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Related Experiment Videos

Vasopressin and oxytocin decrease excitatory amino acid release in adult rat supraoptic nucleus.

M C Currás-Collazo1, E R Gillard, J Jin

  • 1Department of Cell Biology and Neuroscience, University of California, Riverside, California, USA. margarita.curras@ucr.edu

Journal of Neuroendocrinology
|January 22, 2003
PubMed
Summary

Oxytocin and vasopressin decrease excitatory amino acid release in the supraoptic nucleus (SON), suggesting a role in regulating neuroendocrine cell activity. This peptide action appears specific to the SON, not the cortex.

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Area of Science:

  • Neuroendocrinology
  • Neuropharmacology
  • Cellular Neuroscience

Background:

  • Oxytocin and vasopressin are known to reduce excitatory postsynaptic responses in magnocellular neuroendocrine cells of the supraoptic nucleus (SON).
  • The precise mechanisms by which these neuropeptides influence neuronal activity, particularly regarding excitatory neurotransmitter release, remain incompletely understood.

Purpose of the Study:

  • To investigate whether synaptic glutamate release is modulated by oxytocin and vasopressin.
  • To examine the effects of these neuropeptides on depolarization-induced glutamate and aspartate release in the rat SON and fronto-parietal cortex.

Main Methods:

  • Acute dissection of rat SON and fronto-parietal cortex punches.
  • Stimulation of glutamate and aspartate release using high potassium (60 mM K+).

Related Experiment Videos

  • Measurement of amino acid release via ion exchange chromatography or high-performance liquid chromatography; assessment of receptor involvement using antagonists.

    • Main Results:

    • High K+ significantly increased glutamate levels in both SON and cortex.
    • Oxytocin and vasopressin significantly reduced K+-stimulated glutamate and aspartate release in the SON by 34% and 62%, respectively.
    • In cortical punches, oxytocin and vasopressin did not significantly alter glutamate/aspartate release, and receptor antagonist studies indicated involvement of oxytocin and V1a receptors in the SON.

    Conclusions:

    • Locally released oxytocin and vasopressin may autoregulate SON magnocellular neuroendocrine cell activity.
    • This autoregulation is partly achieved by modulating the release of excitatory amino acids from afferent terminals and/or other cellular sources within the SON.
    • The observed effects are specific to the SON, correlating with the denser distribution of relevant peptide receptors compared to the cortex.