Sex-specific single transcript level atlas of vasopressin and its receptor (AVPR1a) in the mouse brain

Vasopressin (AVP), a nonapeptide synthesized primarily by magnocellular neurons of the paraventricular nucleus (PVH) and supraoptic nucleus (SO) of the hypothalamus, is conveyed along axons of magnocellular neurons via the pituitary stalk to the posterior pituitary, where AVP is released into circulation to exert hormonal functions (Brownstein et al., 1980; Young and Gainer, 2003). Involved in the regulation of blood pressure and water balance (Silva et al., 1969; Stockand et al., 2022), AVP also regulates diverse social behaviors, such as pair bonding, social recognition, and cognition in all mammals, including humans (Lukas and Neumann, 2013; Lukas et al., 2013; Veenema and Neumann, 2008; Meyer-Lindenberg et al., 2011; Albers, 2015). It should be noted that similar to OXT, AVP is evolutionarily conserved across invertebrates and vertebrate taxa, differing from OXT by just two amino acids. Importantly, AVP modulates social behaviors in a sex-specific manner, perhaps due to sex differences in AVP and its receptor expression in the brain (Winslow et al., 1993; Insel and Hulihan, 1995; Dantzer et al., 1987; Rigney et al., 2023; Landgraf et al., 2003; Veenema et al., 2012).

AVP receptors are G protein-coupled receptors consisting of two major subtypes, the V1 receptor (AVPR1) and V2 receptor (AVPR2) (Dumais and Veenema, 2016). AVPR1 has two subtypes, namely AVPR1a and AVPR1b, that mediate the effects of AVP on social behaviors. Avpr1a will be the overarching focus of this study given its abundance and ubiquity in brain regions (Albers, 2015). In fact, differences in AVPR1a genetic variability and expression patterns determine specific social phenotypes (French et al., 2016; Phelps et al., 2017; Lim et al., 2004; Fink et al., 2007; Ren et al., 2014). There is evidence that AVPR1a is involved in maternal care, pair bonding, behavioral aggression, anxiety, social recognition and social play (Lukas et al., 2013; Albers, 2015; Lim et al., 2004; Bielsky et al., 2004; Neumann and Landgraf, 2012; Lago et al., 2021; Thompson et al., 2006). The sex-dependent distribution of Avpr1a across the brain in different species provides a proxy for the distribution of AVP binding and, therefore, provides further evidence for central AVP neural nodes of physiological relevance.

Blocking AVPR1a inhibits social recognition in the rat, while AVPR1a knockout mice fail to display social recognition (Veenema et al., 2012; Bielsky et al., 2004; Bielsky et al., 2005). These effects of AVP in enhancing social recognition are mediated via AVPR1a in the lateral septum (Veenema et al., 2012; Bielsky et al., 2005). Sex differences in Avpr1a binding densities have been described in several brain sites of Wistar rats. Namely, males display higher AVPR1a binding densities in the following forebrain areas: somatosensory and piriform cortex, medial posterior bed nucleus of the stria terminalis (BNST), nucleus of the lateral olfactory tract (LOT), anteroventral thalamic nucleus (VA), tuberal lateral hypothalamus (LH), stigmoid hypothalamus (Stg), and dentate gyrus (DG) (Dumais and Veenema, 2016). In male prairie voles, central AVP infusion facilitates selective aggression associated with pair bond formation and partner preference, and the Avpr1a antagonist 1-(β-mercapto-β, β-cyclopentamethylene propionic acid) does not seem to inhibit aggression (Winslow et al., 1993). In contrast, central AVP infusion induces partner preference in female prairie voles (Insel and Hulihan, 1995). Comparative analysis of AVPR1a distribution has revealed higher densities of AVPR1a binding in the ventral pallidum, amygdala, and thalamus of prairie voles than that of meadow or montane voles (Insel et al., 1994; Wang et al., 1997). It has also been reported that AVPR1a antagonism specifically in the ventral pallidum prevents mating-induced partner preference in male prairie voles (Lim and Young, 2004).

Although osmotically stimulated AVP release with short latency and duration from hypothalamic PVH and SO magnocellular axon terminals occurs in the pituitary (Summy‐Long and Kadekaro, 2001; Stricker et al., 2002), it is also released locally from somata and dendrites in the SO with a longer delay responding to osmotic challenge (Ludwig et al., 1994; Ludwig and Leng, 1997). Such local release is likely to facilitate autocrine and/or paracrine regulation of SO magnocellular neuronal activity and inhibit further systemic AVP output (Ludwig and Leng, 1997; Wang et al., 1982). Of note, somatodendritic AVP release in response to direct hypertonic stimulation is attenuated by V1/V2 receptor antagonism, implying that AVP may facilitate its own release by acting on autoreceptors within magnocellular neurons of the SO (Wotjak et al., 1994). The importance of autofacilitation to local AVP release may lie in fine-tuned regulation of AVP actions toward physiological demands. Alternatively, AVP could putatively diffuse over longer distances to bind to adjacent receptors. The relative contribution of AVP autoreceptor subtypes, including AVPR1a, to this phenomenon awaits further clarification.

Current studies implicate posterior pituitary hormones, traditionally thought of as master regulators of a single physiological target, in the control of multiple bodily systems, either directly or via their receptors in the brain (Neumann and Landgraf, 2012; Zaidi et al., 2018; Carter, 2014; Koshimizu et al., 2012; Jurek and Neumann, 2018). Non-traditional actions of AVP include its ability to affect skeletal homeostasis, wherein it negatively regulates osteoblasts and stimulates osteoclasts. This explains the bone loss that accompanies hyponatremia in patients with elevated AVP levels (Tamma et al., 2013). Furthermore, we have shown that AVP (via AVPR1a) and oxytocin (via OXTR) have opposing skeletal actions—effects that may relate to the pathogenesis of bone loss in chronic hyponatremia, and pregnancy and lactation, respectively (Tamma et al., 2013; Sun et al., 2019; Sun et al., 2016; Tamma et al., 2009).

Detecting specific AVPR1a and AVPR1b in the brain has had limitations for a long time due to the availability of only nonselective radioligands, such as tritium labeled (³H) AVP ligands, which bind to both receptors (Phillips et al., 1990). Although there is a large body of integrative studies for the expression of AVP and AVPR1a in various brain regions, and their functions in regulating central and peripheral actions, there remains the need for detailed, sex-specific mapping of the AVP/AVPR1a neuronal nodes in the brain. We utilized RNAscope—a technology that detects single RNA transcripts—to create a comprehensive atlas of AVP and AVPR1a in the mouse brain. It may seem somewhat remarkable that newly discovered brain areas for receptors of such evolutionarily conserved and well-studied hormones AVP and OXT are currently emerging, with inferences to novel functions. We believe that this atlas of AVP and its AVPR1a in concrete brain sites at a single transcript level should provide a resource to neuroscientists to deepen our understanding of classical and novel central and peripheral functions of AVP by interrogating AVPR1a site-specifically.

