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

Leptin (Lep) is mainly, although not exclusively, secreted by adipocytes. In addition to regulating lipid metabolism, it is also a proinflammatory factor and involved in the development of neuropathic pain after peripheral nerve injuries (PNI) (Lim et al., 2009; Maeda et al., 2009) [1,2]. Leptin or its messenger ribonucleic acid expression has been found in various brain regions normally and in the dorsal horn after PNI (Lim et al., 2009; Ur et al., 2002; La Cava et al., 2004; White et al., 2004) [1,[3], [4], [5]]. However, the expression pattern of Lep and Leptin receptor (LepR) after preganglionic cervical root avulsion (PCRA) is still unknown. We provide data in this article related to Chang et al. (2017) [6]. Here, our data showed a profound Lep and LepR expression in the neurons of dorsal root ganglion (DRG) after PCRA. Moreover, the expression of Lep and LepR were also identified in significant portions of the neurons and microglia located in the dorsal horn. The roles of these increased expressions in the development of neuropathic pain after PCRA deserve further study.


a b s t r a c t
Leptin (Lep) is mainly, although not exclusively, secreted by adipocytes. In addition to regulating lipid metabolism, it is also a proinflammatory factor and involved in the development of neuropathic pain after peripheral nerve injuries (PNI) (Lim et al., 2009;Maeda et al., 2009) [1,2]. Leptin or its messenger ribonucleic acid expression has been found in various brain regions normally and in the dorsal horn after PNI (Lim et al., 2009;Ur et al., 2002;La Cava et al., 2004;White et al., 2004) [1,[3][4][5]. However, the expression pattern of Lep and Leptin receptor (LepR) after preganglionic cervical root avulsion (PCRA) is still unknown. We provide data in this article related to Chang et al. (2017) [6]. Here, our data showed a profound Lep and LepR expression in the neurons of dorsal root The DRG and DH were labeled using primary antibodies raised against leptin, its receptor, ionized calcium binding adaptor molecule 1 (Iba1, microglia), neuronal nuclei (NeuN, neuron), and glial fibrillary acidic protein (GFAP, astrocyte).

Data source location
Taipei, Taiwan.

Value of the Data
Generalized expression of Lep and LepR was noted 7 days after PCRA in DRG neurons. However, it has been reported that around 95% of DRG neurons die after PCRA [7]. The functions and/or effect of the leptin produced by neurons undergoing apoptosis remain to be clarified.
Substantial intracellular expression of Lep was noted in the neurons of spinal cord after PCRA. It is known that extracellular leptin acts on its receptor located in the cell membrane of neurons. However, the roles of the intraneuronal Lep in the development of neuropathic pain have not been studied.
Significant amount of Lep was noted in the dorsal horn of the spinal cord in neurons and microglia, but not in astrocytes. The control mechanism and the significance of this de novo production of Lep are of interest for future investigation.
It is reported that LepR has been found to be increased after PNI in neurons, and to a lesser extent in astrocytes [1]. But after PCRA, we found that significant number of microglia has LepR expression. Does this difference be relevant to the different clinical presentation of the neuropathic pain after PNI and PCRA requires further research.

Data
We showed that both Lep and LepR were expressed in the DRG on day 7th after PCRA (Fig. 1). By using double immunolabeling for Lep/LepR and markers of specific cell populations, we found that after PCRA, there are increased expression of leptin in the dorsal horn [6]. This increased leptin expression was colocalized with NeuN (19%) and Iba1 (37%), but not with GFAP (Fig. 2). Similarly, increased expression of LepR was also noted [6]. The LepR was also coexpressed with NeuN (56%) and Iba1 (47%), but not with GFAP (Fig. 3).

Animals
Adult male and female C57BL/6J (n ¼ 10) were obtained from the National Laboratory Animal Center in Taiwan. All animals were housed in ventilated and humidity-and temperature-controlled rooms with a 12 h/12 h light/dark cycle. Food and water were provided ad libitum.

Surgical procedures
The 13-week-old male and female C57BL/6J mice (23.5 7 3.8 g) (n ¼ 10) were anaesthetized using isoflurane and placed on a heating pad. Rectal temperatures were monitored during surgery. All animals received a left hemi-laminectomy at the cervical 5th-7th vertebrae. After the dura was opened, the left 6th-8th cervical dorsal roots were identified, gently pulled, and avulsed at their junctions with the spinal cord, leaving no proximal stump.