Experimental study of urinary center change in pons after conus medullaris injury in rats_Chinese Journal of Reparative and Reconstructive Surgery

Authors：

YU Ronghua ^1,2 ,  HOU Chunlin ² , LIN Haodong ² , ZHAO Jianguo ² , ZONG Haiyang ² , LIN Yaofa ²

1. Second Military Medical University, Shanghai, 200433, P.R.China;
2. Department of Orthopaedics, Changzheng Hospital, Shanghai, 200003, P.R.China;

Corresponding author：

HOU Chunlin, Email: chunlin_hou@163.com

Keywords：

Spinal cord injury; pons; Bcl-2; cell apoptosis; neuron; rat

DOI：

10.7507/1002-1892.201708126

Video：

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Objective To observe the structural changes of urinary center and the expression of Bcl-2 after conus medullaris injury in rats brain so as to explore the possible influence factors of degeneration in brain. Methods Thirty-six adult Sprague-Dawley rats were randomly divided into experimental group (n=30) and control group (n=6). In the experimental group, the conus medullaris injury model was established by cutting off the spinal nerve below L₄, and no treatment was done in the control group. The modeling operations in the experimental group were successful, and 2 rats died at 3 months and 5 months after modeling operation respectively, which may be caused by renal failure or urinary tract infection. In the experimental group, 6, 6, 6, 5, and 5 rats were killed at 1 day, 1 week, and 1, 3, 6 months after operation respectively, and 1 rat was killed at each time point in the control group. The dorsolateral tissue of the pontine tegmentum was harvested to perform HE staining and Bcl-2 immunohistochemical SP staining. Results HE staining showed that there was no obvious difference between the experimental group and the control group at 1 day after operation, the neurons were densely packed, arranged neatly, and the nucleoli were clear; at 1 week, the space between the neurons in the experimental group were slightly widened; at 1 month, nucleus retraction in some neurons happened in the experimental group; at 3 and 6 months, the nuclei in the experimental group were more and more condensed, and even some cells disappeared. Bcl-2 immunohistochemical SP staining showed that the expression of Bcl-2 in the control group was weakly positive. The positive expression of Bcl-2 was found at 1 day after operation in the experimental group; the positive expression of Bcl-2 at 7 days after operation was significantly higher than that in the control group, and reached the peak; the positive expression of Bcl-2 decreased gradually at 1, 3, and 6 months after modeling operation, but it was still higher than that of the control group. Conclusion The urinary center appears structure degeneration and necrocytosis after conus medullaris injury in rats brain. The elevated expression of Bcl-2 may be associated with brain tissue repair and function remodeling.

Citation： YU Ronghua, HOU Chunlin, LIN Haodong, ZHAO Jianguo, ZONG Haiyang, LIN Yaofa. Experimental study of urinary center change in pons after conus medullaris injury in rats. Chinese Journal of Reparative and Reconstructive Surgery, 2018, 32(1): 75-79. doi: 10.7507/1002-1892.201708126 Copy

1.	Wang M, Li ZY, Xu WD, et al. Sensory restoration in cortical level after a contralateral C₇ nerve transfer to an injured arm in rats. Neurosurgery, 2010, 67(1): 136-143.
2.	Navarro X, Vivó M, Valero-Cabré A. Neural plasticity after peripheral nerve injury and regeneration. Prog Neurobiol, 2007, 82(4): 163-201.
3.	Lin H, Hou C, Chen A. Reconstructed bladder innervation above the level of spinal cord injury to produce urination by abdomen-to-bladder reflex contractions. J Neurosurg Spine, 2011, 14(6): 799-802.
4.	Lin H, Hou C, Chen A, et al. Reinnervation of atonic bladder after conus medullaris injury using a modified nerve crossover technique in canines. World Neurosurg, 2010, 73(5): 582-586.
5.	Lin H, Hou C, Chen A, et al. Innervation of reconstructed bladder above the levelof spinal cord injury for inducing micturition by contractions of the abdomen-to-bladder reflex arc. Neurosurgery, 2010, 66(5): 948-952.
6.	Lin H, Hou C, Zhen X. Bypassing spinal cord injury: surgical reconstruction of afferent and efferent pathways to the urinary bladder after conus medullaris injury in a rat model. J Reconstr Microsurg, 2008, 24: 575-581.
7.	Satoh K, Shimizu N, Tohyama M, et al. Localization of the micturitionreflex center at dorsolateral pontine tegmentum of the rat. Neurosci Lett, 1978, 8(1): 27-33.
8.	Lee BH, Lee KH, Kim UJ, et al. Injury in the spinal cord may produce cell death in the brain. Brain Res, 2004, 1020(1-2): 37-44.
9.	Wu JF, Stoica BA, Luo T, et al. Isolated spinal cord contusion in rats induces chronic brain neuroinflammation, neurodegeneration, and cognitive impairment. Cell Cycle, 2014, 13(15): 2446-2458.
10.	Felix MS, Popa N, Matarazzo VA, et al. Alteration of forebrain neurogenesis after cervical spinal cord injury in the adult rat. Front Neurosci, 2012, 6: 45.
11.	Wecht JM, Bauman WA. Decentralized cardiovascular autonomic control and cognitive deficits in persons with spinal cord injury. J Spinal Cord Med, 2013, 36(2): 74-81.
12.	Hains BC, Black JA, Waxman SG. Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury. J Comp Neurol, 2003, 462(3): 328-341.
13.	McBride RL, Feringa ER, Garver MK, et al. Prelabeled red nucleus and sensorimotor cortex neurons of the rat survive 10 and 20 weeks after spinal cord transection. J Neuropathol Exp Neurol, 1989, 48(5): 568-576.
14.	Graham SH, Chen J, Clark RS. Bcl-2 family gene products in cerebral ischemia and traumatic brain injury. J Neurotrauma, 2000, 17(10): 831-841.
15.	Schulman JJ, Wright FA, Kaufmann T, et al. The Bcl-2 family member Bok binds to the coupling domain of inositol 1, 4, 5-trisphate receptors and protects them from proteolytic cleavage. Biol Chem, 2013, 288(35): 25340-25349.
16.	Clark RS, Chen J, Watkins SC, et al. Apoptosis suppressor gene Bcl-2 expression after traumatic brain injury in rats. J Neurosci, 1997, 17(23): 9172-9182.
17.	Luo J, Lenke LG, Xu F, et al.In vivo Bcl -2 oncogene neuronal expression in the spinal cord. Spine (Phila Pa1976), 1998, 23(5): 517-523.
18.	Pallini R, Fernandez E, Sbriccoli A. Retrograde degeneration of corticospinal axons following transection of the spinal cord in rats. A quantitative study with anterogradely transported horseradish peroxidase. J Neurosurg, 1988, 68(1): 124-128.

