Vasopressin Inhibits Glutamate Release via Two Distinct Modes in the Brainstem
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The hypothalamus coordinates autonomic responses in part through arginine vasopressin (AVP) released in medial nucleus tractus solitarius (NTS). However, the mechanisms and sites of AVP action within NTS pathways are uncertain. In brainstem slices, we activated solitary tract (ST) primary afferents to release glutamate and tested whether AVP modulated synaptic transmission to second-order neurons. NTS neurons were classified as second order by ST synaptic characteristics or the presence of anterograde tracers from peripheral baroreceptor afferents. Stimulus recruitment curves indicated ST-EPSCs on individual neurons were evoked by stimulation of single ST axons. Variance-mean (V-M) analysis of ST-EPSCs in individual neurons revealed uniformly high release probability (p approximately 0.9) from an average of 19 release sites (N) and a quantal size (q) of 34.0 +/- 4.7 pA. In 26 of 49 neurons, AVP inhibited afferent synaptic transmission. In most neurons, AVP reduced ST-EPSC amplitudes (n = 20) by decreasing p to 0.65, whereas q, N, and conduction times were unaffected. The V1a antagonist SR49059 alone decreased ST-EPSC V and increased M, suggesting tonic AVP actions, and blocked exogenous AVP action (n = 4). In other neurons with identical ST release properties, AVP induced synaptic failures and increased conduction time without altering the V-M relationship of successful ST-EPSCs (n = 6). Interestingly, frequency-depressed ST-EPSCs were not affected by AVP. AVP failed to alter holding or voltage-dependent potassium currents. Thus, AVP regulates NTS neurons by two distinct novel and state-dependent mechanisms: one, an analog, graded presynaptic inhibition of terminal glutamate release and the other, a binary, extraterminal block of conducted excitation.
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Presynaptic V1aR activation leads to an inhibition of glutamate release.
“suggesting that presynaptic V1aR activation leads to an inhibition of glutamate release.”
From Vasopressin regulates social play behavior in sex-specific ways through glutamate modulation in the lateral septum (2025) · cites this paper as Bailey et al., 2006
Bath application of a V1aR antagonist increased glutamate release from solitary tract neurons.
“Interestingly, bath application of a V1aR antagonist increased glutamate release from solitary tract neurons (Bailey et al., 2006)”
From Vasopressin regulates social play behavior in sex-specific ways through glutamate modulation in the lateral septum (2025) · cites this paper as Bailey et al., 2006
AVP acts on presynaptically expressed V1aR to modulate glutamate release in the parabrachial nucleus and the nucleus of the solitary tract.
“in vitro studies have suggested that AVP acts on presynaptically expressed V1aR to modulate glutamate release in other brain regions, namely the parabrachial nucleus and the nucleus of the solitary tract (Chen & Pittman, 1999;Bailey et al., 2006).”
From Vasopressin regulates social play behavior in sex-specific ways through glutamate modulation in the lateral septum (2025) · cites this paper as Bailey et al., 2006
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Uraemia: an unrecognized driver of central neurohumoral dysfunction in chronic kidney disease?
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Self-citationDistinct Calcium Sources Support Multiple Modes of Synaptic Release from Cranial Sensory Afferents
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Dedicated C-fiber vagal sensory afferent pathways to the paraventricular nucleus of the hypothalamus
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Extensive Inhibitory Gating of Viscerosensory Signals by a Sparse Network of Somatostatin Neurons
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Self-citationInterval Walking Training Can Increase Physical Fitness in Middle-Aged and Older People
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“Moreover, bath application of a V1aR antagonist increased glutamate release from solitary tract neurons [64].”
Tonic Regulation of GABAergic Synaptic Activity on Vasopressin Neurones by Cannabinoids
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- Authors
- Bailey, T. W., Jin, Y.-H., Doyle, M. W., Smith, S. M., & Andresen, M. C.
- Affiliations
- Oregon Health & Science University (US)
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2006-06-07
- Volume
- 26
- Issue
- 23
- Pages
- 6131-6142
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2680488
- OpenAlex
- W1964779574
- Cited by
- 112
- References
- 60
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 1 · 2023: 3 · 2021: 4 · 2020: 3 · 2019: 7 · 2018: 6 · 2017: 5 · 2016: 2 · 2015: 9 · 2014: 6 · 2013: 7 · 2012: 13
- FWCI
- 3.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (F32HL070433, HL-56460, HL-70433, HL41119, R01HL041119)
- National Institute of Neurological Disorders and Stroke (R01NS043444, NS-43444)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Keywords
- vasopressin, glutamate release, brainstem, presynaptic inhibition, synaptic transmission, release probability, quantal size, synaptic failure, baroreceptor afferents, V1a receptor, hypothalamus, autonomic regulation
- MeSH terms
- Animals, Arginine Vasopressin, Drug Resistance, Male, Synaptic Transmission, Neurons, Afferent, Pressoreceptors, Probability, Rats, Sprague-Dawley, Receptors, Vasopressin, Solitary Nucleus, Glutamic Acid, Excitatory Postsynaptic Potentials, Rats, In Vitro Techniques
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