AVP receptors are G protein-coupled receptors consisting of two major subtypes, AVPR1 and AVPR2 (Dumais and Veenema, 2016). AVPR1 is further divided into AVPR1a and AVPR1b receptor subtypes that mediate the effects of AVP in the brain on social behaviors. In this study, we have provided not only a distribution mapping of AVP and AVPR1a in the brain, but also assessed sex differences in their expression by RNAscope. Allowing the detection of single transcripts, RNAscope uses ~20 pairs of transcript-specific double Z-probes to hybridize 10-µm-thick whole brain sections. Preamplifiers first hybridize to the ~28 bp binding site formed by each double Z-probe; amplifiers then bind to the multiple binding sites on each preamplifier; and finally, labeled probes containing a chromogenic enzyme bind to multiple sites of each amplifier.

RNAscope data were quantified on every tenth section of the whole brains from coded three female and three male mice. For simplicity and clarity in the graphs, a scatter plot has been shown for three nuclei, subnuclei, and regions with the highest AVP and AVPR1a transcript densities, as well as their absolute transcript counts. Each section was viewed and analyzed using CaseViewer 2.4 (3DHISTECH, Budapest, Hungary) and QuPath v.0.2.3 (University of Edinburgh, UK). The Atlas for the Mouse Brain in Stereotaxic Coordinates (Paxinos and Franklin, 2007) was used to identify every nucleus, subnucleus, or region, which was followed by manual counting of Avp and Avpr1a transcripts by two independent observers (VR and AG) in every tenth section using the tag feature. Receptor density was calculated by dividing the absolute receptor number by the total area (µm², ImageJ) of every nucleus, subnucleus, or region. The highest Avp and Avpr1a values in the brain regions are presented as means ± SE and compared with those of the opposite sex. Photomicrographs were prepared using Photoshop CS5 (Adobe Systems) only to adjust brightness, contrast, and sharpness, to remove artifacts (i.e. obscuring bubbles) and to make composite plates.

RNAscope revealed Avp expression in the hypothalamus, forebrain, hippocampus, and cortex of both female and male mice (Figure 1A); however, Avp expression in the 3rd ventricular region and thalamus was found only in the female mouse (Figure 1B). Whereas the numbers of Avp-expressing cells were greater in females compared with males in the hypothalamus (607 vs 471), 3rd ventricular region (7 vs 0) and thalamus (2 vs 0), those numbers were lower in the hippocampus (58 vs 118), forebrain (50 vs 77) and cortex (5 vs 6) (see Appendix for Glossary and Figure 1—figure supplement 1 for raw count graphs).

Figure 1 with 1 supplement see all

Download asset Open asset

The highest Avp transcript densities were detected in the following brain nuclei, subnuclei, and regions of female and male mice, respectively: ventricular region—3V only for females, hypothalamus—SChVL and PaDC, forebrain—MPOM and VLPO, hippocampus—Py and GrDG, thalamus—ic only for females, and cerebral cortex—Pir for both (Figure 1B). Representative micrographs of some of the hypothalamic and forebrain regions with highest Avp expression are shown in Figure 1C.

We found that Avpr1a transcript expression in several brain nuclei, e.g., the MS of the forebrain, medullary 12N, IRt, LRt, MdV (Figure 2—figure supplement 1B), displayed individual patterns of expression compared with more ubiquitous and even expression noted in most of the other brain areas, suggesting brain-site-specific functional diversity and context-selective regulation of Avpr1a-mediated signaling. We report the expression of the Avpr1a in 398 and 375 brain nuclei, subnuclei, and regions of the female and male mice, respectively. Avpr1a transcripts were detected bilaterally, with no apparent ipsilateral dominance. Probe specificity was established by detecting a positive signal in renal tubules (positive control) with an absent signal in the FrA of the frontal cortex (negative control) (Figure 2A). Representative micrographs of the sex-specific medullary CC and hypothalamic Arc with highest Avpr1a expression are shown in Figure 2B.

Figure 2 with 1 supplement see all

Download asset Open asset

In the female, total Avpr1a transcript numbers were the highest in the medulla followed in descending order by the hypothalamus, cortex, midbrain and pons, forebrain, thalamus, cerebellum, hippocampus, olfactory bulb, and ventricular regions (Figure 2—figure supplement 1A). In the male, Avpr1a transcripts were the highest in the forebrain, followed by the medulla, midbrain and pons, hypothalamus, cortex, hippocampus, thalamus, olfactory bulb, cerebellum, and ventricular regions (Figure 2—figure supplement 1A). Detailed Avpr1a transcript counts are shown in Figures 3 and 4.

Figure 3 with 1 supplement see all

Download asset Open asset

Figure 4 with 1 supplement see all

Download asset Open asset

Using the RNAscope dataset, we further calculated Avpr1a density in all brain divisions (Figure 2C), nuclei, subnuclei, and regions (Figures 3 and 4). Highest Avpr1a densities in the female and male mice, respectively, were noted in nuclei, subnuclei, and regions as follows: ventricular regions—CC ependymal region for both with 2.92-fold greater in the male; hypothalamus—Arc for both; medulla—IOBe and InM; midbrain and pons—vtgx and DRI; forebrain—AC and LSI; olfactory bulb—Mi and Tu; hippocampus—TS and df; thalamus—PV and Xi; cortex—MPtA and AID; and cerebellum—1Cb for both with 2.58-fold greater in the female (Figures 3 and 4).

In addition, RNAscope analysis revealed that various brain nuclei, subnuclei, and regions in both female and male mice co-localized Avp and Avpr1a transcripts. Avpr1a to Avp ratios within the same brain nucleus, subnucleus, and region in both sexes are demonstrated in Figure 5. Finally, RNAscope showed Avp and Avpr1a expression in the posterior pituitary lobe with Avp and Avpr1a transcript densities that were higher in male compared with female mice, however, without statistical significance (Figure 6).

Figure 5

Download asset Open asset

Figure 6

Download asset Open asset

Here, we attempted to integrate previous information on sex-specific AVP and its AVPR1a expression in the murine brain. AVPR1a is the most abundant and widespread receptor in the brain (Albers, 2015) that plays a dominant role in regulating behavior. In addition, we focused on paradigm-shifting non-traditional roles of central AVP signaling in light of newly discovered AVPR1a. We report AVP expression in 41 female and 13 male brain nuclei, subnuclei, and regions. Moreover, we identified abundant AVPR1a expression in 398 female and 375 male brain nuclei, subnuclei, and regions. Therefore, this report is the most exhaustive atlas of brain Avp and Avpr1a expression at the single transcript level.

It has been reported that AVP synthesis and AVP fiber projections are sexually dimorphic in specific brain sites (for review, see: Dumais and Veenema, 2016). To our knowledge, the first discovery of the sexually dimorphic nature of AVP in the rat brain was made by de Vries et al., 1981. That is, males displayed more AVP-immunoreactive fibers in the lateral septum and lateral habenular nucleus over females (de Vries et al., 1981). Surprisingly, sex differences in AVP fiber density in the LS and medial amygdala (MeA) originate from the BNST, given only lesions to the BNST, but not the PVH, result in decreased AVP fiber density in the LS (de Vries and Buijs, 1983; Caffé et al., 1989). In adult rats, AVP fiber density from the BNST and MeA is dependent on circulating gonadal hormones, as gonadectomy eliminates AVP expression and hormone replacement restores AVP fiber network (de Vries et al., 1984; Miller et al., 1992). Nonetheless, gonadal hormones appear to only partially explain sex differences in AVP expression because both females and males, exposed to a similar gonadal steroid hormone regime, still differ sexually (de Vries and al-Shamma, 1990; de Vries et al., 1994).

