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Updated: Mar 11, 2026

Microfluidic Chip for Axonal Injury Models Construction and Enabling Multi-Omics Analysis
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Study of local intracellular signals regulating axonal morphogenesis using a microfluidic device.

Daiki Uryu1, Tomohiro Tamaru1, Azusa Suzuki1

  • 1Department of Human and Artificial Intelligent Systems, Faculty of Engineering, University of Fukui , Fukui , Japan.

Science and Technology of Advanced Materials
|November 24, 2016
PubMed
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Microfluidic devices precisely control local Ca2+ signals and protein levels in neurons. This technology reveals L-type calcium channel activity is essential for axonal branching in cerebellar granule neurons.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biotechnology

Background:

  • Axonal patterning is vital for neuronal connectivity and function.
  • Understanding local molecular mechanisms controlling axonal structure requires precise subcellular manipulation.
  • Microfluidic devices offer a powerful platform for localized, long-term functional studies.

Purpose of the Study:

  • To investigate the role of local calcium (Ca2+) signals in axonal branching using microfluidics.
  • To develop and apply a microfluidic system for localized control of protein levels in neurons.
  • To elucidate the contribution of axonal Ca2+ entry via L-type voltage-dependent calcium channels (L-VDCC) to axonal growth.

Main Methods:

  • Utilized polydimethylsiloxane (PDMS)-based microfluidic devices for localized drug delivery (nifedipine).
Keywords:
200 Applications60 New topics/Others600 Applications/Cell biologyMicrofluidic deviceaxoncerebellar granule neuronsdepolarizationdihydrofolate reductase

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  • Employed genetic engineering with an E. coli dihydrofolate reductase (ecDHFR)-destabilizing domain fused to EGFP for protein level control.
  • Combined microfluidics with electroporation and trimethoprim (TMP) to achieve differential protein manipulation between axons and somatodendrites.

    • Main Results:

    • Membrane depolarization induced significant axonal branch extension in cultured cerebellar granule neurons (CGNs).
    • Local application of nifedipine confirmed that Ca2+ influx through L-VDCCs in the axon is necessary for branch extension.
    • Successfully demonstrated localized manipulation of fusion protein levels (EGFP-ecDHFR) using microfluidics and TMP.

    Conclusions:

    • Microfluidic devices are effective tools for studying fundamental biological processes at the subcellular level.
    • Local Ca2+ signaling, specifically via L-VDCCs, plays a critical role in axonal branching.
    • The developed microfluidic system enables precise, localized control of protein expression, advancing research in neuronal development and function.