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Postweaning Development Influences Endogenous VPAC1 Modulation of LTP Induced by Theta-Burst Stimulation: A Link to

Marta Gil1, Ana Caulino-Rocha1, Marta Bento1

  • 1BioISI-Biosystems & Integrative Sciences Institute, Faculdade de Ciências, Universidade de Lisboa, 1749-016 Lisbon, Portugal.

Biomolecules
|March 28, 2024
PubMed

Insights

Vasoactive intestinal peptide (VIP) receptor VPAC1 influences long-term potentiation (LTP) during brain development. Its modulation of hippocampal LTP is stronger in juveniles than adults, linked to GABAergic circuit maturation.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Synaptic Plasticity

Background:

  • Long-term potentiation (LTP), a key mechanism for learning and memory, undergoes significant developmental changes postweaning.
  • Vasoactive intestinal peptide (VIP) and its VPAC1 receptor are known to modulate hippocampal LTP, but their role during postweaning development and its relation to GABAergic maturation remain unclear.
  • Understanding these developmental changes is crucial given the involvement of VIP interneurons in learning, neurodevelopmental disorders, and epilepsy.

Purpose of the Study:

  • To investigate how VPAC1 receptor modulation of LTP changes from weaning to adulthood.
  • To examine the relationship between VPAC1's influence on LTP and the maturation of hippocampal GABAergic circuits.
  • To determine the role of VPAC2 receptor activation in TBS-induced LTP during postweaning development.

Main Methods:

  • Theta-burst stimulation (TBS) was used to induce LTP in rats at different postweaning ages (3, 6-7, and 12 weeks).
  • The effect of a VPAC1 receptor antagonist (PG 97-269) on TBS-induced LTP was assessed.
  • Synaptic levels of VPAC1 receptors and markers for GABAergic and glutamatergic synaptic contacts were analyzed.
  • The influence of VPAC2 receptor activation on LTP was also evaluated.

Main Results:

  • TBS-induced LTP increased progressively from weaning to adulthood.
  • VPAC1 receptor antagonism significantly inhibited LTP more in juveniles than in adults, despite similar synaptic VPAC1 levels.
  • GABAergic synaptic markers increased more prominently than glutamatergic markers during this developmental period, suggesting enhanced GABAergic circuit maturation.
  • VPAC2 receptor activation did not significantly affect TBS-induced LTP.

Conclusions:

  • VPAC1 receptor modulation of hippocampal LTP is developmentally regulated, being more potent in younger animals.
  • This developmental shift in VPAC1's influence is associated with, but not solely explained by, the maturation of GABAergic circuits.
  • The findings offer insights into the role of VIP signaling in hippocampal plasticity during brain development and its potential implications for neurological conditions.

Keywords:
PSD-95VGATVGlut1VIPVPAC1 receptorgephyrinhippocampustheta-burst LTP

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