Integrin α3 is required for high‐frequency repetitive transcranial magnetic stimulation‐induced glutamatergic synaptic transmission in mice with ischemia

Background Repetitive transcranial magnetic stimulation (rTMS) is an effective therapy in post‐stroke motor recovery. However, the underlying mechanisms of rTMS regulates long‐lasting changes with synaptic transmission and glutamate receptors function (including AMPARs or NMDARs) remains unclear. Me...

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Veröffentlicht in:CNS neuroscience & therapeutics 2024-04, Vol.30 (4), p.e14498-n/a
Hauptverfasser: Liu, Li, Hu, Han, Wu, Junfa, Koleske, Anthony J., Chen, Hongting, Wang, Nianhong, Yu, Kewei, Wu, Yi, Xiao, Xiao, Zhang, Qun
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Sprache:eng
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Zusammenfassung:Background Repetitive transcranial magnetic stimulation (rTMS) is an effective therapy in post‐stroke motor recovery. However, the underlying mechanisms of rTMS regulates long‐lasting changes with synaptic transmission and glutamate receptors function (including AMPARs or NMDARs) remains unclear. Methods Mice were received 10‐Hz rTMS treatment once daily on the third day after photothrombotic (PT) stroke for 18 days. Motor behaviors and the Western blot were used to evaluate the therapeutic efficacy of 10‐Hz rTMS in the mice with PT model. Moreover, we used wild‐type (WT) and NEX‐α3−/− mice to further explore the 10‐Hz rTMS effect. Results We found that 10‐Hz rTMS improved the post‐stroke motor performance in the PT mice. Moreover, the levels of AMPAR, vGlut1, and integrin α3 in the peri‐infarct were significantly increased in the rTMS group. In contrast, 10‐Hz rTMS did not induce these aforementioned effects in NEX‐α3−/− mice. The amplitude of AMPAR‐mediated miniature excitatory postsynaptic currents (EPSCs) and evoked EPSCs was increased in the WT + rTMS group, but did not change in NEX‐α3−/− mice with rTMS. Conclusions In this study, 10‐Hz rTMS improved the glutamatergic synaptic transmission in the peri‐infract cortex through effects on integrin α3 and AMPARs, which resulted in motor function recovery after stroke. Model for integrin α3 involvement in the rTMS‐modulated glutamatergic synaptic transmission after PT stroke.
ISSN:1755-5930
1755-5949
DOI:10.1111/cns.14498