Related Experiment Video
Updated: May 28, 2026

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
Summary
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.
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.
Related Concept Videos
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 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
If over time, all...
Calcium Ion Concentration Mechanism
If over time, all...
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.
Hebbian LTP
LTP can occur when presynaptic neurons...
Hebbian LTP
LTP can occur when presynaptic neurons...
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.