Magnocellular neurons of the PVN, SO, and SCh of the hypothalamus are the predominant source of AVP synthesis. Hypothalamic AVP synthesis in most rodent species is similar between males and females in the PVH and SO of mice (Joca et al., 2014; Steinman et al., 2015); PVH, SO, and SCh of voles (Wang, 1995; Wang et al., 1996); PVH, MPOA, LH, and AHA of Mongolian gerbils and Chinese striped hamsters (Wang et al., 2013) (for review, see Dumais and Veenema, 2016). In concordance with these reports, we also found no sex differences in Avp synthesis, as evidenced by similar numbers of Avp-expressing neurons in the PVH and SO of mice; however, we did note sex differences in Avp expression density in specific hypothalamic nuclei. Notably, Avp expression density was higher in several PVH (PaLM and PaMM) and suprachiasmatic (SChVL and RCh) subnuclei of female compared to male mice. No sex differences in SO-Avp expression density were found.

Furthermore, Avpr1a transcript density was highest in the arcuate nucleus (Arc) and retrochiasmatic subnucleus (RCh) in female compared with Arc and suprachiasmatic nucleus (SCh) of male mice. Avpr1a expression in the Arc has previously been reported (Ostrowski et al., 1992); however, its role was unclear until a recent report demonstrating a critical involvement of Arc-NPY in the regulation of fluid homeostasis and the induction of salt water-induced hypertension through AVP modulation in the SO (Zhang et al., 2022); the latter receives direct projections from the Arc (Pineda et al., 2016). In contrast, it is plausible, but by no means proven, that PVH- and/or SO-AVP may modulate Arc anorexigenic neurons to inhibit ingestive behavior, which has previously been shown with PVH oxytocinergic neurons (Maejima et al., 2014). Indeed, increasing evidence suggests that AVP reduces feeding in mammals (Meyer et al., 1989; Langhans et al., 1991).

It has been reported that in the rat, AVP is an important output of the SCh targeting AVP cells in other hypothalamic areas—its release into the CSF peaks in the early morning and declines later in a day (Kalsbeek et al., 2010). Specifically, SCh-AVP secreted during late sleep activates osmosensory afferents to AVP neurons in the SO and organum vasculosum of the lamina terminalis (Trudel and Bourque, 2010; Gizowski et al., 2016). Similar to rodents, studies in humans also determined that the main AVP projections from the SCh target the anteroventral hypothalamic area, sub-PVH, as well as ventral parts of the PVH and DMH—a remarkable evolutionary conservation of SCh innervation from rodent to human (Dai et al., 1998a; Dai et al., 1998b). The fact that the SCh is another brain nucleus with high AVP and AVPR1a expression density (greater in males vs females) accentuates an important role of SCh-AVP in circadian rhythmicity, notably impacting neuroendocrine day/night rhythms, feeding timing, period, precision, and synchronization of SCh neurons (Kalsbeek et al., 2010; Rohr et al., 2021; Yoshimura et al., 2021).

In the hindbrain, the highest Avpr1a transcript density was noted in the inferior olive, beta subnucleus (IOBe) of female mice, and intermedius nucleus (InM) of male mice. It has been reported that AVP fibers are apparent in the hindbrain, such as the parabrachial nucleus, locus coeruleus, and near inferior olive nuclei (Young et al., 1999). In this regard, Avpr1a mRNA expression has been noted in the inferior olive (Ostrowski et al., 1992). Given this nucleus has been implicated in various functions, including learning and timing of movements, it is possible that AVPR1a in the inferior olive may be activated by the paracrine release of AVP from distant nuclei, such as the SCh, to control motor learning and timing. Alternatively, AVPR1a in the inferior olive may respond to other ligands (e.g., OXT) found in nearby regions (Szczepanska-Sadowska et al., 2021). The role of AVPR1 in the InM of male mice is less clear, but because the InM sends monosynaptic projections to the NTS (Edwards et al., 2009) that is essential for blood pressure control by AVP and receiving information from the cardiovascular receptors (Zanutto et al., 2010), a possible coordinated control by hindbrain AVP of blood pressure and cardiovascular function.

Although the midbrain, pons, and forebrain displayed less abundant Avpr1a transcript density, they revealed further sex differences. In the midbrain and pons, the highest Avpr1a density was observed in the ventral tegmental decussation (vtgx) in females and dorsal raphe nucleus, interfascicular part (DRI), in males. AVP and OXT in the ventral tegmental area are known to regulate social interactions with rewarding properties. Indeed, humans, as inherently social beings, show a strong inclination to affiliate and share their emotions with each other (Baumeister and Leary, 1995; Wagner et al., 2015). Sex differences in ventral tegmental AVPR1a make biological sense, as social interaction of females, specifically, with pups and, generally, with counterparts throughout their lives, has rewarding properties fundamental to maternal behavior and survival. Modulation of AVPR1a in the dorsal raphe nucleus has also been linked to social and emotional behaviors (Dumais and Veenema, 2016; Rigney et al., 2020; Rood et al., 2013). Sexual dimorphism in AVP innervation of and AVPR1a expression in the DRI appears to imprint dimorphic social behaviors. That is, AVPR1a blockade in the lateral habenular nucleus (LHb) of males, but not females who have lesser AVP innervation of the LHb and dorsal raphe nucleus, results in reduced urine marking to unfamiliar males and ultrasonic vocalizations to unfamiliar, sexually receptive females, whereas AVPR1a blockade in the dorsal raphe nucleus of only males reduces urine marking to unfamiliar males (Rigney et al., 2020).

In the forebrain, both sexes displayed high Avpr1a transcript density in septal nuclei. The highest Avpr1a density was in the anterior commissural nucleus (AC) within the septal nuclei of females, and lateral (LSI) and medial (MS) septal nuclei of males. It is not surprising that Avpr1a transcript density was significantly greater in septal nuclei of males than females, given that in many rodent species males have more AVP-immunoreactive fibers in the lateral septum (de Vries et al., 1981). Notably, the effects of AVP on social recognition is mediated via AVPR1a in the lateral septum (Veenema et al., 2012; Bielsky et al., 2005). For example, AVPR1a blockade inhibits social recognition in the rat, while AVPR1a knockout mice fail to display social recognition (Veenema et al., 2012; Bielsky et al., 2004; Bielsky et al., 2005).

Despite Avpr1a transcript densities in other brain divisions being significantly lower, sexually dimorphic differences are worth mentioning here. In the olfactory bulb, females had the high Avpr1a density in the mitral cell layer (Mi), whereas males had high receptor expression in the olfactory tubercle (Tu). A population of AVP neurons in the olfactory bulb of the rat that plays a role in social recognition via AVPR1a has been reported (Tobin et al., 2010). Silencing the AVPR1a by siRNA impairs habituation/dishabituation to juvenile cues, but not to volatile odors (Tobin et al., 2010). Of note, AVP is a retrograde signal that filters activation of the Mi cells in the ewe, likely through presynaptic modulation of norepinephrine or acetylcholine. The secretion of both transmitters is stimulated by AVP in the olfactory bulb (Tobin et al., 2010; Lévy et al., 1995). The functional relevance of AVP signaling via AVPR1a activation in the Tu requires additional studies. There is, however, evidence in the rat that AVP via AVPR1a has, at least, an indirect impact on Tu function, as seen by a reduction in activation responding to a noxious odor of butyric acid, when the AVPR1a is blocked (Reed et al., 2013). The presence of AVPR1a in the hippocampus, thalamus, cortex, and ventricular regions is consistent with the reported effects of AVP on memory (de Wied, 1971), emotional and reward-motivated behavior (Zhang et al., 2006), blood pressure (Matsuguchi et al., 1982), blood flow, and CSF production (Faraci et al., 1988). Functional roles of many other nuclei shown here to express AVPR1a and not mentioned in this report are much less clear. The importance of revealing novel AVP-triggered functions by interrogating AVPR1a site-specifically will require further investigations.

