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. 2012;7(5):e37621.
doi: 10.1371/journal.pone.0037621. Epub 2012 May 18.

Effects of exogenous galanin on neuropathic pain state and change of galanin and its receptors in DRG and SDH after sciatic nerve-pinch injury in rat

Xiaofeng Xu  1 , Xiangdong Yang, Ping Zhang, Xiuying Chen, Huaxiang Liu, Zhenzhong Li
Affiliations

Effects of exogenous galanin on neuropathic pain state and change of galanin and its receptors in DRG and SDH after sciatic nerve-pinch injury in rat

Xiaofeng Xu et al. PLoS One. 2012.

Abstract

A large number of neuroanatomical, neurophysiologic, and neurochemical mechanisms are thought to contribute to the development and maintenance of neuropathic pain. However, mechanisms responsible for neuropathic pain have not been completely delineated. It has been demonstrated that neuropeptide galanin (Gal) is upregulated after injury in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH) where it plays a predominantly antinociceptive role. In the present study, sciatic nerve-pinch injury rat model was used to determine the effects of exogenous Gal on the expression of the Gal and its receptors (GalR1, GalR2) in DRG and SDH, the alterations of pain behavior, nerve conduction velocity (NCV) and morphology of sciatic nerve. The results showed that exogenous Gal had antinociceptive effects in this nerve-pinch injury induced neuropathic pain animal model. It is very interesting that Gal, GalR1 and GalR2 change their expression greatly in DRG and SDH after nerve injury and intrathecal injection of exougenous Gal. Morphological investigation displays a serious damage after nerve-pinch injury and an amendatory regeneration after exogenous Gal treatment. These findings imply that Gal, via activation of GalR1 and/or GalR2, may have neuroprotective effects in reducing neuropathic pain behaviors and improving nerve regeneration after nerve injury.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. The mechanical threshold alterations with different treatment from day 0 to day 24.
The data are presented as means ± SD (n = 7). *P<0.05 vs. control, **P<0.01 vs. control, ***P<0.001 vs. control, # P<0.05 vs. pinch + Gal group, ## P<0.01 vs. pinch + Gal group, ### P<0.001 vs. pinch + Gal group.
Figure 2
Figure 2. The thermal threshold alterations with different treatment from day 0 to day 24.
The data are presented as means ± SD (n = 7). *P<0.05 vs. control, **P<0.01 vs. control, ***P<0.001 vs. control, # P<0.05 vs. pinch + Gal group, ## P<0.01 vs. pinch + Gal group, ### P<0.001 vs. pinch + Gal group.
Figure 3
Figure 3. The NCV alterations at different experimental conditions.
Panel A: MNCV decreased significantly after sciatic nerve-pinch injury at day 16 and 24 as compared with that in sham-operated control animals. Gal treatment improved MNCV significantly at the same experimental time point. Panel B: SNCV decreased significantly after sciatic nerve-pinch injury at day 16 and 24 as compared with that in sham-operated control animals. Gal treatment improved SNCV significantly at the same experimental time point. The data are presented as mean ± SD (n = 7). *P<0.05, **P<0.01, ***P<0.001.
Figure 4
Figure 4. Expression of mRNAs for Gal, GalR1, and GalR2 in DRG and SDH.
Panel A: Gal mRNA levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel B: Gal mRNA levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel C: GalR1 mRNA levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel D: GalR1 mRNA levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel E: GalR2 mRNA levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel F: GalR2 mRNA levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. The mRNA level was expressed as the ratio of control. The data are presented as mean ± SD (n = 7). *P<0.05, **P<0.01, ***P<0.001.
Figure 5
Figure 5. Expression of Gal, GalR1, and GalR2 in DRG and SDH.
Panel A1, A2: Gal protein levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel B1, B2: Gal protein levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel C1, C2: GalR1 protein levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel D1, D2: GalR1 protein levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel E1, E2: GalR2 protein levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel F1, F2: GalR2 protein levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Lane 1: pinch 8 d; Lane 2: pinch + Gal 8 d; Lane 3: control 8 d; Lane 4: pinch 16 d; Lane 5: pinch + Gal 16 d; Lane 6: control 16 d; Lane 7: pinch 24 d; Lane 8: pinch + Gal 24 d; Lane 9: control 24 d. The protein level was expressed as the ratio of control. The data are presented as mean ± SD (n = 7). *P<0.05, **P<0.01, ***P<0.001.
Figure 6
Figure 6. Semi-thin cross sections of sciatic nerve with toluidine blue staining.
Panel A1, A2 and A3: The dystrophy appearance of nerve fibers after sciatic nerve-pinch injury at day 8, 16, and 24, respectively. The internal structure of the nerve was severely disorganized, sometimes with apparently enlarged nerve fibers (arrows) in Panel A1 or A2. Panel B1 and B2: The dystrophy appearance improved at day 8 and 16, respectively, after sciatic nerve-pinch injury with Gal treatment as compared with that in Panel A1 and A2. Panel B3: Most of the nerve fibers recovered to almost normal status at day 24 after sciatic nerve-pinch injury with Gal treatment. Panel C1, C2, and C3: Normal appearance of the sciatic nerve, with small and large diameter myelinated fibers regularly distributed in sham-operated control animals at day 8, 16 and day 24, respectively, after sham operation. Scale bar = 10 µm.
Figure 7
Figure 7. TEM micrograph of ultrathin cross sections of sciatic nerve.
Panel A1, A2 and A3: Myelinated axons after sciatic nerve-pinch injury at day 8, 16, and 24, respectively. Degenerating myelinated axons are characterized by loss of axoplasm and subsequent myelin breakdown in Panel A1 and A2. Panel A3 showed the recovered myelin without clearly layers. The lost axoplasm is partially recovered. Panel B1, B2 and B3: Myelinated axons after sciatic nerve-pinch injury with Gal treatment at day 8, 16, and 24, respectively. The axoplasm loss and myelin breakdown in Panel B1 are less severe than those in Panel A1. The lost axoplasm is almost recovered and the broken myelin is recovering in most of the area in Panel B2. Panel B3 showed the recovered myelin with clearly layers. Only small areas have myelin debris (arrows) in Panel B3. Panel C1, C2, and C3: The ultrastructurally normal myelinated axons of sciatic nerve in sham-operated control animals at day 8, 16 and day 24, respectively, after sham operation. Scale bar = 1 µm.
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