Cited by 204Neuroendocrine regulation and behaviorNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

Role of the vasopressin 1b receptor in rodent aggressive behavior and synaptic plasticity in hippocampal area CA2

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Pagani, J H, Zhao, M, Cui, Z, Williams Avram, S K, Caruana, D A, Dudek, S M, Young, W S·2015·Molecular Psychiatry

Abstract

The vasopressin 1b receptor (Avpr1b) is critical for social memory and social aggression in rodents, yet little is known about its specific roles in these behaviors. Some clues to Avpr1b function can be gained from its profile of expression in the brain, which is largely limited to the pyramidal neurons of the CA2 region of the hippocampus, and from experiments showing that inactivation of the gene or antagonism of the receptor leads to a reduction in social aggression. Here we show that partial replacement of the Avpr1b through lentiviral delivery into the dorsal CA2 region restored the probability of socially motivated attack behavior in total Avpr1b knockout mice, without altering anxiety-like behaviors. To further explore the role of the Avpr1b in this hippocampal region, we examined the effects of Avpr1b agonists on pyramidal neurons in mouse and rat hippocampal slices. We found that selective Avpr1b agonists induced significant potentiation of excitatory synaptic responses in CA2, but not in CA1 or in slices from Avpr1b knockout mice. In a way that is mechanistically very similar to synaptic potentiation induced by oxytocin, Avpr1b agonist-induced potentiation of CA2 synapses relies on NMDA (N-methyl-D-aspartic acid) receptor activation, calcium and calcium/calmodulin-dependent protein kinase II activity, but not on cAMP-dependent protein kinase activity or presynaptic mechanisms. Our data indicate that the hippocampal CA2 is important for attacking in response to a male intruder and that the Avpr1b, likely through its role in regulating CA2 synaptic plasticity, is a necessary mediator.

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  • Oxytocin lowers the threshold for depolarizing inputs to induce long-term potentiation (LTP) in hippocampal CA2 and olfactory bulb.

    “For example, oxytocin lowers the threshold for depolarizing inputs to induce long-term potentiation (LTP) in hippocampal CA2 (Pagani et al. 2015, Carstens & Dudek 2019) and olfactory bulb (Fang et al. 2008).”

    From Oxytocin, Neural Plasticity, and Social Behavior (2021) · cites this paper as Pagani et al. 2015

    The Discussion (page unavailable) proposes that oxytocin decreases the threshold for LTP in CA2, supported by potentiation during baseline stimulation. The Results (page unavailable) show potentiation with an oxytocin-receptor agonist, but the paper presents the threshold claim as a proposal rather than an established finding. The olfactory-bulb portion is attributed to Fang et al., not Pagani et al. (LLM, conf=0.86)

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Research works printed but not linked: 1

  1. [80]Save E Nerad L Poucet B Contribution of multiple sensory information to place field stability in hippocampal place cells Hippocampus 2000 10 1 64 76 10706218

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Authors
Pagani, J. H., Zhao, M., Cui, Z., Williams Avram, S. K., Caruana, D. A., Dudek, S. M., & Young, W. S.
Affiliations
National Institutes of Health (US)
Corresponding author
  • Dudek, S M
  • Young, W S
Venue
Molecular Psychiatry
Published
2014-05-27
Volume
20
Issue
4
Pages
490-499
ISSN
  • 1359-4184 (ISSN-L)
  • 1476-5578
OpenAlex
W2117023704
Cited by
204
References
85
Citations by year
2026: 11 · 2025: 15 · 2024: 15 · 2023: 19 · 2022: 14 · 2021: 16 · 2020: 22 · 2019: 21 · 2018: 20 · 2017: 16 · 2016: 20 · 2015: 11 · 2014: 4
FWCI
25.22
Type
journal article
Language
en
Open access
Locations
  • Molecular Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Aston Publications Explorer (Aston University) (submittedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (ZIAMH002498, Z01-MH-002498-24, Z01MH002498)
  • National Institute of Environmental Health Sciences (Z01ES100221)
Topics
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
AVPR1B, social aggression, hippocampal CA2, synaptic plasticity, NMDA receptor, CaMKII, oxytocin, social memory, pyramidal neurons
MeSH terms
Aggression, Animals, Cell Count, Exploratory Behavior, Female, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Neuronal Plasticity, Synapses, Transduction, Genetic, Lentivirus, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Receptors, Vasopressin, Receptors, Oxytocin, Maze Learning, Mice, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, CA2 Region, Hippocampal, Antidiuretic Hormone Receptor Antagonists

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