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

Xian Ping Dong; Tian Le Xu

doi:10.1016/S0006-8993(02)02555-6

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

Xian Ping Dong, Tian Le Xu

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22 Citas (Scopus)

Resumen

The effect of Radix paeoniae rubra (RPR) on voltage-gated sodium channel (VGSC) currents (I_Na) was examined in freshly isolated rat hippocampal CA1 neurons using whole-cell patch-clamp technique under voltage-clamp conditions. RPR suppressed I_Na without affecting the current activation, inactivation and deactivation. The amplitude of I_Na 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 I_Na to negative potentials, with hyperpolarizing direction shift of V_1/2 of 10.0 mV. The time course of I_Na recovery from inactivation was prolonged significantly by 0.8 mg/ml RPR. RPR (0.8 mg/ml) also enhanced the activity-dependent attenuation of I_Na and decreased the fraction of activated channels. These results suggested that RPR suppressed hippocampal CA1 I_Na 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 I_Na might predict the protective effect during brain ischemia in hippocampal CA1 neurons.

Idioma original	English
Páginas (desde-hasta)	1-9
Número de páginas	9
Publicación	Brain Research
Volumen	940
N.º	1-2
DOI	https://doi.org/10.1016/S0006-8993(02)02555-6
Estado	Published - jun. 14 2002
Publicado de forma externa	Sí

Nota bibliográfica

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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10.1016/S0006-8993(02)02555-6

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title = "Radix paeoniae rubra suppression of sodium current in acutely dissociated rat hippocampal CA1 neurons",

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.",

author = "Dong, {Xian Ping} and Xu, {Tian Le}",

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.",

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AU - Dong, Xian Ping

AU - Xu, Tian Le

N1 - 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.

PY - 2002/6/14

Y1 - 2002/6/14

N2 - 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.

AB - 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.

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

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ASJC Scopus Subject Areas

PubMed: MeSH publication types

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