, Satoko Harada, Michihiro Fujiwara
    Abstract:

    The arginine Vasopressin (AVP) system plays an important role in social behavior. Autism, with its hallmark disturbances in social behavior, has been associated with the V1a Receptor (V1aR) gene. Furthermore, impairments of social function are often observed in symptoms of schizophrenia. Subchronic phencyclidine (PCP) produces behaviors relating to certain aspects of schizophrenic symptoms such as impairing social interaction in animals and it reduces the density of V1aR binding sites in several brain regions. Here, we report that V1aR knockout (KO) mice exhibited impairment of social behavior in a social interaction test, and showed reduced anxiety-related behavior in elevated plus-maze and marble-burying behavior tests. Given the current findings, the V1aR may be involved in the regulation of social interaction, and V1aR KO mice could be used as an animal model of psychiatric disorders associated with social behavior deficits, such as autism and schizophrenia.

  • V1a Receptor knockout mice exhibit impairment of spatial memory in an eight arm radial maze
    Neuroscience Letters, 2004
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Gozoh Tsujimoto, Fuminori Higashihara, Kenichi Mishima, Yoshihiko Fukue, Yukio Takano, Katsunori Iwasaki, Michihiro Fujiwara
    Abstract:

    Abstract In this study, we examined the performance of Vasopressin V1a Receptor (V1aR) and Vasopressin V1b Receptor (V1bR) knockout (KO) mice compared to wild-type (WT) mice in an eight-arm radial maze. V1aR KO mice exhibited an impairment of spatial memory in comparison to WT mice. By contrast, we did not observe any significant differences between the V1bR KO mice and the WT mice in the eight-arm radial maze. Moreover, OPC-21268, a selective V1aR antagonist, impaired spatial memory in the eight-arm radial maze in WT mice characterized by an increased number of errors. These results suggest that the V1aR controls spatial memory in mice.

Gozoh Tsujimoto - One of the best experts on this subject based on the ideXlab platform.

  • Decreased susceptibility to salt-induced hypertension in subtotally nephrectomized mice lacking the Vasopressin V1a Receptor
    Cardiovascular research, 2010
    Co-Authors: Ryo Oikawa, Akito Tanoue, Gozoh Tsujimoto, Chihiro Hosoda, Yoshihisa Nasa, Takuya Daicho, Norio Takagi, Kouichi Tanonaka, Satoshi Takeo
    Abstract:

    Aims By examining Vasopressin V1a Receptor (V1aR) knockout (KO) mice, we previously found that the V1aR is critically involved in the regulation of normal blood pressure. The present study was undertaken to elucidate the role of the V1aR in salt-induced hypertension. Methods and results We compared haemodynamic responses induced by subtotal nephrectomy + salt loading in V1aR KO mice with those of wild-type (WT) controls. The time course of changes in the systolic blood pressure and heart rate during the salt loading was attenuated in the KO mice compared with that for the WT mice. The elevation of the plasma norepinephrine level caused by the subtotal nephrectomy + salt loading was also reduced in the V1aR KO mice. A V1aR antagonist markedly lowered the arterial blood pressure in the salt-loaded WT mice but not in the normotensive WT mice or in the salt-loaded or normotensive V1aR KO mice. Whereas arginine Vasopressin (AVP) administered to the lateral ventricle of the brain induced pressor and tachycardiac responses accompanied by sympathetic activation in the WT mice, these events were completely abolished in the V1aR KO mice. Also, pressor and tachycardiac responses induced by intraventricularly administered hypertonic saline in the WT mice were diminished in the V1aR KO mice. Moreover, the pressor response induced by intraventricularly administered AVP was reduced in α1d adrenoceptor KO mice, whereas the tachycardiac response did not differ from that of the WT mice. Conclusion These results suggest that the V1aR is involved in the elevation of arterial blood pressure caused by dietary salt and that a V1aR antagonist, in particular regarding its effect in the brain, could have significant therapeutic potential in the treatment of hypertension.

  • impaired social interaction and reduced anxiety related behavior in Vasopressin V1a Receptor knockout mice
    Behavioural Brain Research, 2007
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Gozoh Tsujimoto, Kenichi Mishima, Yukio Takano, Katsunori Iwasaki, Emi Koushi, Tomomi Matsuda, Satoko Harada, Michihiro Fujiwara
    Abstract:

    The arginine Vasopressin (AVP) system plays an important role in social behavior. Autism, with its hallmark disturbances in social behavior, has been associated with the V1a Receptor (V1aR) gene. Furthermore, impairments of social function are often observed in symptoms of schizophrenia. Subchronic phencyclidine (PCP) produces behaviors relating to certain aspects of schizophrenic symptoms such as impairing social interaction in animals and it reduces the density of V1aR binding sites in several brain regions. Here, we report that V1aR knockout (KO) mice exhibited impairment of social behavior in a social interaction test, and showed reduced anxiety-related behavior in elevated plus-maze and marble-burying behavior tests. Given the current findings, the V1aR may be involved in the regulation of social interaction, and V1aR KO mice could be used as an animal model of psychiatric disorders associated with social behavior deficits, such as autism and schizophrenia.