Collectively, our results provide compelling evidence of distinct and novel AVP/AVPR1a neuronal nodes in the brain. While studies on central AVP signaling and its control of blood pressure, water balance, and diverse social behaviors in mammals occupy the vast majority of the literature (Silva et al., 1969; Stockand et al., 2022; Lukas and Neumann, 2013; Lukas et al., 2013; Veenema and Neumann, 2008; Meyer-Lindenberg et al., 2011; Albers, 2015), we expect that this comprehensive compendium of sex-specific AVP/AVPR1a expression in the brain will deepen our understanding of the functional and neuroanatomical basis underlying old and new paradigm-shifting functions of central AVP signaling. As appears to be the case for most brain areas, the original discovery of function tends to become dogma, thereby leading to an oversimplification of multiple functions of those brain areas as they interact in circuits. Finally, the approach of direct mapping of receptor expression in the brain and periphery provides the groundwork for greater discernment of new functional arrangements of ancient pituitary glycoprotein hormones and nonapeptides, such as AVP and OXT, and provides helpful pointers toward improving pharmacological interventions in disease.

The authors uploaded the dataset in Dryad to maintain high standards of research reproducibility.

1. 1. Gumerova AA
   2. Pevnev G
   3. Korkmaz F
   4. Cheliadinova U
   5. Burganova G
   6. Vasilyeva D
   7. Cullen L
   8. Barak O
   9. Sultana F
   10. Zhou W
   11. Sims SL
   12. Weiss E
   13. Laurencin V
   14. Frolinger T
   15. Kim S
   16. Goosens KA
   17. Yuen T
   18. Zaidi M
   19. Ryu V

   (2026) Dryad Digital Repository

   Sex-specific Single Transcript Level Atlas of Vasopressin and its Receptor (AVPR1a) in the Mouse Brain.

   https://doi.org/10.5061/dryad.np5hqc08h

1. 1. Albers HE

   (2015) Species, sex and individual differences in the vasotocin/vasopressin system: relationship to neurochemical signaling in the social behavior neural network

   Frontiers in Neuroendocrinology 36:49–71.

   https://doi.org/10.1016/j.yfrne.2014.07.001

   • PubMed
   • Google Scholar
2. 1. Baumeister RF
   2. Leary MR

   (1995)

   The need to belong: desire for interpersonal attachments as a fundamental human motivation

   Psychological Bulletin 117:497–529.

   • PubMed
   • Google Scholar
3. 1. Bielsky IF
   2. Hu SB
   3. Szegda KL
   4. Westphal H
   5. Young LJ

   (2004) Profound impairment in social recognition and reduction in anxiety-like behavior in vasopressin V1a receptor knockout mice

   Neuropsychopharmacology 29:483–493.

   https://doi.org/10.1038/sj.npp.1300360

   • PubMed
   • Google Scholar
4. 1. Bielsky IF
   2. Hu SB
   3. Ren X
   4. Terwilliger EF
   5. Young LJ

   (2005) The V1a vasopressin receptor is necessary and sufficient for normal social recognition: a gene replacement study

   Neuron 47:503–513.

   https://doi.org/10.1016/j.neuron.2005.06.031

   • PubMed
   • Google Scholar
5. 1. Brownstein MJ
   2. Russell JT
   3. Gainer H

   (1980) Synthesis, transport, and release of posterior pituitary hormones

   Science 207:373–378.

   https://doi.org/10.1126/science.6153132

   • PubMed
   • Google Scholar
6. 1. Caffé AR
   2. van Ryen PC
   3. van der Woude TP
   4. van Leeuwen FW

   (1989) Vasopressin and oxytocin systems in the brain and upper spinal cord of Macaca fascicularis

   The Journal of Comparative Neurology 287:302–325.

   https://doi.org/10.1002/cne.902870304

   • PubMed
   • Google Scholar
7. 1. Carter CS

   (2014) Oxytocin pathways and the evolution of human behavior

   Annual Review of Psychology 65:17–39.

   https://doi.org/10.1146/annurev-psych-010213-115110

   • PubMed
   • Google Scholar
8. 1. Dai J
   2. Swaab DF
   3. Buijs RM

   (1998a) Recovery of axonal transport in “dead neurons”

   Lancet 351:499–500.

   https://doi.org/10.1016/S0140-6736(05)78689-X

   • PubMed
   • Google Scholar
9. 1. Dai J
   2. Swaab DF
   3. van Der Vliet J
   4. Buijs RM

   (1998b) Postmortem tracing reveals the organization of hypothalamic projections of the suprachiasmatic nucleus in the human brain

   The Journal of Comparative Neurology 400:87–102.

   https://doi.org/10.1002/(SICI)1096-9861(19981012)400:1<87::AID-CNE6>3.0.CO;2-P

   • Google Scholar
10. 1. Dantzer R
    2. Bluthe RM
    3. Koob GF
    4. Le Moal M

    (1987) Modulation of social memory in male rats by neurohypophyseal peptides

    Psychopharmacology 91:363–368.

    https://doi.org/10.1007/BF00518192

    • PubMed
    • Google Scholar
11. 1. de Vries GJ
    2. Buds RM
    3. Swaab DF

    (1981) Ontogeny of the vasopressinergic neurons of the suprachiasmatic nucleus and their extrahypothalamic projections in the rat brain—presence of a sex difference in the lateral septum

    Brain Research 218:67–78.

    https://doi.org/10.1016/0006-8993(81)90989-6

    • Google Scholar
12. 1. de Vries GJ
    2. Buijs RM

    (1983) The origin of the vasopressinergic and oxytocinergic innervation of the rat brain with special reference to the lateral septum

    Brain Research 273:307–317.

    https://doi.org/10.1016/0006-8993(83)90855-7

    • Google Scholar
13. 1. de Vries GJ
    2. Buijs RM
    3. Sluiter AA

    (1984) Gonadal hormone actions on the morphology of the vasopressinergic innervation of the adult rat brain

    Brain Research 298:141–145.

    https://doi.org/10.1016/0006-8993(84)91157-0

    • PubMed
    • Google Scholar
14. 1. de Vries GJ
    2. al-Shamma HA

    (1990) Sex differences in hormonal responses of vasopressin pathways in the rat brain

    Journal of Neurobiology 21:686–693.

    https://doi.org/10.1002/neu.480210503

    • PubMed
    • Google Scholar
15. 1. de Vries G
    2. Wang Z
    3. Bullock N
    4. Numan S

    (1994) Sex differences in the effects of testosterone and its metabolites on vasopressin messenger RNA levels in the bed nucleus of the stria terminalis of rats

    The Journal of Neuroscience 14:1789–1794.

    https://doi.org/10.1523/JNEUROSCI.14-03-01789.1994

    • Google Scholar
16. 1. de Wied D

    (1971) Long term effect of vasopressin on the maintenance of a conditioned avoidance response in rats

