Oxytocin-Induced Analgesia and Scratching Are Mediated by the Vasopressin-1A Receptor in the Mouse
Open accessAbstract
The neuropeptides oxytocin (OXT) and arginine vasopressin (AVP) contribute to the regulation of diverse cognitive and physiological functions including nociception. Indeed, OXT has been reported to be analgesic when administered directly into the brain, the spinal cord, or systemically. Here, we characterized the phenotype of oxytocin receptor (OTR) and vasopressin-1A receptor (V1AR) null mutant mice in a battery of pain assays. Surprisingly, OTR knock-out mice displayed a pain phenotype identical to their wild-type littermates. Moreover, systemic administration of OXT dose-dependently produced analgesia in both wild-type and OTR knock-out mice in three different assays, the radiant-heat paw withdrawal test, the von Frey test of mechanical sensitivity, and the formalin test of inflammatory nociception. In contrast, OXT-induced analgesia was completely absent in V1AR knock-out mice. In wild-type mice, OXT-induced analgesia could be fully prevented by pretreatment with a V1AR but not an OTR antagonist. Receptor binding studies demonstrated that the distribution of OXT and AVP binding sites in mouse lumbar spinal cord resembles the pattern observed in rat. AVP binding sites diffusely label the lumbar spinal cord, whereas OXT binding sites cluster in the substantia gelatinosa of the dorsal horn. In contrast, quantitative real-time reverse transcription (RT)-PCR revealed that V1AR but not OTR mRNA is abundantly expressed in mouse dorsal root ganglia, where it localizes to small- and medium-diameter cells as shown by single-cell RT-PCR. Hence, V1ARs expressed in dorsal root ganglia might represent a previously unrecognized target for the analgesic action of OXT and AVP.
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It is less likely that AVP and OXT may have acted via each other's receptors.
“Additionally, the neuropeptide- and receptor antagonist-specific effects on social play suggests that it is less likely that AVP and OXT may have acted via each other's receptors (Chini and Manning, 2007; Schorscher-Petcu et al., 2010).”
From Sex-specific modulation of juvenile social play behavior by vasopressin and oxytocin depends on social context (2014) · cites this paper as Schorscher-Petcu et al., 2010
The Introduction states that both OXT and AVP can activate both receptors. More decisively, the Results (Oxytocin and vasopressin 1a receptor antagonists) report that a V1AR antagonist prevented OXT-induced analgesia, supporting OXT action through AVP’s receptor rather than making cross-receptor action unlikely. The paper studies analgesia, not social play. (LLM, conf=0.83)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredOXT-induced analgesia in mice is mediated by vasopressin-1A receptors.
“Future studies are needed to elucidate the exact neurochemical cascade underlying the observed OXT effect on approach behavior since OXT-induced analgesia in mice, for example, is mediated by vasopressin-1A receptors (Schorscher-Petcu et al., 2010).”
From Oxytocin Modulates Social Distance between Males and Females (2012) · cites this paper as Schorscher-Petcu et al., 2010
Some actions of oxytocin are mediated via vasopressin receptors and vice versa.
“Some actions of oxytocin are mediated via vasopressin receptors and vice versa”
From Oxytocin, Neural Plasticity, and Social Behavior (2021) · cites this paper as Schorscher-Petcu et al. 2010
Several previous studies suggested that the effects of oxytocin and vasopressin result from activation of the opposite receptor.
“This concept is not new; several previous studies suggested that the effects of OT and AVP are a result of the activation of the ‘opposite’ receptor (4,80,86-89).”
From Comparative Perspectives on Oxytocin and Vasopressin Receptor Research in Rodents and Primates: Translational Implications (2016) · cites this paper as [88]
Peripheral administration of OT or AVP induces analgesia in OTR but not in V1aR knock-out male and female mice.
“Peripheral administration of OT or AVP induces analgesia in OTR but not in V1aR knock-out male and female mice [40].”
From Cross-talk among oxytocin and arginine-vasopressin receptors: Relevance for basic and clinical studies of the brain and periphery (2018) · cites this paper as [40]
Selective V1aR but not OTR antagonists inhibit both OT- and AVP-induced analgesia in wild-type mice.
“In addition, selective V1aR but not OTR antagonists inhibit both OT- and AVP- induced analgesia in wild-type mice.”
From Cross-talk among oxytocin and arginine-vasopressin receptors: Relevance for basic and clinical studies of the brain and periphery (2018) · cites this paper as [40]
Central administration of OT or AVP induces scratching behavior in wild-type and OTR knock-out male and female mice but not in V1aR knock-out mice.
“Central administration of OT or AVP induces scratching behavior in wild-type and OTR knock-out male and female mice but not in V1aR knock-out mice [40].”
