Cited by 34Neuroendocrine regulation and behaviorNeuropeptides and Animal PhysiologyNeuroscience and Neuropharmacology Research

Vasopressin autoreceptors and nitric oxide-dependent glutamate release are required for somatodendritic vasopressin release from rat magnocellular neuroendocrine cells responding to osmotic stimuli

Gillard, E. R., Coburn, C. G., de Leon, A., Snissarenko, E. P., Bauce, L. G., Pittman, Q. J., Hou, B., Currás-Collazo, M. C.·2007·Endocrinology

Abstract

Magnocellular neuroendocrine cells of the supraoptic nucleus (SON) release vasopressin (VP) systemically and locally during osmotic challenge. Although both central VP and nitric oxide (NO) release appear to reduce osmotically stimulated systemic VP release, it is unknown whether they interact locally in the SON to enhance somatodendritic release of VP, a phenomenon believed to regulate systemic VP release. In this study, we examined the contribution of VP receptor subtypes and NO to local VP release from the rat SON elicited by systemic injection of 3.5 m saline. Treatment of SON punches with VP receptor antagonists decreased osmotically stimulated intranuclear VP release. Similarly, blockade of NO production, or addition of NO scavengers, reduced stimulated VP, glutamate, and aspartate release, suggesting that local NO production and activity are critical for osmotically induced intranuclear VP and excitatory amino acid release. An increase in endogenous NO release from SON punches in response to hyperosmolality was confirmed by enzymatic NO assay. Consistent with enhanced glutamate and VP release from stimulated rat SON punches, the ionotropic glutamate receptor blocker kynurenate decreased stimulated local VP release without affecting NO release. These data suggest that NO enhances local VP release in part by facilitating local release of glutamate/aspartate and that glutamate receptor activity is required for the stimulation of local VP release by osmotic challenge. Coll…

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Crossref · 10.1210/en.2006-0995

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  • These AVP neurons receive osmosensitive inputs from the organum vasculosum lamina terminalis via glutamatergic synapses and are modulated by nitric oxide (NO) signaling pathways.

    “These AVP neurons receive osmosensitive inputs from the organum vasculosum lamina terminalis via glutamatergic synapses and are modulated by nitric oxide (NO) signaling pathways (146–148).”

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Authors
Gillard, E. R., Coburn, C. G., de Leon, A., Snissarenko, E. P., Bauce, L. G., Pittman, Q. J., Hou, B., & Currás-Collazo, M. C.
Affiliations
  • University of California, Riverside (US)
  • University of Calgary (CA)
Corresponding author
Gillard, E. R.
Venue
Endocrinology
Published
2007-02
Volume
148
Issue
2
Pages
479-489
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
OpenAlex
W2006244847
Cited by
34
References
0
Citations by year
2025: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2017: 3 · 2015: 3 · 2014: 4 · 2013: 2
FWCI
3.89
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
vasopressin, nitric oxide, glutamate release, aspartate release, supraoptic nucleus, osmotic stimulation, hyperosmolarity, kynurenic acid, glutamate receptors, osmoregulation
MeSH terms
Amino Acids, Animals, Neurosecretory Systems, Nitric Oxide, Osmosis, Sodium Chloride, Supraoptic Nucleus, Vasopressins, Water-Electrolyte Balance, Signal Transduction, Rats, Sprague-Dawley, Receptors, Vasopressin, Autoreceptors, Glutamic Acid, Excitatory Amino Acids, Protein Isoforms, Rats, In Vitro Techniques

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