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Related Experiment Video

Updated: Sep 11, 2025

Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy
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TRPC4 regulates limbic behavior and neuronal development by stabilizing dendrite branches through actomyosin-driven

Jaepyo Jeon1, Travis I Moore1, Insuk So2

  • 1Department of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030.

Proceedings of the National Academy of Sciences of the United States of America
|August 14, 2025
PubMed
Summary

Transient Receptor Potential Canonical 4 (TRPC4) channels are crucial for early neurodevelopment and motivated behaviors. TRPC4 deficiency in mice impairs dendritic growth and causes autism-like behavioral deficits.

Keywords:
dendritic developmenthippocampusintegrinslimbic-related behaviormGluRs

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Transient Receptor Potential Canonical 4 (TRPC4) channels are linked to neurological functions and autism.
  • The role of TRPC4 in neurodevelopment is not well understood.

Purpose of the Study:

  • To investigate the role of TRPC4 in neurodevelopment and behavior.
  • To elucidate the molecular mechanisms underlying TRPC4's function in neuronal development.

Main Methods:

  • Utilized TRPC4 knockout (Trpc4-/-) mice to assess neurobehavioral deficits.
  • Examined dendritic arborization in hippocampal neurons in vivo and in vitro.
  • Performed live-cell imaging to study glutamate-induced dendritic branching.
  • Investigated TRPC4's role in calcium (Ca2+) signaling downstream of metabotropic glutamate receptors.

Main Results:

  • Trpc4-/- mice exhibited early-onset neurobehavioral deficits post-weaning, affecting nesting, burrowing, and social interactions.
  • Hippocampal neurons from Trpc4-/- mice showed reduced dendritic branching.
  • TRPC4 mediates Ca2+ entry, influencing nonmuscle myosin light chain (MLC) phosphorylation via myosin light chain kinase (MLCK), crucial for integrin activation and dendrite stability.
  • Glutamate stimulation led to new branch formation but subsequent retraction in Trpc4-/- neurons.

Conclusions:

  • TRPC4 channels are essential for dendrite morphogenesis and motivated behaviors.
  • Impaired TRPC4 function leads to deficits in dendritic development and abnormal behaviors in juvenile mice.
  • Findings offer insights into neurodevelopmental disorders like autism spectrum disorder and suggest potential therapeutic targets.