  • Vasopressin V1a Receptor enhances baroreflex via the central component of the reflex arc
    European Journal of Pharmacology, 2007
    Co-Authors: Ryo Oikawa, Akito Tanoue, Gozoh Tsujimoto, Yoshihisa Nasa, Rie Ishii, Tomoyuki Kuwaki, Satoshi Takeo
    Abstract:

    Abstract The neurohypophyseal peptide [Arg 8 ]-Vasopressin (AVP) exerts its physiological actions via 3 distinct Receptor isoforms designated V1a, V1B, and V2. We recently showed that V1a Receptor was involved in the baroreflex control of heart rate using V1a Receptor knockout mice. The present study was undertaken to further clarify this finding. In conscious mice, resting blood pressure of the knockout group was lower than that of the wild-type group (wild-type, 108 ± 2.0 mm Hg; knockout, 98 ± 3.8 mm Hg; n  = 6–7) without notable change in heart rate. Although phenylephrine and nitroprusside-induced changes in blood pressure did not differ in these strains, the subsequent bradycardia and tachycardia were markedly blunted in the knockout mice (mean slopes for baroreflex curve after phenylephrine treatment; wild-type, − 5.65 ± 0.30 bpm/mm Hg; knockout, − 3.97 ± 0.52 bpm/mm Hg; those after nitroprusside treatment; wild-type, − 0.51 ± 0.10 bpm/mm Hg; knockout, − 0.18 ± 0.05 bpm/mm Hg; n  = 6–7). Under urethane anesthesia (1.0–1.2 g/kg, i.p.), electrical stimulation of the vagal afferent nerve evoked frequency-dependent hypotension and bradycardia in the wild-type mice. In contrast, in the knockout mice such stimulation induced a pressor, not a depressor, response and diminished bradycardia. Moreover, electrical stimulation-induced hemodynamic changes through the vagal afferent nerve in the wild-type mice were significantly attenuated by pretreatment with intravenously administered V1a Receptor antagonist d(CH 2 ) 5 Tyr(Me)AVP. Electrical stimulation of the vagal efferent nerve-induced hemodynamic changes (depressor and bradycardia) and chronotropic responses to adrenergic and cholinergic stimuli were not different between the 2 strains. These results suggest that the V1a Receptor in the central nervous system is involved in the regulation of the heart rate via the baroreflex arc.

  • V1a Receptor knockout mice exhibit impairment of spatial memory in an eight arm radial maze
    Neuroscience Letters, 2004
    Co-Authors: Nobuaki Egashira, Akito Tanoue, Gozoh Tsujimoto, Fuminori Higashihara, Kenichi Mishima, Yoshihiko Fukue, Yukio Takano, Katsunori Iwasaki, Michihiro Fujiwara
    Abstract:

    Abstract In this study, we examined the performance of Vasopressin V1a Receptor (V1aR) and Vasopressin V1b Receptor (V1bR) knockout (KO) mice compared to wild-type (WT) mice in an eight-arm radial maze. V1aR KO mice exhibited an impairment of spatial memory in comparison to WT mice. By contrast, we did not observe any significant differences between the V1bR KO mice and the WT mice in the eight-arm radial maze. Moreover, OPC-21268, a selective V1aR antagonist, impaired spatial memory in the eight-arm radial maze in WT mice characterized by an increased number of errors. These results suggest that the V1aR controls spatial memory in mice.

  • Key amino acids of Vasopressin V1a Receptor responsible for the species difference in the affinity of OPC-21268.
    FEBS Letters, 2000
    Co-Authors: Hitomi Shinoura, Akira Hirasawa, Keitaro Hashimoto, Hitoshi Take, Kazuhide Inoue, Yasuo Ohno, Gozoh Tsujimoto
    Abstract:

    Abstract A non-peptide, Vasopressin V1a Receptor-selective antagonist, OPC-21268, exhibited a markedly higher affinity for the rat V1a Receptor ( K i =380 nM) than for the human V1a Receptor ( K i =140 μM). To delineate the region responsible for the high affinity binding of OPC-21268 for the rat V1a Receptor, we have constructed a series of chimeric human and rat V1a Receptors, and examined the chimeric and point-mutated Receptors by competitive radioligand binding analysis. The results showed that the transmembrane domain (TMD) VI–VII of the Vasopressin V1a Receptor, in particular the amino acid residue Ala-342 in TMD VII, is the major component conferring the rat-selective binding of OPC-21268 to the V1a Receptor.