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Related Concept Videos

Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
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Long-term Potentiation01:25

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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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: May 28, 2026

Barnes Maze Testing Strategies with Small and Large Rodent Models
12:59

Barnes Maze Testing Strategies with Small and Large Rodent Models

Published on: February 26, 2014

DIP/WISH deficiency enhances synaptic function and performance in the Barnes maze.

Suhail Asrar1, Keiko Kaneko, Keizo Takao

  • 1Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), Japan.

Molecular Brain
|October 25, 2011
PubMed
Summary
This summary is machine-generated.

Deleting diaphanous interacting protein (DIP)/WASP interacting SH3 protein (WISH) enhances long-term potentiation in hippocampal neurons. This leads to improved learning and memory in mice, as shown by faster Barnes maze test performance.

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Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
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Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Diaphanous interacting protein (DIP)/WASP interacting SH3 protein (WISH) is implicated in cytoskeletal signaling, regulating actin dynamics and microtubule activity.
  • Spine-head volumes dynamically reflect synaptic strength and are crucial for long-term synaptic plasticity.
  • The role of DIP/WISH in synaptic plasticity and spine formation remains largely unexplored.

Purpose of the Study:

  • To investigate the involvement of DIP/WISH in synaptic plasticity and spine formation.
  • To determine the effects of DIP/WISH deficiency on hippocampal function and cognitive performance.

Main Methods:

  • Electrophysiological recordings in hippocampal CA1 neurons from DIP/WISH-deficient mice.
  • Behavioral testing using the Barnes maze to assess learning and memory.

Main Results:

  • DIP/WISH-deficient hippocampal CA1 neurons showed enhanced long-term potentiation, affecting both pre- and post-synaptic events.
  • DIP/WISH-deficient mice demonstrated improved performance in the Barnes maze test, particularly at younger ages.

Conclusions:

  • DIP/WISH deletion enhances hippocampal long-term potentiation.
  • The absence of DIP/WISH improves cognitive performance in mice, likely mediated by enhanced synaptic plasticity.