From Cross-talk among oxytocin and arginine-vasopressin receptors: Relevance for basic and clinical studies of the brain and periphery (2018) · cites this paper as [40]
The antinociceptive effects of intranasal oxytocin observed in the present study could be explained by the activation of peripheral receptors, mainly the vasopressin 1A receptor.
“Additionally, it is also possible that the antinociceptive effects of intranasal oxytocin observed in the present study are explained by the activation of peripheral receptors, mainly the vasopressin 1A receptor 76.”
From The Analgesic Effect of Oxytocin in Humans: A Double‐Blind, Placebo‐Controlled Cross‐Over Study Using Laser‐Evoked Potentials (2016) · cites this paper as [76]
Oxytocin mediates its central effects by binding with high affinity to oxytocin receptors and/or with lower affinity to vasopressin 1a receptors.
“OT mediates its central effects by binding with high affinity to OT receptors (OTRs) and/or with lower affinity to vasopressin 1a (V1aR) receptors (Schorscher-Petcu et al., 2010; Song et al., 2014).”
From Central oxytocin receptors mediate mating-induced partner preferences and enhance correlated activation across forebrain nuclei in male prairie voles (2016) · cites this paper as Schorscher-Petcu et al., 2010
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“Some actions of oxytocin are mediated via vasopressin receptors and vice versa (Chini et al. 2008, Schorscher-Petcu et al. 2010, Xiao et al. 2017, Song & Albers 2018).”
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“Future studies are needed to elucidate the exact neurochemical cascade underlying the observed OXT effect on approach behavior since OXT-induced analgesia in mice, for example, is mediated by vasopressin-1A receptors (Schorscher-Petcu et al., 2010).”
BackgroundBiased Oxytocinergic Modulation of Midbrain Dopamine Systems
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“This concept is not new; several previous studies suggested that the effects of OT and AVP are a result of the activation of the ‘opposite’ receptor (4,80,86-89).”
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“, 2012), and some of the behavioral effects of OT are mediated by AVPR1A (Schorscher-Petcu et al., 2010; Song et al., 2013).”
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Oxytocin, vasopressin, and the motivational forces that drive social behaviors
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Vasopressin, oxytocin, and social odor recognition
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A Review of Oxytocin’s Effects on the Positive, Negative, and Cognitive Domains of Schizophrenia
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Oxytocin Gene Polymorphisms Influence Human Dopaminergic Function in a Sex-Dependent Manner
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Sex differences in the regulation of offensive aggression and dominance by arginine-vasopressin
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Oxytocin and behavior: lessons from knockout mice
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“, 1999), implying that the behavioral effects seen in this study might be explained independently of OXTR activation (Schorscher-Petcu et al., 2010).”
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- Authors
- Schorscher-Petcu, A., Sotocinal, S., Ciura, S., Dupre, A., Ritchie, J., Sorge, R. E., Crawley, J. N., Hu, S.-B., Nishimori, K., Young, L. J., Tribollet, E., Quirion, R., & Mogil, J. S.
- Affiliations
- McGill University (CA)
- University of Geneva (CH)
- National Institutes of Health (US)
- Tohoku University (JP)
- Emory University (US)
- Douglas Mental Health University Institute (CA)
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-06-16
- Volume
- 30
- Issue
- 24
- Pages
- 8274-8284
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2902996
- OpenAlex
- W2006909083
- Cited by
- 189
- References
- 80
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 10 · 2023: 5 · 2022: 9 · 2021: 8 · 2020: 13 · 2019: 11 · 2018: 14 · 2017: 18 · 2016: 14 · 2015: 20 · 2014: 17 · 2013: 10 · 2012: 11
- FWCI
- 7.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institutes of Health
- Canadian Institutes of Health Research
- National Center for Research Resources (M01RR000082)
- Topics
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- oxytocin, vasopressin, vasopressin 1a receptor, oxytocin receptor, analgesia, scratching behavior, nociception, pain, knockout mice, lumbar spinal cord, dorsal root ganglia, substantia gelatinosa, inflammatory nociception, mechanical sensitivity, receptor binding
- MeSH terms
- Analgesics, Analysis of Variance, Animals, Arginine Vasopressin, Autoradiography, Behavior, Animal, Dose-Response Relationship, Drug, Female, Ganglia, Spinal, Gene Expression Regulation, Hyperalgesia, Impulsive Behavior, Male, Mice, Inbred C57BL, Ornipressin, Oxytocin, Pain Measurement, Physical Stimulation, Protein Binding, Sensory Receptor Cells, RNA, Messenger, Receptors, Vasopressin, Receptors, Oxytocin, Mice, Knockout, Mice, Antidiuretic Hormone Receptor Antagonists
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