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Synaptic effects of xenon on NMDA receptor-mediated response in rat spinal neuron
•Glutamatergic synaptic transmission of spinal SDCN neurons was investigated.•Kinetic properties of AMPA/KA- and NMDA-induced sEPSC and eEPSC were analysed.•Xe equally inhibited isolated sEPSCNMDA and eEPSCNMDA at both pre- and postsynaptic side. To investigate the precise mechanism of xenon (Xe), p...
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Published in: | Neuroscience letters 2024-07, Vol.836, p.137885, Article 137885 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | •Glutamatergic synaptic transmission of spinal SDCN neurons was investigated.•Kinetic properties of AMPA/KA- and NMDA-induced sEPSC and eEPSC were analysed.•Xe equally inhibited isolated sEPSCNMDA and eEPSCNMDA at both pre- and postsynaptic side.
To investigate the precise mechanism of xenon (Xe), pharmacologically isolated AMPA/KA and NMDA receptor-mediated spontaneous (s) and evoked (e) excitatory postsynaptic currents (s/eEPSCAMPA/KA and s/eEPSCNMDA) were recorded from mechanically isolated single spinal sacral dorsal commissural nucleus (SDCN) neurons attached with glutamatergic nerve endings (boutons) using conventional whole-cell patch-clamp technique. We analysed kinetic properties of both s/eEPSCAMPA/KA and s/eEPSCNMDA by focal single- and/or paired-pulse electrical stimulation to compare them. The s/eEPSCNMDA showed smaller amplitude, slower rise time, and slower 1/e decay time constant (τDecay) than those of s/eEPSCAMPA/KA. We previously examined how Xe modulates s/eEPSCAMPA/KA, therefore, examined the effects on s/eEPSCNMDA in the present study. Xe decreased the frequency and amplitude of sEPSCNMDA, and decreased the amplitude but increased the failure rate and paired-pulse ratio of eEPSCNMDA without affecting their τDecay. It was concluded that Xe might suppress NMDA receptor-mediated synaptic transmission via both presynaptic and postsynaptic mechanisms. |
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ISSN: | 0304-3940 1872-7972 1872-7972 |
DOI: | 10.1016/j.neulet.2024.137885 |