Collateral Sprouting of Uninjured Primary Afferent A-Fibers into the Superﬁcial Dorsal Horn of the Adult Rat Spinal Cord after Topical Capsaicin Treatment to the Sciatic Nerve

The Journal of Neuroscience, 1996 · DOI: · Published: August 15, 1996

Spinal Cord Injury Neurology Pain Management

Simple Explanation

This study investigates how nerve damage affects the spinal cord. Specifically, it looks at whether damage to certain nerve fibers (C-fibers) can cause other nerve fibers (A-fibers) to grow into areas of the spinal cord where they don't normally go. The researchers used a chemical called capsaicin to damage the C-fibers in rats. They then looked to see if the A-fibers started growing into a specific region of the spinal cord called lamina II. The results showed that when C-fibers were damaged, A-fibers did indeed grow into lamina II. This suggests that damage to one type of nerve fiber can cause other nerve fibers to reorganize and grow into new areas of the spinal cord.

Study Duration

2 Weeks

Participants

24 Adult male Sprague Dawley rats

Evidence Level

Level III, Experimental Study

Key Findings

1
Topical capsaicin treatment to the sciatic nerve results in novel transganglionic B-HRP staining in lamina II.
2
The somatotopic distribution of the sprouted B-HRP terminals in lamina II overlapped almost exactly with the zone of TMP depletion.
3
No difference was found between the extent and distribution of B-HRP staining in lamina II after axotomy or capsaicin treatment of the sciatic nerve.

Research Summary

This study demonstrates that topical capsaicin treatment to the sciatic nerve results in novel transganglionic B-HRP staining in lamina II, suggesting that uninjured A-fiber central terminals can collaterally sprout into lamina II of the dorsal horn after C-fiber injury. The somatotopic distribution of the sprouted B-HRP terminals in lamina II overlapped almost exactly with the zone of TMP depletion, indicating a close relationship between C-fiber degeneration and A-fiber sprouting. The sprouting produced by complete section of the sciatic nerve and local damage restricted to the C-fiber component of the nerve was indistinguishable.

Practical Implications

Understanding Neuropathic Pain

The study suggests that the pain associated with C-fiber neuropathies may be explained by the sprouting of uninjured A-fibers into lamina II, an area of the spinal cord that normally only processes C-fiber input.

Potential Therapeutic Targets

Identifying the signaling mechanisms responsible for A-fiber sprouting after C-fiber injury could lead to the development of novel therapeutic strategies for managing neuropathic pain.

Reassessing Capsaicin Use

The findings suggest a need for careful assessment of the potential for low-dose capsaicin cream to introduce novel neuropathic pain, especially in patients already experiencing allodynia.

Study Limitations

1
The study was conducted on rats, and the findings may not be directly applicable to humans.
2
It is not possible to quantify the extent of denervation produced by either peripheral axotomy or perineural capsaicin application or determine whether the amount of denervation correlates with the amount of collateral sprouting.
3
The signaling mechanism responsible for A-fiber sprouting both after nerve injury and after a neurotoxic injury restricted to C-fibers is unknown.

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