Capsaicin-induced neuronal death and proliferation of the primary sensory neurons located in the nodose ganglia of adult rats
Capsaicin-induced neuronal death and proliferation of the primary sensory neurons located in the nodose ganglia of adult rats
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DOI：
10.1016/j.neuroscience.2008.03.055
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发表时间：
2008-06-23
期刊：
影响因子：
3.3
通讯作者：
Ritter, R. C.
中科院分区：
文献类型：
--
作者：
Czaja, K.;Burns, G. A.;Ritter, R. C.
为了评估迷走神经传入神经元被破坏后神经元替换的可能性，我们检查了ip.辣椒素对成年大鼠的治疗作用。大鼠接受辣椒素或赋形剂，然后注射5‘-溴-2’-脱氧尿苷(BrdU)以显示DNA复制。治疗后不同时间取结状神经节，行4‘，6-二氨基-2-苯吲哚(DAPI)核染色和免疫荧光染色，计数神经元数目，测定香草样受体、裂解半胱氨酸天冬氨酸氨基转移酶3(TUNEL)、BrdU、神经元选择性标志物蛋白基因产物(PGP)-9.5和神经丝蛋白-M免疫反应性。辣椒素处理24小时后，约40%的结状神经节神经元表达裂解的caspase3免疫反应阳性，16%的神经元显示TUNEL染色，表明辣椒素处理成年大鼠的初级感觉神经元被杀死。DAPI染色的神经元核计数证实了神经元死亡的发生，这表明辣椒素处理30d后结节神经元数量减少了50%。然而，在辣椒素处理60d后，辣椒素处理组大鼠结状神经节中的神经元核总数与对照组没有差异，这表明结状神经节中增加了新的神经元。辣椒素处理后30天和60天，神经元特异性抗原PGP-9.5免疫反应阳性的结状神经节细胞胞核内有明显的BrdU掺入，证实神经元的增殖。总之，这些观察表明，在辣椒素诱导的神经元破坏后，成年大鼠的结状神经节发生了大规模的神经再生。因此，成体结状神经节为研究初级感觉神经元外周损伤后的神经可塑性和成体神经发生提供了一个新的系统。爱思唯尔有限公司代表伊布罗出版。
To evaluate the potential for neuronal replacement following destruction of vagal afferent neurons, we examined nodose ganglia following i.p. capsaicin treatment of adult rats. Rats received capsaicin or vehicle followed by a regimen of 5'-bromo-2'-deoxyuridine injections (BrdU) to reveal DNA replication. Nodose ganglia were harvested at various times post-treatment and processed for 4',6-diamidino-2-phenylindole (DAPI) nuclear staining and immunofluorescence to estimate neuronal numbers and to determine vanilloid receptor, cleaved caspase 3, TUNEL, BrdU, the neuron-selective marker protein gene product (PGP) -9.5 and neurofilament-M-immunoreactivity. Twenty-four hours after capsaicin approximately 40% of nodose ganglion neurons expressed cleaved caspase 3-immunoreactivity and 16% revealed TUNEL staining, indicating that primary sensory neurons are killed by the capsaicin treatment of adult rats. The occurrence of neuronal death was confirmed by counts of DAPI-stained neuronal nuclei, which revealed >= 50% reduction of nodose neuron number by 30 days post-capsaicin. However, by 60 days post-capsaicin, the total numbers of neuronal nuclei in nodose ganglia from capsaicin-treated rats were not different from controls, suggesting that new neurons had been added to the nodose ganglia. Neuronal proliferation was confirmed by significant BrdU incorporation in nuclei of nodose ganglion cells immunoreactive for the neuron-specific antigen PGP-9.5 revealed 30 and 60 days post-capsaicin. Collectively, these observations suggest that in adult rats massive scale neurogenesis occurs in nodose ganglia following capsaicin-induced neuronal destruction. The adult nodose ganglion, therefore, provides a novel system for studying neural plasticity and adult neurogenesis after peripheral injury of primary sensory neurons. Published by Elsevier Ltd on behalf of IBRO.