Data on the expression of leptin and leptin receptor in the dorsal root ganglion and spinal cord after preganglionic cervical root avulsion

Data in Brief, 2017 · DOI: 10.1016/j.dib.2017.10.005 · Published: October 7, 2017

Spinal Cord Injury Neurology Pain Management

Simple Explanation

This study investigates the expression of leptin (Lep) and its receptor (LepR) in the dorsal root ganglion (DRG) and spinal cord after preganglionic cervical root avulsion (PCRA). Leptin, primarily secreted by adipocytes, is known to be involved in neuropathic pain after peripheral nerve injuries. The researchers found profound Lep and LepR expression in DRG neurons after PCRA. They also identified Lep and LepR in neurons and microglia within the dorsal horn of the spinal cord. These findings suggest a potential role for leptin signaling in the development of neuropathic pain following PCRA, warranting further investigation into the mechanisms and implications of these increased expressions.

Study Duration

7 days

Participants

10 C57BL/6J mice

Evidence Level

Not specified

Key Findings

1
Generalized expression of Lep and LepR was noted 7 days after PCRA in DRG neurons.
2
Substantial intracellular expression of Lep was noted in the neurons of spinal cord after PCRA.
3
Significant amount of Lep was noted in the dorsal horn of the spinal cord in neurons and microglia, but not in astrocytes.

Research Summary

This data article presents findings on the expression patterns of leptin (Lep) and its receptor (LepR) in the dorsal root ganglion (DRG) and spinal cord following preganglionic cervical root avulsion (PCRA) in mice. The study demonstrates increased expression of both Lep and LepR in DRG neurons and in neurons and microglia within the dorsal horn after PCRA. These findings suggest a potential role for leptin signaling in the pathophysiology of neuropathic pain following PCRA, highlighting the need for further research to elucidate the underlying mechanisms.

Practical Implications

Neuropathic Pain Mechanisms

The increased expression of Lep and LepR in neurons and microglia after PCRA suggests a role for leptin signaling in the development and maintenance of neuropathic pain.

Microglial Activation

The finding that a significant number of microglia exhibit LepR expression after PCRA, unlike after PNI, indicates a potentially distinct mechanism of microglial activation in PCRA-induced neuropathic pain.

Therapeutic Targets

Understanding the roles of Lep and LepR in neuropathic pain after PCRA may lead to the development of targeted therapies to alleviate pain symptoms in patients with nerve root avulsions.

Study Limitations

1
The functions and/or effect of the leptin produced by neurons undergoing apoptosis remain to be clarified.
2
The roles of the intraneuronal Lep in the development of neuropathic pain have not been studied.
3
The control mechanism and the significance of this de novo production of Lep are of interest for future investigation.

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