Regulation of Hippocampal Synaptic Plasticity by the Tyrosine Kinase Receptor, REK7/EphA5, and its Ligand, AL-1/Ephrin-A5
| Autor: | Ingrid W. Caras, Paul Moran, Zheng Jl, Natasha Shinsky, H S Phillips, Mendoza-Ramirez Jl, Wei-Qiang Gao, Mark Armanini, John W. Winslow |
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| Rok vydání: | 1998 |
| Předmět: |
Time Factors
Long-Term Potentiation Fluorescent Antibody Technique Nonsynaptic plasticity Biology Neurotransmission Synaptic Transmission Gene Expression Regulation Enzymologic Mice Cellular and Molecular Neuroscience Organ Culture Techniques Memory Synaptic augmentation Animals RNA Messenger Molecular Biology Cells Cultured Neuronal Plasticity Synaptic scaling Ephrin-A2 Excitatory Postsynaptic Potentials Receptor Protein-Tyrosine Kinases Receptor EphA5 Long-term potentiation Dendrites Cell Biology Axons Electric Stimulation Rats Mice Inbred C57BL Synaptic fatigue Solubility nervous system Immunoglobulin G CD4 Antigens Dentate Gyrus Synaptic plasticity Neuroscience Synaptic tagging Transcription Factors |
| Zdroj: | Molecular and Cellular Neuroscience. 11:247-259 |
| ISSN: | 1044-7431 |
| Popis: | The Eph-related tyrosine kinase receptor, REK7/EphA5, mediates the effects of AL-1/Ephrin-A5 and related ligands and is involved in the guidance of retinal, cortical, and hippocampal axons during development. The continued expression of REK7/EphA5 in the adult brain, in particular in areas associated with a high degree of synaptic plasticity such as the hippocampus, raises the question of its function in the mature nervous system. In this report we examined the role of REK7/EphA5 in synaptic remodeling by asking if agents that either block or activate REK7/EphA5 affect synaptic strength in hippocampal slices from adult mouse brain. We show that a REK7/EphA5 antagonist, soluble REK7/EphA5–IgG, impairs the induction of long-term potentiation (LTP) without affecting other synaptic parameters such as normal synaptic transmission or paired-pulse facilitation. In contrast, perfusion with AL-1/Ephrin-A5–IgG, an activator of REK7/EphA5, induces a sustained increase in normal synaptic transmission that partially mimics LTP. The sustained elevation of normal synaptic transmission could be attributable to a long-lasting binding of the AL-1/Ephrin-A5–IgG to the endogenous REK7/EphA5 receptor, as revealed by immunohistochemistry. Furthermore, maximal electrical induction of LTP occludes the potentiating effects of subsequent treatment with AL-1/Ephrin-A5–IgG. Taken together these results implicate REK7/EphA5 in the regulation of synaptic plasticity in the mature hippocampus and suggest that REK7/EphA5 activation is recruited in the LTP induced by tetanization. |
| Databáze: | OpenAIRE |
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