    Nature 232:58–60.

    https://doi.org/10.1038/232058a0

    • PubMed
    • Google Scholar
17. 1. Dumais KM
    2. Veenema AH

    (2016) Vasopressin and oxytocin receptor systems in the brain: Sex differences and sex-specific regulation of social behavior

    Frontiers in Neuroendocrinology 40:1–23.

    https://doi.org/10.1016/j.yfrne.2015.04.003

    • PubMed
    • Google Scholar
18. 1. Edwards IJ
    2. Deuchars SA
    3. Deuchars J

    (2009) The intermedius nucleus of the medulla: a potential site for the integration of cervical information and the generation of autonomic responses

    Journal of Chemical Neuroanatomy 38:166–175.

    https://doi.org/10.1016/j.jchemneu.2009.01.001

    • PubMed
    • Google Scholar
19. 1. Faraci FM
    2. Mayhan WG
    3. Farrell WJ
    4. Heistad DD

    (1988) Humoral regulation of blood flow to choroid plexus: role of arginine vasopressin

    Circulation Research 63:373–379.

    https://doi.org/10.1161/01.RES.63.2.373

    • Google Scholar
20. 1. Fink S
    2. Excoffier L
    3. Heckel G

    (2007) High variability and non-neutral evolution of the mammalian avpr1a gene

    BMC Evolutionary Biology 7:176.

    https://doi.org/10.1186/1471-2148-7-176

    • PubMed
    • Google Scholar
21. 1. French JA
    2. Taylor JH
    3. Mustoe AC
    4. Cavanaugh J

    (2016) Neuropeptide diversity and the regulation of social behavior in New World primates

    Frontiers in Neuroendocrinology 42:18–39.

    https://doi.org/10.1016/j.yfrne.2016.03.004

    • PubMed
    • Google Scholar
22. 1. Gizowski C
    2. Zaelzer C
    3. Bourque CW

    (2016) Clock-driven vasopressin neurotransmission mediates anticipatory thirst prior to sleep

    Nature 537:685–688.

    https://doi.org/10.1038/nature19756

    • PubMed
    • Google Scholar
23. 1. Insel TR
    2. Wang ZX
    3. Ferris CF

    (1994) Patterns of brain vasopressin receptor distribution associated with social organization in microtine rodents

    The Journal of Neuroscience 14:5381–5392.

    https://doi.org/10.1523/JNEUROSCI.14-09-05381.1994

    • PubMed
    • Google Scholar
24. 1. Insel TR
    2. Hulihan TJ

    (1995) A gender-specific mechanism for pair bonding: oxytocin and partner preference formation in monogamous voles

    Behavioral Neuroscience 109:782–789.

    https://doi.org/10.1037//0735-7044.109.4.782

    • PubMed
    • Google Scholar
25. 1. Joca L
    2. Zuloaga DG
    3. Raber J
    4. Siegel JA

    (2014) Long-term effects of early adolescent methamphetamine exposure on depression-like behavior and the hypothalamic vasopressin system in mice

    Developmental Neuroscience 36:108–118.

    https://doi.org/10.1159/000360001

    • PubMed
    • Google Scholar
26. 1. Jurek B
    2. Neumann ID

    (2018) The oxytocin receptor: from intracellular signaling to behavior

    Physiological Reviews 98:1805–1908.

    https://doi.org/10.1152/physrev.00031.2017

    • PubMed
    • Google Scholar
27. 1. Kalsbeek A
    2. Fliers E
    3. Hofman MA
    4. Swaab DF
    5. Buijs RM

    (2010) Vasopressin and the output of the hypothalamic biological clock

    Journal of Neuroendocrinology 22:362–372.

    https://doi.org/10.1111/j.1365-2826.2010.01956.x

    • PubMed
    • Google Scholar
28. 1. Koshimizu T
    2. Nakamura K
    3. Egashira N
    4. Hiroyama M
    5. Nonoguchi H
    6. Tanoue A

    (2012) Vasopressin V1a and V1b receptors: from molecules to physiological systems

    Physiological Reviews 92:1813–1864.

    https://doi.org/10.1152/physrev.00035.2011

    • Google Scholar
29. 1. Lago TR
    2. Brownstein MJ
    3. Page E
    4. Beydler E
    5. Manbeck A
    6. Beale A
    7. Roberts C
    8. Balderston N
    9. Damiano E
    10. Pineles SL
    11. Simon N
    12. Ernst M
    13. Grillon C

    (2021) The novel vasopressin receptor (V1aR) antagonist SRX246 reduces anxiety in an experimental model in humans: a randomized proof-of-concept study

    Psychopharmacology 238:2393–2403.

    https://doi.org/10.1007/s00213-021-05861-4

    • Google Scholar
30. 1. Landgraf R
    2. Frank E
    3. Aldag JM
    4. Neumann ID
    5. Sharer CA
    6. Ren X
    7. Terwilliger EF
    8. Niwa M
    9. Wigger A
    10. Young LJ

    (2003) Viral vector‐mediated gene transfer of the vole V1a vasopressin receptor in the rat septum: improved social discrimination and active social behaviour

    European Journal of Neuroscience 18:403–411.

    https://doi.org/10.1046/j.1460-9568.2003.02750.x

    • Google Scholar
31. 1. Langhans W
    2. Delprete E
    3. Scharrer E

    (1991) Mechanisms of vasopressin’s anorectic effect

    Physiology & Behavior 49:169–176.

    https://doi.org/10.1016/0031-9384(91)90251-I

    • Google Scholar
32. 1. Lévy F
    2. Kendrick KM
    3. Goode JA
    4. Guevara-Guzman R
    5. Keverne EB

    (1995) Oxytocin and vasopressin release in the olfactory bulb of parturient ewes: changes with maternal experience and effects on acetylcholine, gamma-aminobutyric acid, glutamate and noradrenaline release

    Brain Research 669:197–206.

    https://doi.org/10.1016/0006-8993(94)01236-b

    • PubMed
    • Google Scholar
33. 1. Lim MM
    2. Wang Z
    3. Olazábal DE
    4. Ren X
    5. Terwilliger EF
    6. Young LJ

    (2004) Enhanced partner preference in a promiscuous species by manipulating the expression of a single gene

    Nature 429:754–757.

    https://doi.org/10.1038/nature02539

    • Google Scholar
34. 1. Lim MM
    2. Young LJ

    (2004) Vasopressin-dependent neural circuits underlying pair bond formation in the monogamous prairie vole

    Neuroscience 125:35–45.

    https://doi.org/10.1016/j.neuroscience.2003.12.008

    • PubMed
    • Google Scholar
35. 1. Ludwig M
    2. Callahan MF
    3. Neumann I
    4. Landgraf R
    5. Morris M

    (1994) Systemic osmotic stimulation increases vasopressin and oxytocin release within the supraoptic nucleus

    Journal of Neuroendocrinology 6:369–373.

    https://doi.org/10.1111/j.1365-2826.1994.tb00595.x

    • Google Scholar
36. 1. Ludwig M
    2. Leng G

    (1997) Autoinhibition of supraoptic nucleus vasopressin neurons in vivo: a combined retrodialysis/electrophysiological study in rats

    The European Journal of Neuroscience 9:2532–2540.

