Activation of arginine vasopressin receptor 1a facilitates the induction of long-term potentiation in the accessory olfactory bulb of male mice
Abstract
Olfaction plays an important role in social recognition in most mammals. Central arginine vasopressin (AVP) plays a role in this olfaction-based recognition. The high level of expression of AVP receptors in the accessory olfactory bulb (AOB) at the first relay of the vomeronasal system highlights the importance of AVP signaling at this stage. We therefore analyzed the effects of AVP on the synaptic plasticity of glutamatergic transmission from mitral cells to granule cells in AOB slices from male mice. To monitor the strength of the glutamatergic transmission, we measured the maximal initial slope of the lateral olfactory tract-evoked field potential, which represents the granule cell response to mitral cell activation. AVP paired with 100-Hz stimulation that only produced short-term potentiation enhanced the induction of long-term potentiation (LTP) in a dose-dependent manner. AVP-paired LTP was blocked by the selective AVP receptor 1a (AVPR1a) antagonist, d(CH 2)5[Tyr(Me)2]AVP (Manning compound), but not by the AVPR1b antagonist SSR149415, and it was mimicked by the selective AVPR1a agonist [Phe 2, Ile 3, Orn 8]-vasopressin. We further examined the effect of AVP on the reciprocal transmission between mitral and granule cells by stimulating a mitral cell and recording the evoked inhibitory postsynaptic currents (IPSCs) from the same cell using conventional whole-cell patch-clamp techniques. AVP reduced the reciprocal IPSCs triggered by endogenous glutamate release from the excited mitral cell. These results suggest that AVP promotes the induction of LTP at the mitral-to-granule cell synapse via the activation of AVPR1a through an as-yet-to-be-determined mechanism in the AOB of male mice.
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Oxytocin increases the salience of social stimuli.
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This modulation of signal to noise may be a common neural circuit mechanism to enhance the salience of multimodal social stimuli.
“This modulation of signal to noise may be a common neural circuit mechanism to enhance the salience of multimodal social stimuli (10,78).”
From Oxytocin, Vasopressin, and Social Behavior: From Neural Circuits to Clinical Opportunities (2022) · cites this paper as [78]
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- Authors
- Namba, T., Taniguchi, M., Murata, Y., Tong, J., Wang, Y., Okutani, F., Yamaguchi, M., & Kaba, H.
- Affiliations
- Kōchi University (JP)
- University of Kochi (JP)
- Corresponding author
- Kaba, Hideto
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2016-11
- Volume
- 634
- Pages
- 107-113
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2528390936
- Cited by
- 12
- References
- 51
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 2 · 2018: 1 · 2017: 2
- FWCI
- 0.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Kochi University
- Topics
- Life Sciences › Neuroscience › Sensory Systems › Olfactory and Sensory Function Studies
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- vasopressin, AVPR1A, long-term potentiation, accessory olfactory bulb, vomeronasal system, mitral cells, granule cells, glutamatergic neurotransmission, synaptic plasticity, lateral olfactory tract, inhibitory postsynaptic currents, vasopressin receptor antagonists, vasopressin analogue, social recognition, male mice
- MeSH terms
- Animals, Arginine Vasopressin, Electric Stimulation, Indoles, Male, Mice, Inbred BALB C, Synaptic Transmission, Neurons, Olfactory Bulb, Pyrrolidines, Vasopressins, Receptors, Vasopressin, Long-Term Potentiation, Glutamic Acid, Inhibitory Postsynaptic Potentials, Antidiuretic Hormone Receptor Antagonists
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