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首页> 外文期刊>Clinical and experimental pharmacology & physiology >Effects of sodium valproate on synaptic transmission and neuronal excitability in rat hippocampus.
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Effects of sodium valproate on synaptic transmission and neuronal excitability in rat hippocampus.

机译：丙戊酸钠对大鼠海马突触传递和神经元兴奋性的影响。

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1. Valproate (VPA) has long been used in the treatment of both generalized and partial seizures. However, its cellular mechanisms of action remain unclear. 2. In the present study, the effects of VPA on synaptic transmission and neuronal excitability were examined in the hippocampal CA1 region using whole-cell patch clamp recordings. 3. Perfusion with VPA, at therapeutically attainable concentrations (i.e. 0.3 and 0.6 mmol/L), significantly increased the frequency (112 +/- 2 and 133 +/- 2% of control, respectively; n = 5; both P < 0.05), but not the average amplitude, of miniature inhibitory post-synaptic currents (mIPSCs). Perfusion with VPA had no effect on either the amplitude or the frequency of miniature excitatory post-synaptic currents (mEPSCs). 4. In acutely dissociated CA1 pyramidal neurons, VPA had no effect on 10 micromol/L GABA-induced currents. Furthermore, following the administration of 0.3 and 0.6 mmol/L VPA, the frequency of action potential firing was significantly reduced from 18.0 +/- 1.1 to 15.3 +/- 0.9 and from 18.6 +/- 0.9 to 12.6 +/- 0.6, respectively (n = 8; both P < 0.05). In contrast, 0.3 and 0.6 mmol/L VPA significantly increased spike frequency adaptation from 4.02 +/- 0.47 to 4.72 +/- 0.55 and from 3.47 +/- 0.41 to 4.48 +/- 0.58, respectively (n = 8; P < 0.05). 5. The results of the present study suggest that VPA presynaptically increases inhibitory synaptic activity without modifying excitatory synaptic transmission and reduces neuronal excitability. Any or all of these effects may contribute to its anticonvulsant action.
机译：1.丙戊酸盐（VPA）长期用于治疗全身性和部分性癫痫。但是，其细胞作用机制仍不清楚。 2.在本研究中，使用全细胞膜片钳记录检查了VPA对海马CA1区突触传递和神经元兴奋性的影响。 3.在治疗上可达到的浓度（即0.3和0.6 mmol / L）下用VPA灌注，显着增加了频率（分别为对照组的112 +/- 2和133 +/- 2％; n = 5;两者P <0.05 ），而不是微型抑制突触后电流（mIPSC）的平均幅度。 VPA灌注对微型兴奋性突触后电流（mEPSC）的幅度或频率均无影响。 4.在急性解离的CA1锥体神经元中，VPA对10 micromol / L GABA诱导的电流没有影响。此外，在施用0.3和0.6 mmol / L VPA之后，动作电位触发的频率分别从18.0 +/- 1.1降低到15.3 +/- 0.9和从18.6 +/- 0.9降低到12.6 +/- 0.6 （n = 8;均P <0.05）。相反，0.3和0.6 mmol / L VPA分别将尖峰频率适应性分别从4.02 +/- 0.47增加到4.72 +/- 0.55和从3.47 +/- 0.41到4.48 +/- 0.58（n = 8; P <0.05 ）。 5.本研究的结果表明，VPA在不改变兴奋性突触传递和降低神经元兴奋性的情况下，先突触增加抑制性突触活性。这些效应中的任何一种或全部都可能有助于其抗惊厥作用。

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