1. Wang M, Li ZY, Xu WD, et al. Sensory restoration in cortical level after a contralateral C₇ nerve transfer to an injured arm in rats. Neurosurgery, 2010, 67(1): 136-143.
2. Navarro X, Vivó M, Valero-Cabré A. Neural plasticity after peripheral nerve injury and regeneration. Prog Neurobiol, 2007, 82(4): 163-201.
3. Lin H, Hou C, Chen A. Reconstructed bladder innervation above the level of spinal cord injury to produce urination by abdomen-to-bladder reflex contractions. J Neurosurg Spine, 2011, 14(6): 799-802.
4. Lin H, Hou C, Chen A, et al. Reinnervation of atonic bladder after conus medullaris injury using a modified nerve crossover technique in canines. World Neurosurg, 2010, 73(5): 582-586.
5. Lin H, Hou C, Chen A, et al. Innervation of reconstructed bladder above the levelof spinal cord injury for inducing micturition by contractions of the abdomen-to-bladder reflex arc. Neurosurgery, 2010, 66(5): 948-952.
6. Lin H, Hou C, Zhen X. Bypassing spinal cord injury: surgical reconstruction of afferent and efferent pathways to the urinary bladder after conus medullaris injury in a rat model. J Reconstr Microsurg, 2008, 24: 575-581.
7. Satoh K, Shimizu N, Tohyama M, et al. Localization of the micturitionreflex center at dorsolateral pontine tegmentum of the rat. Neurosci Lett, 1978, 8(1): 27-33.
8. Lee BH, Lee KH, Kim UJ, et al. Injury in the spinal cord may produce cell death in the brain. Brain Res, 2004, 1020(1-2): 37-44.
9. Wu JF, Stoica BA, Luo T, et al. Isolated spinal cord contusion in rats induces chronic brain neuroinflammation, neurodegeneration, and cognitive impairment. Cell Cycle, 2014, 13(15): 2446-2458.
10. Felix MS, Popa N, Matarazzo VA, et al. Alteration of forebrain neurogenesis after cervical spinal cord injury in the adult rat. Front Neurosci, 2012, 6: 45.
11. Wecht JM, Bauman WA. Decentralized cardiovascular autonomic control and cognitive deficits in persons with spinal cord injury. J Spinal Cord Med, 2013, 36(2): 74-81.
12. Hains BC, Black JA, Waxman SG. Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury. J Comp Neurol, 2003, 462(3): 328-341.
13. McBride RL, Feringa ER, Garver MK, et al. Prelabeled red nucleus and sensorimotor cortex neurons of the rat survive 10 and 20 weeks after spinal cord transection. J Neuropathol Exp Neurol, 1989, 48(5): 568-576.
14. Graham SH, Chen J, Clark RS. Bcl-2 family gene products in cerebral ischemia and traumatic brain injury. J Neurotrauma, 2000, 17(10): 831-841.
15. Schulman JJ, Wright FA, Kaufmann T, et al. The Bcl-2 family member Bok binds to the coupling domain of inositol 1, 4, 5-trisphate receptors and protects them from proteolytic cleavage. Biol Chem, 2013, 288(35): 25340-25349.
16. Clark RS, Chen J, Watkins SC, et al. Apoptosis suppressor gene Bcl-2 expression after traumatic brain injury in rats. J Neurosci, 1997, 17(23): 9172-9182.
17. Luo J, Lenke LG, Xu F, et al.In vivo Bcl -2 oncogene neuronal expression in the spinal cord. Spine (Phila Pa1976), 1998, 23(5): 517-523.
18. Pallini R, Fernandez E, Sbriccoli A. Retrograde degeneration of corticospinal axons following transection of the spinal cord in rats. A quantitative study with anterogradely transported horseradish peroxidase. J Neurosurg, 1988, 68(1): 124-128.

Chinese Journal of Reparative and Reconstructive Surgery

Experimental study of urinary center change in pons after conus medullaris injury in rats

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