    https://doi.org/10.1111/j.1460-9568.1997.tb01682.x

    • PubMed
    • Google Scholar
37. 1. Lukas M
    2. Neumann ID

    (2013) Oxytocin and vasopressin in rodent behaviors related to social dysfunctions in autism spectrum disorders

    Behavioural Brain Research 251:85–94.

    https://doi.org/10.1016/j.bbr.2012.08.011

    • PubMed
    • Google Scholar
38. 1. Lukas M
    2. Toth I
    3. Veenema AH
    4. Neumann ID

    (2013) Oxytocin mediates rodent social memory within the lateral septum and the medial amygdala depending on the relevance of the social stimulus: Male juvenile versus female adult conspecifics

    Psychoneuroendocrinology 38:916–926.

    https://doi.org/10.1016/j.psyneuen.2012.09.018

    • Google Scholar
39. 1. Maejima Y
    2. Sakuma K
    3. Santoso P
    4. Gantulga D
    5. Katsurada K
    6. Ueta Y
    7. Hiraoka Y
    8. Nishimori K
    9. Tanaka S
    10. Shimomura K
    11. Yada T

    (2014) Oxytocinergic circuit from paraventricular and supraoptic nuclei to arcuate POMC neurons in hypothalamus

    FEBS Letters 588:4404–4412.

    https://doi.org/10.1016/j.febslet.2014.10.010

    • Google Scholar
40. 1. Matsuguchi H
    2. Sharabi FM
    3. Gordon FJ
    4. Johnson AK
    5. Schmid PG

    (1982) Blood pressure and heart rate responses to microinjection of vasopressin into the nucleus tractus solitarius region of the rat

    Neuropharmacology 21:687–693.

    https://doi.org/10.1016/0028-3908(82)90012-0

    • Google Scholar
41. 1. Meyer AH
    2. Langhans W
    3. Scharrer E

    (1989) Vasopressin reduces food intake in goats

    Quarterly Journal of Experimental Physiology 74:465–473.

    https://doi.org/10.1113/expphysiol.1989.sp003294

    • PubMed
    • Google Scholar
42. 1. Meyer-Lindenberg A
    2. Domes G
    3. Kirsch P
    4. Heinrichs M

    (2011) Oxytocin and vasopressin in the human brain: social neuropeptides for translational medicine

    Nature Reviews Neuroscience 12:524–538.

    https://doi.org/10.1038/nrn3044

    • Google Scholar
43. 1. Miller MA
    2. DeVries GJ
    3. al-Shamma HA
    4. Dorsa DM

    (1992) Decline of vasopressin immunoreactivity and mRNA levels in the bed nucleus of the stria terminalis following castration

    The Journal of Neuroscience 12:2881–2887.

    https://doi.org/10.1523/JNEUROSCI.12-08-02881.1992

    • Google Scholar
44. 1. Neumann ID
    2. Landgraf R

    (2012) Balance of brain oxytocin and vasopressin: implications for anxiety, depression, and social behaviors

    Trends in Neurosciences 35:649–659.

    https://doi.org/10.1016/j.tins.2012.08.004

    • PubMed
    • Google Scholar
45. 1. Ostrowski NL
    2. Lolait SJ
    3. Bradley DJ
    4. O’Carroll AM
    5. Brownstein MJ
    6. Young WS

    (1992) Distribution of V1a and V2 vasopressin receptor messenger ribonucleic acids in rat liver, kidney, pituitary and brain

    Endocrinology 131:533–535.

    https://doi.org/10.1210/endo.131.1.1535312

    • Google Scholar
46. Book

    1. Paxinos G
    2. Franklin KBJ

    (2007)

    The Mouse Brain in Stereotaxic Coordinates (3rd)

    New York: Academic Press.

    • Google Scholar
47. 1. Phelps SM
    2. Okhovat M
    3. Berrio A

    (2017) Individual differences in social behavior and cortical vasopressin receptor: genetics, epigenetics, and evolution

    Frontiers in Neuroscience 11:537.

    https://doi.org/10.3389/fnins.2017.00537

    • PubMed
    • Google Scholar
48. 1. Phillips PA
    2. Abrahams JM
    3. Kelly JM
    4. Mooser V
    5. Trinder D
    6. Johnston CI

    (1990) Localization of vasopressin binding sites in rat tissues using specific V1 and V2 selective ligands

    Endocrinology 126:1478–1484.

    https://doi.org/10.1210/endo-126-3-1478

    • Google Scholar
49. 1. Pineda R
    2. Sabatier N
    3. Ludwig M
    4. Millar RP
    5. Leng G

    (2016) A direct neurokinin B projection from the arcuate nucleus regulates magnocellular vasopressin cells of the supraoptic nucleus

    Journal of Neuroendocrinology 28:12342.

    https://doi.org/10.1111/jne.12342

    • PubMed
    • Google Scholar
50. 1. Reed MD
    2. Price KE
    3. Archbold J
    4. Moffa A
    5. Febo M

    (2013) Predator odor-evoked BOLD activation in the awake rat: Modulation by oxytocin and V1a vasopressin receptor antagonists

    Brain Research 1494:70–83.

    https://doi.org/10.1016/j.brainres.2012.11.045

    • Google Scholar
51. 1. Ren D
    2. Chin KR
    3. French JA

    (2014) Molecular Variation in AVP and AVPR1a in new world monkeys (primates, platyrrhini): evolution and implications for social monogamy

    PLOS ONE 9:e111638.

    https://doi.org/10.1371/journal.pone.0111638

    • Google Scholar
52. 1. Rigney N
    2. Beaumont R
    3. Petrulis A

    (2020) Sex differences in vasopressin 1a receptor regulation of social communication within the lateral habenula and dorsal raphe of mice

    Hormones and Behavior 121:104715.

    https://doi.org/10.1016/j.yhbeh.2020.104715

    • PubMed
    • Google Scholar
53. 1. Rigney N
    2. de Vries GJ
    3. Petrulis A

    (2023) Modulation of social behavior by distinct vasopressin sources

    Frontiers in Endocrinology 14:1127792.

    https://doi.org/10.3389/fendo.2023.1127792

    • PubMed
    • Google Scholar
54. 1. Rohr KE
    2. Telega A
    3. Savaglio A
    4. Evans JA

    (2021) Vasopressin regulates daily rhythms and circadian clock circuits in a manner influenced by sex

    Hormones and Behavior 127:104888.

    https://doi.org/10.1016/j.yhbeh.2020.104888

    • PubMed
    • Google Scholar
55. 1. Rood BD
    2. Stott RT
    3. You S
    4. Smith CJW
    5. Woodbury ME
    6. De Vries GJ

    (2013) Site of origin of and sex differences in the vasopressin innervation of the mouse (Mus musculus) brain

    Journal of Comparative Neurology 521:2321–2358.

    https://doi.org/10.1002/cne.23288

    • Google Scholar
56. 1. Silva YJ
    2. Moffat RC
    3. Walt AJ

    (1969)

    Vasopressin effect on portal and systemic hemodynamics. Studies in intact, unanesthetized humans

    JAMA 210:1065–1068.

