Spinal HDAC6 mediates nociceptive behaviors induced by chronic constriction injury via neuronal activation and neuroinﬂammation

Molecular Pain, 2023 · DOI: 10.1177/17448069231218352 · Published: November 10, 2023

Simple Explanation

This study investigates the role of HDAC6, an enzyme, in neuropathic pain (NP) development following nerve injury in mice. They found that HDAC6 levels increase in the spinal cord after injury. The researchers used a drug called ACY-1215 to block HDAC6 and found it reduced pain and suppressed neuron activation and neuroinflammation in the mice. The results suggest that HDAC6 could be a target for new treatments for neuropathic pain.

Study Duration

Not specified

Participants

Male C57BL/6 mice (8 weeks old, weighing 21–25 g)

Evidence Level

Not specified

Key Findings

1
HDAC6 expression is upregulated in the spinal cord following chronic constriction injury (CCI).
2
Inhibition of HDAC6 with ACY-1215 alleviates mechanical allodynia in CCI mice.
3
HDAC6 inhibition suppresses CCI-induced pyroptosis and neuroinflammatory responses via the NF-κB/NLRP3 pathway.

Research Summary

The study investigates the role of HDAC6 in neuropathic pain (NP) induced by chronic constriction injury (CCI) in mice, finding that HDAC6 expression is upregulated in the spinal cord following CCI. The researchers found that inhibiting HDAC6 with ACY-1215 reduced mechanical allodynia and suppressed neuron activation, pyroptosis, and neuroinflammation in the CCI mice. The study concludes that HDAC6 contributes to the development and maintenance of NP through neuronal activation and neuroinflammation, suggesting it as a potential therapeutic target for NP.

Practical Implications

Therapeutic Target

HDAC6 may be a promising therapeutic target for treating neuropathic pain.

Drug Development

ACY-1215, a specific HDAC6 inhibitor, shows potential for alleviating mechanical allodynia.

Mechanism Understanding

HDAC6 contributes to NP through neuronal activation and neuroinflammation, providing insights into the pathogenesis of neuropathic pain.

Study Limitations

1
The study was conducted on mice, and results may not directly translate to humans.
2
The specific types of receptors on neurons affected by neuroinflammation were not determined.
3
Further investigations are needed to determine the pathways and potential transmitter-receptor interactions that regulate glial activation.

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