胶质纤维酸性蛋白
背根神经节
SNi公司
星形胶质细胞
病理
生物
GFAP染色
神经胶质
神经损伤
神经科学
细胞生物学
解剖
中枢神经系统
背
免疫组织化学
医学
生物化学
水解
酸水解
作者
Elena A. Konnova,Alexandru‐Florian Deftu,Paul Chu Sin Chung,Marie Pertin,Guylène Kirschmann,Isabelle Décosterd,Marc R. Suter
标识
DOI:10.3390/ijms242115559
摘要
Satellite glial cells (SGCs), enveloping primary sensory neurons’ somas in the dorsal root ganglion (DRG), contribute to neuropathic pain upon nerve injury. Glial fibrillary acidic protein (GFAP) serves as an SGC activation marker, though its DRG satellite cell specificity is debated. We employed the hGFAP-CFP transgenic mouse line, designed for astrocyte studies, to explore its expression within the peripheral nervous system (PNS) after spared nerve injury (SNI). We used diverse immunostaining techniques, Western blot analysis, and electrophysiology to evaluate GFAP+ cell changes. Post-SNI, GFAP+ cell numbers increased without proliferation, and were found near injured ATF3+ neurons. GFAP+ FABP7+ SGCs increased, yet 75.5% of DRG GFAP+ cells lacked FABP7 expression. This suggests a significant subset of GFAP+ cells are non-myelinating Schwann cells (nmSC), indicated by their presence in the dorsal root but not in the ventral root which lacks unmyelinated fibres. Additionally, patch clamp recordings from GFAP+ FABP7−cells lacked SGC-specific Kir4.1 currents, instead displaying outward Kv currents expressing Kv1.1 and Kv1.6 channels specific to nmSCs. In conclusion, this study demonstrates increased GFAP expression in two DRG glial cell subpopulations post-SNI: GFAP+ FABP7+ SGCs and GFAP+ FABP7− nmSCs, shedding light on GFAP’s specificity as an SGC marker after SNI.
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