    • PubMed
    • Google Scholar
57. 1. Steinman MQ
    2. Laredo SA
    3. Lopez EM
    4. Manning CE
    5. Hao RC
    6. Doig IE
    7. Campi KL
    8. Flowers AE
    9. Knight JK
    10. Trainor BC

    (2015) Hypothalamic vasopressin systems are more sensitive to the long term effects of social defeat in males versus females

    Psychoneuroendocrinology 51:122–134.

    https://doi.org/10.1016/j.psyneuen.2014.09.009

    • Google Scholar
58. 1. Stockand JD
    2. Mironova EV
    3. Xiang H
    4. Soares AG
    5. Contreras J
    6. McCormick JA
    7. Gurley SB
    8. Pao AC

    (2022) Chronic activation of vasopressin-2 receptors induces hypertension in Liddle mice by promoting Na ⁺ and water retention

    American Journal of Physiology-Renal Physiology 323:F468–F478.

    https://doi.org/10.1152/ajprenal.00384.2021

    • Google Scholar
59. 1. Stricker EM
    2. Huang W
    3. Sved AF

    (2002) Early osmoregulatory signals in the control of water intake and neurohypophyseal hormone secretion

    Physiology & Behavior 76:415–421.

    https://doi.org/10.1016/S0031-9384(02)00752-7

    • Google Scholar
60. 1. Summy‐Long JY
    2. Kadekaro M

    (2001) Circumventricular Organs: Gateways to the Brain Role Of Circumventricular Organs (CVO) In Neuroendocrine Responses: Interactions Of CVO And The Magnocellular Neuroendocrine System In Different Reproductive States

    Clinical and Experimental Pharmacology and Physiology 28:590–601.

    https://doi.org/10.1046/j.1440-1681.2001.03491.x

    • Google Scholar
61. 1. Sun L
    2. Tamma R
    3. Yuen T
    4. Colaianni G
    5. Ji Y
    6. Cuscito C
    7. Bailey J
    8. Dhawan S
    9. Lu P
    10. Calvano CD
    11. Zhu L-L
    12. Zambonin CG
    13. di Benedetto A
    14. Stachnik A
    15. Liu P
    16. Grano M
    17. Colucci S
    18. Davies TF
    19. New MI
    20. Zallone A
    21. Zaidi M

    (2016) Functions of vasopressin and oxytocin in bone mass regulation

    PNAS 113:164–169.

    https://doi.org/10.1073/pnas.1523762113

    • Google Scholar
62. 1. Sun L
    2. Lizneva D
    3. Ji Y
    4. Colaianni G
    5. Hadelia E
    6. Gumerova A
    7. Ievleva K
    8. Kuo TC
    9. Korkmaz F
    10. Ryu V
    11. Rahimova A
    12. Gera S
    13. Taneja C
    14. Khan A
    15. Ahmad N
    16. Tamma R
    17. Bian Z
    18. Zallone A
    19. Kim SM
    20. New MI
    21. Iqbal J
    22. Yuen T
    23. Zaidi M

    (2019) Oxytocin regulates body composition

    PNAS 116:26808–26815.

    https://doi.org/10.1073/pnas.1913611116

    • Google Scholar
63. 1. Szczepanska-Sadowska E
    2. Wsol A
    3. Cudnoch-Jedrzejewska A
    4. Żera T

    (2021) Complementary role of oxytocin and vasopressin in cardiovascular regulation

    International Journal of Molecular Sciences 22:11465.

    https://doi.org/10.3390/ijms222111465

    • PubMed
    • Google Scholar
64. 1. Tamma R
    2. Colaianni G
    3. Zhu L
    4. DiBenedetto A
    5. Greco G
    6. Montemurro G
    7. Patano N
    8. Strippoli M
    9. Vergari R
    10. Mancini L
    11. Colucci S
    12. Grano M
    13. Faccio R
    14. Liu X
    15. Li J
    16. Usmani S
    17. Bachar M
    18. Bab I
    19. Nishimori K
    20. Young LJ
    21. Buettner C
    22. Iqbal J
    23. Sun L
    24. Zaidi M
    25. Zallone A

    (2009) Oxytocin is an anabolic bone hormone

    PNAS 106:7149–7154.

    https://doi.org/10.1073/pnas.0901890106

    • Google Scholar
65. 1. Tamma R
    2. Sun L
    3. Cuscito C
    4. Lu P
    5. Corcelli M
    6. Li J
    7. Colaianni G
    8. Moonga SS
    9. di Benedetto A
    10. Grano M
    11. Colucci S
    12. Yuen T
    13. New MI
    14. Zallone A
    15. Zaidi M

    (2013) Regulation of bone remodeling by vasopressin explains the bone loss in hyponatremia

    PNAS 110:18644–18649.

    https://doi.org/10.1073/pnas.1318257110

    • Google Scholar
66. 1. Thompson RR
    2. George K
    3. Walton JC
    4. Orr SP
    5. Benson J

    (2006) Sex-specific influences of vasopressin on human social communication

    PNAS 103:7889–7894.

    https://doi.org/10.1073/pnas.0600406103

    • PubMed
    • Google Scholar
67. 1. Tobin VA
    2. Hashimoto H
    3. Wacker DW
    4. Takayanagi Y
    5. Langnaese K
    6. Caquineau C
    7. Noack J
    8. Landgraf R
    9. Onaka T
    10. Leng G
    11. Meddle SL
    12. Engelmann M
    13. Ludwig M

    (2010) An intrinsic vasopressin system in the olfactory bulb is involved in social recognition

    Nature 464:413–417.

    https://doi.org/10.1038/nature08826

    • Google Scholar
68. 1. Trudel E
    2. Bourque CW

    (2010) Central clock excites vasopressin neurons by waking osmosensory afferents during late sleep

    Nature Neuroscience 13:467–474.

    https://doi.org/10.1038/nn.2503

    • PubMed
    • Google Scholar
69. 1. Veenema AH
    2. Neumann ID

    (2008) Central vasopressin and oxytocin release: regulation of complex social behaviours

    Progress in Brain Research 170:261–276.

    https://doi.org/10.1016/S0079-6123(08)00422-6

    • PubMed
    • Google Scholar
70. 1. Veenema AH
    2. Bredewold R
    3. De Vries GJ

    (2012) Vasopressin regulates social recognition in juvenile and adult rats of both sexes, but in sex- and age-specific ways

    Hormones and Behavior 61:50–56.

    https://doi.org/10.1016/j.yhbeh.2011.10.002

    • Google Scholar
71. 1. Wagner U
    2. Galli L
    3. Schott BH
    4. Wold A
    5. van der Schalk J
    6. Manstead ASR
    7. Scherer K
    8. Walter H

    (2015) Beautiful friendship: Social sharing of emotions improves subjective feelings and activates the neural reward circuitry

    Social Cognitive and Affective Neuroscience 10:801–808.

    https://doi.org/10.1093/scan/nsu121

    • Google Scholar
72. 1. Wang BC
    2. Share L
    3. Crofton JT

    (1982) Central infusion of vasopressin decreased plasma vasopressin concentration in dogs

    The American Journal of Physiology 243:E365–E369.

    https://doi.org/10.1152/ajpendo.1982.243.5.E365

    • PubMed
    • Google Scholar
73. 1. Wang Z

    (1995) Species differences in the vasopressin-immunoreactive pathways in the bed nucleus of the stria terminalis and medial amygdaloid nucleus in prairie voles (Microtus ochrogaster) and meadow voles (Microtus pennsylvanicus)

    Behavioral Neuroscience 109:305–311.

