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Related Concept Videos

Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.

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Related Experiment Video

Updated: Jul 17, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
12:47

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates

Published on: March 20, 2014

A TREK-1/AQP4/TRPA1/BDNF Signaling Axis Is Associated With Astrocytic Volume Transients, Synaptic Plasticity, and

Victor James Drew1, Junsung Woo2, Jung Moo Lee1

  • 1Center for Memory and Glioscience, Institute for Basic Science (IBS), Daejeon, Republic of Korea.

Glia
|July 16, 2026
PubMed
Summary

Astrocytes regulate memory and synaptic plasticity through volume changes. Key ion channels and BDNF are crucial for these processes, offering potential therapeutic targets for memory disorders.

Keywords:
AQP4BDNFTREK‐1TRPA1astrocytic volume transientspatial memorysynaptic plasticity

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Last Updated: Jul 17, 2026

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Synaptic Plasticity

Background:

  • Astrocytes, traditionally viewed as support cells, are increasingly recognized for their active roles in brain function.
  • Astrocytic volume transients are emerging as key regulators of synaptic plasticity and memory formation.
  • Previous work identified TREK-1, TRPA1, Best1 channels, and BDNF as involved in these volume changes, but mechanisms remain unclear.

Purpose of the Study:

  • To investigate the roles of TREK-1 and TRPA1 channels in astrocytic volume dynamics.
  • To elucidate the downstream effects of astrocytic volume transients on synaptic plasticity and memory.
  • To explore the involvement of BDNF in mediating these effects.

Main Methods:

  • Intrinsic optical signal imaging to observe astrocytic swelling.
  • Electrophysiology to measure synaptic potentiation (LTP).
  • Behavioral assays (object-place recognition, passive avoidance) to assess spatial memory.

Main Results:

  • Neuronal stimulation triggers astrocytic swelling via K+ uptake (TREK-1) and Ca2+ influx (TRPA1).
  • Astrocytic swelling correlates with short- and long-term potentiation (LTP).
  • BDNF administration restored LTP during calcium sequestration; channel disruption impaired spatial memory.

Conclusions:

  • Astrocytic volume transients, modulated by TREK-1, TRPA1, and BDNF, are critical for synaptic plasticity and memory.
  • These mechanisms represent potential therapeutic targets for cognitive and memory dysfunction.