Spinal cord injury-mediated changes in electrophysiological properties of rat gastric nodose ganglion neurons.
Spinal cord injury-mediated changes in electrophysiological properties of rat gastric nodose ganglion neurons.
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DOI：
10.1016/j.expneurol.2021.113927
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发表时间：
2022-03
影响因子：
5.3
通讯作者：
Holmes GM
中科院分区：
文献类型：
--
作者：
Blanke EN;Ruiz-Velasco V;Holmes GM
在临床前啮齿动物模型中，脊髓损伤(SCI)表现为急性和慢性胃迷走神经传入功能障碍。然而，这种功能障碍背后的机制仍不清楚。在本研究中，我们观察了脊髓损伤对急性(3天)和慢性(3周)大鼠胃结节(NG)神经元兴奋性和电压门控Na+(NAV)通道表达和功能的影响。大鼠在实验前3天或3周随机接受T3-SCI或假手术对照手术，并向胃内注射3%DiI溶液以鉴定胃NG神经元。对急性分离的DiI标记的NG神经元进行单细胞qRT-PCR检测Nav1.7、NaV1.8和NaV1.9的表达水平。结果表明，3种通道亚型均有不同程度降低。在急性分离的DiI标记的NG神经元上进行电流和电压钳全细胞膜片钳记录，以测量胃NG神经元C-纤维和A-纤维的主动和被动特性以及NAV1.8通道的生物物理特性。急性和慢性脊髓损伤对分离的胃NG神经元的被动特性和NAV1.8的生物物理特性均无不良影响。这些发现表明，虽然NAV基因表达水平在脊髓损伤后发生了变化，但NAV1.8的功能没有改变。整个迷走神经传入神经元的破坏还有待研究。
In preclinical rodent models, spinal cord injury (SCI) manifests in gastric vagal afferent dysfunction both acutely and chronically. However, the mechanism that underlies this dysfunction remains unknown. In the current study, we examined the effect of SCI on gastric nodose ganglia (NG) neuron excitability and voltage-gated Na+ (NaV) channels expression and function in rats after an acute (i.e. 3-days) and chronic period (i.e. 3-weeks). Rats randomly received either T3-SCI or sham control surgery 3-days or 3-weeks prior to experimentation as well as injections of 3% DiI solution into the stomach to identify gastric NG neurons. Single cell qRT-PCR was performed on acutely dissociated DiI-labeled NG neurons to measure NaV1.7, NaV1.8 and NaV1.9 expression levels. The results indicate that all 3 channel subtypes decreased. Current- and voltage-clamp whole-cell patch-clamp recordings were performed on acutely dissociated DiI-labeled NG neurons to measure active and passive properties of C- and A-fibers as well as the biophysical characteristics of NaV1.8 channels in gastric NG neurons. Acute and chronic SCI did not demonstrate deleterious effects on either passive properties of dissociated gastric NG neurons or biophysical properties of NaV1.8. These findings suggest that although NaV gene expression levels change following SCI, NaV1.8 function is not altered. The disruption throughout the entirety of the vagal afferent neuron has yet to be investigated.
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影响因子：
2.5
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