Identification and validation of Rab11a in Rat orofacial inflammatory pain model induced by CFA

Liu, Miaomiao; Li, Xin; Wang, Jian; Ji, Yuanyuan; Gu, Jianying; Yi, Wei; Peng, Liwei; Tian, Chunjuan; Lv, Peiyuan; Wang, Peng; Liu, X.; Li, Weixin

doi:10.1016/j.neuint.2023.105550

Cited by 2 publications

(8 citation statements)

References 40 publications

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“…It’s shown that 89.15% Rab11a-immunoreactivities were in cytoplasm of neurons (Fig. 1 C1-C4 and D), which is consistent with previous reports [ 14 ]. In contrast, only a small proportion of Rab11a-positive cells were co-labeled with glial fibrillary acidic protein (GFAP) (Fig.…”

Section: Resultssupporting

confidence: 92%

“…Consistent with our recent study [ 14 ] on a rat orofacial inflammatory pain model induced by CFA, we observed that approximately 89.15% of Rab11a-positive cells in the SDH of mice were positive for NeuN. Immunofluorescence and Western blotting analyses demonstrated a substantial increase in Rab11a expression in the SDH in mice with CFA injection, as quantified by both semi-quantitative and quantitative methods.…”

Section: Discussionsupporting

confidence: 91%

“…The morphological results suggest that the expression of Rab11a is correlated with the process of inflammatory pain, we thus want to test whether knockdown of the Rab11a will rescue the pain responses. Rab11a-specific short hairpin RNA (Rab11a-shRNA) binding to AAV2/9 virus or control virus (scrambled-shRNA), which has been confirmed in previous work [ 14 , 15 ], was then injected into the SDH ipsilateral to the CFA injected paw (Fig. 3 A).…”

Section: Resultssupporting

confidence: 70%

“…Electrophysiologically, application of Rab11a-shRNA did not affect the presynaptic glutamate release and the postsynaptic AMPA receptor-mediated responses but reduced the NMDA receptor-mediated EPSCs and the number of spikes of neurons in lamina II of the spinal cord in mice with CFA injection. In our recent work in testing the Rab11a’s function in a CFA-induced orofacial inflammatory pain model in rats [ 14 ], we notice that Rab11a-shRNA similarly reduces the spike number of Sp5C neurons. However, Rab11a-shRNA also reversed the potentiated sEPSC frequency and amplitude [ 14 ].…”

Section: Discussionmentioning

confidence: 93%

“…Rab11a, a member of small molecule guanosine triphosphate (GTP) enzymes of Rab family [ 8 – 10 ], is reported to be involved in traumatic brain injury, Alzheimer’s disease, and so on [ 11 – 13 ]. Our recent study reveals that Rab11a is closely related to Complete Freund’s Adjuvant (CFA)-induced orofacial pain [ 14 ]. Downregulation of Rab11a expression in the caudal part of the spinal trigeminal nucleus (Sp5C) significantly alleviates CFA-induced orofacial mechanical and thermal pain.…”

Section: Introductionmentioning

confidence: 99%

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Rab11a in the spinal cord: an essential contributor to complete Freund’s adjuvant-induced inflammatory pain in mice

Gu,

Wang,

et al. 2023

Mol Brain

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Inflammatory pain is a commonly observed clinical symptom in a range of acute and chronic diseases. However, the mechanism of inflammatory pain is far from clear yet. Rab11a, a small molecule guanosine triphosphate enzyme, is reported to regulate orofacial inflammatory pain in our previous works. However, the mechanism of Rab11a’s involvement in the regulation of inflammatory pain remains obscure. Here, we aim to elucidate the potential mechanisms through which Rab11a contributes to the development of inflammatory pain in the spinal level. It’s shown that neurons, rather than glial cells, were the primary cell type expressing Rab11a in the spinal dorsal horn (SDH). After intra-plantar injection of CFA, both the number of Fos/Rab11a-immunopositive neurons and the expression of Rab11a were increased. Administration of Rab11a-shRNA into the SDH resulted in significantly analgesic effect in mice with CFA injection. Application of Rab11a-shRNA also reduced the NMDA receptor-mediated excitatory post-synaptic current (EPSC) and the spike number of neurons in lamina II of the SDH in mice with CFA injection, without affecting the presynaptic glutamate release and the postsynaptic AMPA receptor-mediated EPSC. Our results thus suggest that the enhanced expression of neuronal Rab11a may be important for the process of inflammatory pain in mice with CFA injection, which is likely mediated by Rab11a’s potentiation of the competence of post-synaptic NMDAR and spiking of SDH neurons.

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Section: Resultssupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%