Lee Jeung Woon, Jergova Stanislava, Furmanski Orion, Gajavelli Shyam, Sagen Jacqueline
Miami Project to Cure Paralysis, Miller School of Medicine, University of Miami Miami, FL, USA.
Front Physiol. 2012 May 31;3:167. doi: 10.3389/fphys.2012.00167. eCollection 2012.
Intraspinal quisqualic acid (QUIS) injury induce (i) mechanical and thermal hyperalgesia, (ii) progressive self-injurious overgrooming of the affected dermatome. The latter is thought to resemble painful dysesthesia observed in spinal cord injury (SCI) patients. We have reported previously loss of endogenous GABA immunoreactive (IR) cells in the superficial dorsal horn of QUIS rats 2 weeks post injury. Further histological evaluation showed that GABA-, glycine-, and synaptic vesicular transporter VIAAT-IR persisted but were substantially decreased in the injured spinal cord. In this study, partially differentiated GABA-IR embryonic neural precursor cells (NPCs) were transplanted into the spinal cord of QUIS rats to reverse overgrooming by replenishing lost inhibitory circuitry. Rat E14 NPCs were predifferentiated in 0.1 ng/ml FGF-2 for 4 h prior to transplantation. In vitro immunocytochemistry of transplant cohort showed large population of GABA-IR NPCs that double labeled with nestin but few colocalized with NeuN, indicating partial maturation. Two weeks following QUIS lesion at T12-L1, and following the onset of overgrooming, NPCs were transplanted into the QUIS lesion sites; bovine adrenal fibroblast cells were used as control. Overgrooming was reduced in >55.5% of NPC grafted animals, with inverse relationship between the number of surviving GABA-IR cells and the size of overgrooming. Fibroblast-control animals showed a progressive worsening of overgrooming. At 3 weeks post-transplantation, numerous GABA-, nestin-, and GFAP-IR cells were present in the lesion site. Surviving grafted GABA-IR NPCs were NeuN(+) and GFAP(-). These results indicate that partially differentiated NPCs survive and differentiate in vivo into neuronal cells following transplantation into an injured spinal cord. GABA-IR NPC transplants can restore lost dorsal horn inhibitory signaling and are useful in alleviating central pain following SCI.
脊髓内注射喹啉酸(QUIS)损伤会导致:(i)机械性和热痛觉过敏,(ii)对受影响皮节进行渐进性自残性过度梳理。后者被认为类似于脊髓损伤(SCI)患者中观察到的疼痛性感觉异常。我们之前报道过,在损伤后2周,QUIS大鼠浅层背角内源性γ-氨基丁酸免疫反应性(IR)细胞缺失。进一步的组织学评估显示,γ-氨基丁酸、甘氨酸和突触囊泡转运体VIAAT-IR在损伤脊髓中持续存在,但大量减少。在本研究中,将部分分化的γ-氨基丁酸-IR胚胎神经前体细胞(NPCs)移植到QUIS大鼠脊髓中,通过补充丢失的抑制性神经回路来逆转过度梳理行为。大鼠E14 NPCs在移植前于0.1 ng/ml碱性成纤维细胞生长因子-2中预分化4小时。移植组的体外免疫细胞化学显示,大量γ-氨基丁酸-IR NPCs与巢蛋白双标,但很少与神经元核抗原共定位,表明部分成熟。在T12-L1节段进行QUIS损伤两周后,在过度梳理行为开始后,将NPCs移植到QUIS损伤部位;牛肾上腺成纤维细胞用作对照。超过55.5%的NPC移植动物的过度梳理行为减少,存活的γ-氨基丁酸-IR细胞数量与过度梳理行为的程度呈负相关。成纤维细胞对照动物的过度梳理行为逐渐恶化。移植后3周,损伤部位出现大量γ-氨基丁酸、巢蛋白和胶质纤维酸性蛋白-IR细胞。存活的移植γ-氨基丁酸-IR NPCs为神经元核抗原阳性和胶质纤维酸性蛋白阴性。这些结果表明,部分分化的NPCs在移植到损伤脊髓后能在体内存活并分化为神经元细胞。γ-氨基丁酸-IR NPC移植可恢复丢失的背角抑制性信号,有助于减轻SCI后的中枢性疼痛。