Abstract
In this study, we investigated temporal changes in galanin receptor type 2 (GalR2) expression in NF200-, galanin-, neuropeptide Y (NPY)-, and neuronal nitric oxide synthase (nNOS)-like immunoreactive (LI) dorsal root ganglion (DRG) neurons after median nerve chronic constriction injury (CCI), and the effects of GalR2 on c-Fos expression in the cuneate nucleus (CN). Double immunofluorescence labeling methods were used to appraise changes in GalR2 expression in NF200-LI, galanin-LI, NPY-LI, and nNOS-LI DRG neurons after CCI. The von Frey assay was used to assess the efficiency of intraplantar administration of saline, M871 (a GalR2 antagonist), or AR-M1896 (a GalR2 agonist) on neuropathic signs of rats with CCI. The effects of alterations in c-Fos expression were assessed in all treatments. The percentage of GalR2-LI neurons in lesioned DRGs increased and peaked at 1 week after CCI. We further detected that percentages of GalR2-LI neurons labeled for NF200, galanin, NPY, and nNOS significantly increased following CCI. Furthermore, M871 remarkably attenuated tactile allodynia, but the sensation was slightly aggravated by AR-M1896 after CCI. Consequentially, after electrical stimulation of the CCI-treated median nerve, the number of c-Fos-LI neurons in the cuneate nucleus (CN) was significantly reduced in the M871 group, whereas it increased in the AR-M1896 group. These results suggest that activation of GalR2, probably through NPY or nitric oxide, induces c-Fos expression in the CN and transmits mechanical allodynia sensations to the thalamus.
Highlights
The cuneate nucleus (CN) receives innocuous tactile and proprioceptive signals from forelimb areas through primary Aβ afferent fibers and relays the information to the contralateral thalamus [1,2,3,4,5]
With double-labeling, percentages of galanin receptor type 2 (GalR2)-like immunoreactive (LI) neurons in constriction injury (CCI) dorsal root ganglion (DRG) colocalized with NF200 (Fig 3), galanin (Fig 4), neuropeptide Y (NPY) (Fig 5), and neuronal nitric oxide synthase (nNOS) (Fig 6) had significantly increased compared to the control group
The present study revealed that median nerve injury upregulated amounts of galanin-LI and GalR2-LI neurons in injured DRGs
Summary
The cuneate nucleus (CN) receives innocuous tactile and proprioceptive signals from forelimb areas through primary Aβ afferent fibers and relays the information to the contralateral thalamus [1,2,3,4,5]. The CN plays a role in transmission of neuropathic pain signaling, which is partly mediated by changes in neuropeptide expression [1, 6–. Previous studies showed that median nerve injury leads to significant increase in neuropeptide Y (NPY) and neuronal nitric oxide synthase (nNOS) in the lesioned side of the CN and cervical dorsal root ganglion (DRG) neurons [6, 8, 10]. Microinjection of NPY receptor antagonist ameliorated median nerve injury-induced tactile hypersensitivity and decreased c-Fos expression in the CN [7]. A previous study showed that galanin is dramatically induced in the injured side of the CN following median nerve injury [8]; detailed information about galanin immunolabeling in cervical DRG neurons after median nerve injury is not available
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