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Related Experiment Video

Updated: Feb 8, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
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TRPM7 Is Required for Normal Synapse Density, Learning, and Memory at Different Developmental Stages.

Yuqiang Liu1, Cui Chen1, Yunlong Liu2

  • 1Department of Neurology, Huashan Hospital, and Institutes of Brain Science, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China.

Cell Reports
|June 21, 2018
PubMed
Summary

The transient receptor potential melastatin 7 (TRPM7) chanzyme is crucial for synaptic density and cognitive functions in the brain. Its α-kinase domain, not the ion channel, is key for maintaining learning and memory.

Keywords:
TRPM7cofilinlearning and memoryneurodegenerative disorderssynapse densitysynaptic plasticityα-kinase

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Ion Channel Physiology

Background:

  • The transient receptor potential melastatin 7 (TRPM7) chanzyme has known roles in various tissues, but its function in the central nervous system (CNS) under normal physiological conditions is not well understood.
  • TRPM7 possesses both ion channel and kinase activities, suggesting diverse biological functions.

Purpose of the Study:

  • To investigate the role of TRPM7 in the CNS, specifically its contribution to synaptic structure, plasticity, and cognitive functions under physiological conditions.
  • To determine which domain of TRPM7 (ion channel or α-kinase) is responsible for its observed effects in the brain.

Main Methods:

  • TRPM7 knockdown was performed in hippocampal neurons and adult rat hippocampi.
  • Conditional knockout of TRPM7 was generated in mice during early postnatal development.
  • Synapse density, synaptic plasticity, learning, and memory were assessed.
  • Rescue experiments were conducted by restoring specific TRPM7 domains.

Main Results:

  • TRPM7 knockdown in hippocampal neurons reduced structural synapse density, which was rescued by the α-kinase domain but not the ion channel region.
  • Early postnatal TRPM7 knockout in mice led to impaired learning, memory, synapse density, and plasticity.
  • TRPM7 knockdown in adult rats also impaired learning, memory, synapse density, and synaptic plasticity.
  • Restoring the α-kinase domain in knockout mice rescued synapse density, plasticity, and memory, likely via cofilin phosphorylation.

Conclusions:

  • Brain TRPM7 is essential for normal synaptic structure, plasticity, and cognitive functions under physiological conditions.
  • The α-kinase domain of TRPM7 plays a critical role in maintaining these functions, potentially through interaction with cofilin.
  • TRPM7's contribution to brain function extends beyond its ion channel activity.