Actions of remimazolam on inhibitory transmission of rat spinal dorsal horn neurons

Rintaro Hoshino, Nobuko Ohashi*, Daisuke Uta, Masayuki Ohashi, Hiroyuki Deguchi, Hiroshi Baba

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

2 被引用数 (Scopus)

抄録

Remimazolam is an ultra-short benzodiazepine that acts on the benzodiazepine site of γ-aminobutyric acid (GABA) receptors in the brain and induces sedation. Although GABA receptors are found localized in the spinal dorsal horn, no previous studies have reported the analgesic effects or investigated the cellular mechanisms of remimazolam on the spinal dorsal horn. Behavioral measures, immunohistochemistry, and in vitro whole-cell patch-clamp recordings of dorsal horn neurons were used to assess synaptic transmission. Intrathecal injection of remimazolam induced behavioral analgesia in inflammatory pain-induced mechanical allodynia (six rats/dose; p < 0.05). Immunohistochemical staining revealed that remimazolam suppressed spinal phosphorylated extracellular signal-regulated kinase activation (five rats/group, p < 0.05). In vitro whole-cell patch-clamp analysis demonstrated that remimazolam increased the frequency of GABAergic miniature inhibitory post-synaptic currents, prolonged the decay time (six rats; p < 0.05), and enhanced GABA currents induced by exogenous GABA (seven rats; p < 0.01). However, remimazolam did not affect miniature excitatory post-synaptic currents or amplitude of monosynaptic excitatory post-synaptic currents evoked by Aδ- and C-fiber stimulation (seven rats; p > 0.05). This study suggests that remimazolam induces analgesia by enhancing GABAergic inhibitory transmission in the spinal dorsal horn, suggesting its potential utility as a spinal analgesic for inflammatory pain.

本文言語英語
ページ(範囲)63-73
ページ数11
ジャーナルJournal of Pharmacological Sciences
155
2
DOI
出版ステータス出版済み - 2024/06

ASJC Scopus 主題領域

  • 分子医療
  • 薬理学

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