In vivo methylmercury exposure induced long-lasting epileptiform activity in layer II/III neurons in cortical slices from the rat.

In vivo methylmercury exposure induced long-lasting epileptiform activity in layer II/III neurons in cortical slices from the rat.
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DOI:
10.1016/j.toxlet.2009.12.017
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发表时间:
2010-03-15
期刊:
影响因子:
3.5
通讯作者:
Yuan, Yukun
Yuan, Yukun
中科院分区:
医学3区
文献类型:
--
作者:
Dasari, Sameera;Yuan, Yukun

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产前和产后甲基汞(MeHg)暴露已被证明增加神经元兴奋性和癫痫易感性。为了确定出生后早期MeHg暴露是否会引起类似的影响,我们检测了体内MeHg处理后大鼠皮质切片II/III层神经元场电位的变化。从出生后第5天开始,大鼠皮下注射0 (0.9% NaCl)、0.75或1.5 mg/kg/天MeHg,持续15或30天,之后制备皮层切片进行场电位记录。单脉冲刺激大鼠皮层第4层,可产生典型的单尖峰场兴奋性突触后电位。在给予0.75或1.5 mg/kg/天MeHg治疗15天的大鼠切片中也可见到这种类型的fEPSPs。然而,用任何一种MeHg剂量治疗30天,在40%的受测动物中导致fepsp出现多次尖峰(癫痫样活动)。在终止甲基汞暴露30天后,50% - 60%的动物仍可观察到这种癫痫样活动。然而,对照动物的切片仍然显示单尖峰的fEPSPs。因此,这些数据表明,出生后甲基汞暴露在体内改变了神经元的兴奋性,并诱导了皮质神经元的长期高兴奋性。
Prenatal and postnatal methylmercury (MeHg) exposure has been shown to increase neuronal excitability and seizure susceptibility. To determine if early postnatal MeHg exposure causes a similar effect, we examined changes in field potentials in layer II/III neurons in cortical slices of rat following in vivo MeHg treatment. Rats received 0 (0.9% NaCl), 0.75 or 1.5 mg/kg/day MeHg subcutaneously for 15 or 30 days beginning on postnatal day 5, after which cortical slices were prepared for field potential recordings. In slices from rats treated with vehicle, single pulse stimulation of layer IV of cortical slices induced a typical field excitatory postsynaptic potential (fEPSP) with a single spike. This type of fEPSPs was also seen in slices from rats with 15 day treatment with 0.75 or 1.5 mg/kg/day MeHg. However, 30 day treatment with either MeHg dose resulted in fEPSPs with multiple spikes (epileptiform activity) in 40% of animals examined. This epileptiform activity remained observable in 50 – 60% animals in which MeHg exposure had been terminated for 30 days. However, slices from control animals still showed fEPSPs with single spike. Thus, these data suggest that postnatal MeHg exposure in vivo altered neuronal excitability and induced a long-lasting hyperexcitability in cortical neurons.
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