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Related Concept Videos

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Related Experiment Video

Updated: Dec 27, 2025

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording
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Developmental Time Course of SNAP-25 Isoforms Regulate Hippocampal Long-Term Synaptic Plasticity and

Katisha R Gopaul1, Muhammad Irfan1,2, Omid Miry1

  • 1Department of Cell Biology & Anatomy, New York Medical College, Valhalla, NY 10595, USA.

International Journal of Molecular Sciences
|February 26, 2020
PubMed
Summary

Syntaxin-binding protein 25 (SNAP-25) isoforms influence brain plasticity. SNAP-25b deficiency impairs synaptic plasticity in young mice, but compensatory mechanisms in adults restore function, especially after learning.

Keywords:
SNARE proteinsSchaffer collateral-CA1 synapsescognitionlearning and memorylong-term depressionlong-term potentiation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • SNAP-25 is crucial for neurotransmitter release and synaptic plasticity.
  • Two SNAP-25 splice variants, SNAP-25a and SNAP-25b, are developmentally regulated.
  • These variants may differentially affect hippocampal and neocortical synapses.

Purpose of the Study:

  • To investigate the distinct roles of SNAP-25a and SNAP-25b in synaptic plasticity.
  • To examine the developmental regulation of long-term potentiation (LTP) and long-term depression (LTD) by SNAP-25 isoforms.
  • To assess the impact of SNAP-25b deficiency and learning on hippocampal synaptic function.

Main Methods:

  • Utilized SNAP-25b-deficient mice at different ages (1 and 4 months).
  • Electrophysiological recordings at Schaffer collateral-CA1 synapses in the hippocampus.
  • Assessed synaptic plasticity (LTP and LTD) before and after training on a hippocampus-dependent task.

Main Results:

  • In young (1-month-old) SNAP-25b-deficient mice, faster release kinetics, decreased LTP, and enhanced LTD were observed.
  • By adulthood (4 months), SNAP-25b-deficient mice showed compensatory increases in LTP and normalized LTD.
  • Hippocampus-dependent learning reversed LTP deficits in young mice and prevented LTD up-regulation in adults.

Conclusions:

  • SNAP-25b isoform promotes LTP and reduces LTD in young mice at hippocampal synapses.
  • Compensatory mechanisms can restore synaptic plasticity in adult SNAP-25b-deficient mice.
  • Learning interacts with SNAP-25 isoform expression to modulate synaptic plasticity and memory.