    https://doi.org/10.1037/0735-7044.109.2.305

    • Google Scholar
74. 1. Wang Z
    2. Zhou L
    3. Hulihan TJ
    4. Insel TR

    (1996) Immunoreactivity of central vasopressin and oxytocin pathways in microtine rodents: A quantitative comparative study

    The Journal of Comparative Neurology 366:726–737.

    https://doi.org/10.1002/(SICI)1096-9861(19960318)366:4<726::AID-CNE11>3.0.CO;2-D

    • Google Scholar
75. 1. Wang Z
    2. Young LJ
    3. Liu Y
    4. Insel TR

    (1997) Species differences in vasopressin receptor binding are evident early in development: Comparative anatomic studies in prairie and montane voles

    The Journal of Comparative Neurology 378:535–546.

    https://doi.org/10.1002/(SICI)1096-9861(19970224)378:4<535::AID-CNE8>3.0.CO;2-3

    • Google Scholar
76. 1. Wang Y
    2. Xu L
    3. Pan Y
    4. Wang Z
    5. Zhang Z

    (2013) Species differences in the immunoreactive expression of oxytocin, vasopressin, tyrosine hydroxylase and estrogen receptor alpha in the brain of mongolian gerbils (Meriones unguiculatus) and chinese striped hamsters (Cricetulus barabensis)

    PLOS ONE 8:e65807.

    https://doi.org/10.1371/journal.pone.0065807

    • Google Scholar
77. 1. Winslow JT
    2. Hastings N
    3. Carter CS
    4. Harbaugh CR
    5. Insel TR

    (1993) A role for central vasopressin in pair bonding in monogamous prairie voles

    Nature 365:545–548.

    https://doi.org/10.1038/365545a0

    • PubMed
    • Google Scholar
78. 1. Wotjak CT
    2. Ludwig M
    3. Landgraf R

    (1994) Vasopressin facilitates its own release within the rat supraoptic nucleus in vivo

    Neuroreport 5:1181–1184.

    https://doi.org/10.1097/00001756-199406020-00005

    • PubMed
    • Google Scholar
79. 1. Yoshimura M
    2. Conway-Campbell B
    3. Ueta Y

    (2021) Arginine vasopressin: Direct and indirect action on metabolism

    Peptides 142:170555.

    https://doi.org/10.1016/j.peptides.2021.170555

    • Google Scholar
80. 1. Young LJ
    2. Toloczko D
    3. Insel TR

    (1999) Localization of vasopressin (V1a) receptor binding and mRNA in the rhesus monkey brain

    Journal of Neuroendocrinology 11:291–297.

    https://doi.org/10.1046/j.1365-2826.1999.00332.x

    • PubMed
    • Google Scholar
81. 1. Young WS
    2. Gainer H

    (2003) Transgenesis and the study of expression, cellular targeting and function of oxytocin, vasopressin and their receptors

    Neuroendocrinology 78:185–203.

    https://doi.org/10.1159/000073702

    • Google Scholar
82. 1. Zaidi M
    2. New MI
    3. Blair HC
    4. Zallone A
    5. Baliram R
    6. Davies TF
    7. Cardozo C
    8. Iqbal J
    9. Sun L
    10. Rosen CJ
    11. Yuen T

    (2018) Actions of pituitary hormones beyond traditional targets

    Journal of Endocrinology 237:R83–R98.

    https://doi.org/10.1530/JOE-17-0680

    • Google Scholar
83. 1. Zanutto BS
    2. Valentinuzzi ME
    3. Segura ET

    (2010) Neural set point for the control of arterial pressure: role of the nucleus tractus solitarius

    Biomedical Engineering Online 9:4.

    https://doi.org/10.1186/1475-925X-9-4

    • PubMed
    • Google Scholar
84. 1. Zhang L
    2. Doroshenko P
    3. Cao XY
    4. Irfan N
    5. Coderre E
    6. Kolaj M
    7. Renaud LP

    (2006) Vasopressin induces depolarization and state-dependent firing patterns in rat thalamic paraventricular nucleus neurons in vitro

    American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290:R1226–R1232.

    https://doi.org/10.1152/ajpregu.00770.2005

    • Google Scholar
85. 1. Zhang C-L
    2. Lin Y-Z
    3. Wu Q
    4. Yan C
    5. Wong MW-K
    6. Zeng F
    7. Zhu P
    8. Bowes K
    9. Lee K
    10. Zhang X
    11. Song Z-Y
    12. Lin S
    13. Shi Y-C

    (2022) Arcuate NPY is involved in salt-induced hypertension via modulation of paraventricular vasopressin and brain-derived neurotrophic factor

    Journal of Cellular Physiology 237:2574–2588.

    https://doi.org/10.1002/jcp.30719

    • PubMed
    • Google Scholar

Author details

1. Anisa Azatovna Gumerova

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Data curation, Writing – review and editing

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0002-1449-4000

2. Georgii Pevnev

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Data curation, Formal analysis

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0003-2015-9310

3. Funda Korkmaz

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Investigation

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0002-9174-8369

4. Uliana Cheliadinova

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Data curation, Investigation

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0009-0007-2308-4824

5. Guzel Burganova

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Investigation

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0002-7204-7268

6. Darya Vasilyeva

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Software, Investigation

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0009-0007-5121-9618

7. Liam Cullen

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Data curation

   Competing interests

   No competing interests declared

8. Orly Barak

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Resources

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0002-3041-2343

9. Farhath Sultana

   Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

   Contribution

   Software, Validation

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0003-4186-3390

10. Weibin Zhou

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Validation

    Competing interests

    Reviewing editor, eLife

11. Steven Lee Sims

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Validation

    Competing interests

    No competing interests declared

    "This ORCID iD identifies the author of this article:" 0000-0002-1636-084X

12. Emily Weiss

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Writing – review and editing

    Competing interests

    No competing interests declared

13. Victoria Laurencin

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Investigation

    Competing interests

    No competing interests declared

    "This ORCID iD identifies the author of this article:" 0009-0006-0801-6471

14. Tal Frolinger

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Validation, Visualization

    Competing interests

    No competing interests declared

    "This ORCID iD identifies the author of this article:" 0000-0002-2066-6649

15. Se-Min Kim

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Data curation, Validation

    Competing interests

    No competing interests declared

16. Ki A Goosens

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Validation, Visualization

    Competing interests

    No competing interests declared

    "This ORCID iD identifies the author of this article:" 0000-0002-5246-2261

17. Tony Yuen

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Supervision, Funding acquisition, Validation, Visualization, Writing – review and editing

    Competing interests

    No competing interests declared

18. Mone Zaidi

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Conceptualization, Data curation, Supervision, Funding acquisition, Validation, Writing – review and editing

    For correspondence

    mone.zaidi@mountsinai.org

    Competing interests

    No competing interests declared

    "This ORCID iD identifies the author of this article:" 0000-0001-5911-9522

19. Vitaly Ryu

    Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, United States

    Contribution

    Conceptualization, Data curation, Formal analysis, Supervision, Writing - original draft, Writing – review and editing

    For correspondence

    vitaly.ryu@mssm.edu

    Competing interests

    No competing interests declared

    "This ORCID iD identifies the author of this article:" 0000-0001-8068-4577

• 564

  views

• 18

  downloads

• 0

  citations

Views, downloads and citations are aggregated across all versions of this paper published by eLife.