Radix paeoniae rubra suppression of sodium current in acutely dissociated rat hippocampal CA1 neurons

Xian Ping Dong, Tian Le Xu

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

The effect of Radix paeoniae rubra (RPR) on voltage-gated sodium channel (VGSC) currents (INa) was examined in freshly isolated rat hippocampal CA1 neurons using whole-cell patch-clamp technique under voltage-clamp conditions. RPR suppressed INa without affecting the current activation, inactivation and deactivation. The amplitude of INa decreased by ∼18.4% within a few seconds of 0.8 mg/ml RPR exposure. RPR (0.8 mg/ml) shifted the steady-state inactivation curves of INa to negative potentials, with hyperpolarizing direction shift of V1/2 of 10.0 mV. The time course of INa recovery from inactivation was prolonged significantly by 0.8 mg/ml RPR. RPR (0.8 mg/ml) also enhanced the activity-dependent attenuation of INa and decreased the fraction of activated channels. These results suggested that RPR suppressed hippocampal CA1 INa by shifting the inactivation curve in hyperpolarizing direction, slowing the recovery time course from inactivation, enhancing the activity-dependent attenuation and decreasing the number of activatable channels. RPR suppression on INa might predict the protective effect during brain ischemia in hippocampal CA1 neurons.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalBrain Research
Volume940
Issue number1-2
DOIs
Publication statusPublished - Jun 14 2002
Externally publishedYes

Bibliographical note

Funding Information:
This study was partially supported by the National Natural Science Foundation of China (No. 30125015), the National Basic Research Program of China (G1999054000), and the Training Grant Award for Ph.D. Students Mentor from the Ministry of Education of China (2000035812) to T.-L. Xu.

ASJC Scopus Subject Areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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