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AIP limits neurotransmitter release by inhibiting calcium bursts from the ryanodine receptor

Bojun Chen1, Ping Liu1, Edward J Hujber2,3

  • 1Department of Neuroscience, University of Connecticut Health Center, Farmington, CT, 06030, USA.

Nature Communications
|November 11, 2017
PubMed

Insights

Mutations in AIPR-1 cause neurotransmitter hypersecretion by affecting ryanodine receptors. This conserved function of AIP proteins is to inhibit calcium release, potentially impacting pituitary tumor growth.

Area of Science:

  • Neuroscience
  • Genetics
  • Cell Biology

Background:

  • Pituitary tumors are linked to AIP gene mutations and growth hormone hypersecretion.
  • The precise mechanisms driving hypersecretion beyond pituitary enlargement remain unclear.

Purpose of the Study:

  • To investigate novel genetic factors contributing to neurotransmitter hypersecretion.
  • To elucidate the function of AIP-related proteins in neuronal signaling.

Main Methods:

  • Genetic screening in Caenorhabditis elegans to identify suppressors of reduced neurotransmitter release.
  • Analysis of neurotransmitter release, calcium transients, and vesicle pools in mutant strains.
  • Investigating the interaction between AIPR-1 and ryanodine receptors.

Main Results:

  • A mutation in AIPR-1 led to increased neurotransmitter release and calcium transients.
  • Phenotypes were linked to a leaky ryanodine receptor and reversed by ryanodine receptor mutations.
  • AIPR-1 physically associates with ryanodine receptors at synapses.

Conclusions:

  • A conserved function of AIP proteins is to inhibit calcium release via ryanodine receptors.
  • AIPR-1 regulates neuronal excitability by modulating ryanodine receptor activity.
  • Dysregulation of this pathway may contribute to conditions like pituitary tumors.

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