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Related Experiment Video

Updated: Aug 11, 2025

Assessing Cellular Stress and Inflammation in Discrete Oxytocin-secreting Brain Nuclei in the Neonatal Rat Before and After First Colostrum Feeding
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Endolysosomal TPCs regulate social behavior by controlling oxytocin secretion.

Lora L Martucci1,2,3, Jean-Marie Launay4, Natsuko Kawakami5

  • 1Neuroscience Paris-Saclay Institute, CNRS UMR 9197, Paris-Sud University, Paris-Saclay University, Saclay 91400, France.

Proceedings of the National Academy of Sciences of the United States of America
|February 6, 2023
PubMed
Summary
This summary is machine-generated.

Lysosomes and two-pore channels (TPCs) control oxytocin (OT) release by priming vesicles. TPC activation enhances social behavior, while TPC-deficient mice show deficits restored by OT.

Keywords:
NAADPcalciumchannelhypothalamusneuropeptide

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Oxytocin (OT) regulates social behavior and is stored in large dense-cored vesicles (LDCVs).
  • OT secretion depends on calcium (Ca2+) influx and intracellular Ca2+ release, which primes LDCVs for exocytosis.
  • The precise Ca2+-dependent mechanisms priming OT secretion remain incompletely understood.

Purpose of the Study:

  • To elucidate the role of lysosomes and two-pore channels (TPCs) in regulating oxytocin secretion.
  • To investigate the Ca2+ signaling pathways involved in priming neuropeptide vesicles for release.
  • To determine the impact of TPC function on social behavior.

Main Methods:

  • Investigated lysosome-LDCV interactions in hypothalamic neurons.
  • Utilized TPC knockout mice to assess OT levels and secretion.
  • Examined the effects of TPC activators (nicotinic acid adenine dinucleotide phosphate, TPC2-A1-N) and antagonists (Ned-19).
  • Assessed maternal and social behaviors in wild-type and TPC knockout mice.

Main Results:

  • Lysosomes were found to surround dendritic LDCVs.
  • Direct activation of TPCs provided critical Ca2+ signals that prime OT release by increasing the releasable LDCV pool.
  • TPC knockout mice exhibited reduced plasma OT levels and impaired hypothalamic OT secretion.
  • Activation of metabotropic glutamate receptors recruited TPCs to sustain somatodendritic OT release.
  • Mice lacking TPCs showed impaired social and maternal behaviors, which were restored by OT administration.

Conclusions:

  • Lysosomes and TPCs play an unexpected but crucial role in neuropeptide secretion by priming LDCVs.
  • TPC-mediated Ca2+ signaling is essential for regulating the releasable pool of OT vesicles.
  • Dysregulation of TPCs impairs social behavior, highlighting their importance in neuroendocrine regulation of social interactions.