Upregulation of TRESK Channels Contributes to Motor and Sensory Recovery after Spinal Cord Injury

International Journal of Molecular Sciences, 2020 · DOI: 10.3390/ijms21238997 · Published: November 26, 2020

Simple Explanation

This study investigates the role of TRESK channels after spinal cord injury (SCI), focusing on their impact on motor and sensory recovery. The research utilizes a thoracic spinal cord contusion model in rats and transgenic mice overexpressing the TRESK gene to observe changes in TRESK expression and function after SCI. The findings suggest that TRESK upregulation following SCI contributes to improved motor and sensory function by suppressing neuron excitability, reducing inflammation, and limiting apoptotic processes.

Study Duration

4 weeks

Participants

Sprague-Dawley rats (n = 60) and C57BL/6 mice (n = 60)

Evidence Level

Not specified

Key Findings

1
TRESK expression is upregulated in both dorsal and ventral neurons of the spinal cord following SCI, with significant increases observed at acute time points (6, 24, and 48 hours) post-injury.
2
Transgenic mice overexpressing TRESK (TGTRESK) exhibit faster paralysis recovery and higher mechanical pain thresholds compared to wild-type (WT) mice after SCI.
3
TGTRESK mice show reduced levels of TNF-α in the blood, as well as decreased IL-1β concentrations and apoptotic signals in the caudal spinal cord and dorsal root ganglion (DRG) compared to WT mice after SCI.

Research Summary

The study examines the role of TRESK channels in spinal cord injury (SCI) using a thoracic spinal cord contusion model and transgenic mice overexpressing TRESK. Results indicate that TRESK expression is increased post-SCI in spinal cord neurons and DRGs, particularly at acute time points after the injury. This upregulation contributes to motor and sensory recovery. TGTRESK mice exhibit improved motor and sensory recovery, reduced inflammation, and decreased apoptotic signals, suggesting a protective role for TRESK against SCI-induced pathological conditions.

Practical Implications

Therapeutic Target for SCI

TRESK channels may represent a novel therapeutic target for SCI, with potential for developing analgesic and anti-inflammatory drugs.

Combination Therapy

Combination therapies based on ion channel modulation, including TRESK, may offer an effective approach for treating SCI.

Development of activators/upregulators

TRESK activators and upregulators have the potential to be used for the treatment of the SCI and neuropathic pain.

Study Limitations

1
Changes in membrane potential and excitability in motor and sensory neurons were not measured in WT and TGTRESK sham and SCI models.
2
Subtypes of cells expressing TRESK were not differentiated, limiting a more detailed understanding of the channel's specific roles.
3
Further behavioral tests are needed to comprehensively assess TRESK-related motor and sensory recovery after an SCI.

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