EphB2 receptor cell-autonomous forward signaling mediates auditory memory recall and learning-driven spinogenesis.
Asghar Talebian1, Mark Henkemeyer1
1Department of Neuroscience and Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, TX 75390 USA.
Communications Biology
|October 22, 2019
Summary
Ephrin-B/EphB2 signaling is crucial for memory recall and brain plasticity. This interaction enhances memory formation and retrieval by supporting neural activation and structural changes in learning centers.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Ephrin-B ligands and EphB receptors are highly expressed in brain learning centers.
- The precise role of their trans-synaptic interactions in memory remains largely unknown.
Purpose of the Study:
- To investigate the contribution of EphB2 forward signaling to memory recall.
- To determine the impact of EphB2 signaling on neural activation and structural plasticity in memory-associated brain regions.
Main Methods:
- Assessed memory recall in mice with altered EphB2 signaling.
- Measured neuronal activation using c-Fos staining after encoding and retrieval.
- Analyzed dendritic spine density and maturation in the auditory cortex.
Main Results:
- EphB2 forward signaling is essential for contextual and sound-evoked memory recall.
- Over-activation of EphB2 tyrosine kinase domain enhanced memory.
- Reduced neuronal activation was observed in the auditory cortex and hippocampal CA1 during retrieval in EphB2 mutants.
- Spine density and maturation were reduced in the auditory cortex of mutants.
Conclusions:
- Trans-synaptic ephrin-B-EphB2 interactions and forward signaling are critical for memory generation.
- These interactions facilitate neural activation and structural plasticity in learning-associated neurons.
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