Electrical stimulation of the superior sagittal sinus suppresses A-type K+ currents and increases P/Q- and T-type Ca2+ currents in rat trigeminal ganglion neurons

Autor: Junping Cao, Yuan Zhang, Lei Wu, Lidong Shan, Yufang Sun, Xinghong Jiang, Jin Tao
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Zdroj: The Journal of Headache and Pain, Vol 20, Iss 1, Pp 1-12 (2019)
Druh dokumentu: article
ISSN: 1129-2369
1129-2377
DOI: 10.1186/s10194-019-1037-5
Popis: Abstract Background Migraine is a debilitating neurological disorder involving abnormal trigeminovascular activation and sensitization. However, the underlying cellular and molecular mechanisms remain unclear. Methods A rat model of conscious migraine was established through the electrical stimulation (ES) of the dural mater surrounding the superior sagittal sinus. Using patch clamp recording, immunofluorescent labelling, enzyme-linked immunosorbent assays and western blot analysis, we studied the effects of ES on sensory neuronal excitability and elucidated the underlying mechanisms mediated by voltage-gated ion channels. Results The calcitonin gene-related peptide (CGRP) level in the jugular vein blood and the number of CGRP-positive neurons in the trigeminal ganglia (TGs) were significantly increased in rats with ES-induced migraine. The application of ES increased actional potential firing in both small-sized IB4-negative (IB4 −) and IB4 + TG neurons. No significant changes in voltage-gated Na+ currents were observed in the ES-treated groups. ES robustly suppressed the transient outward K+ current (I A) in both types of TG neurons, while the delayed rectifier K+ current remained unchanged. Immunoblot analysis revealed that the protein expression of Kv4.3 was significantly decreased in the ES-treated groups, while Kv1.4 remained unaffected. Interestingly, ES increased the P/Q-type and T-type Ca2+ currents in small-sized IB4 − TG neurons, while there were no significant changes in the IB4 + subpopulation of neurons. Conclusion These results suggest that ES decreases the I A in small-sized TG neurons and increases P/Q- and T-type Ca2+ currents in the IB4 − subpopulation of TG neurons, which might contribute to neuronal hyperexcitability in a rat model of ES-induced migraine.
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