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低氯培养基在海马切片CA1亚区诱导的癫痫样活动。

Epileptiform activity induced by low chloride medium in the CA1 subfield of the hippocampal slice.

作者信息

Avoli M, Drapeau C, Perreault P, Louvel J, Pumain R

机构信息

Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada.

出版信息

J Neurophysiol. 1990 Dec;64(6):1747-57. doi: 10.1152/jn.1990.64.6.1747.

DOI:10.1152/jn.1990.64.6.1747
PMID:2074462
Abstract
  1. Extracellular and intracellular recordings and measurements of the extracellular concentration of free K+ ([K+]o) were performed in the CA1 subfield of the rat hippocampal slice during perfusion with artificial cerebrospinal fluid (ACSF) in which NaCl had been replaced with equimolar Na-isethionate or Na-methylsulfate (hereafter called low Cl- ACSF). 2. CAl pyramidal cells perfused with low Cl- ACSF generated intracellular epileptiform potentials in response to orthodromic, single-shock stimuli delivered in stratum (S.) radiatum. Low-intensity stimuli evoked a short-lasting epileptiform burst (SB) of action potentials that lasted 40-150 ms and was followed by a prolonged hyperpolarization. When the stimulus strength was increased, a long-lasting epileptiform burst (LB) appeared; it had a duration of 4-15 s and consisted of an early discharge of action potentials similar to the SB, followed by a prolonged, large-amplitude depolarizing plateau. The refractory period of the LB was longer than 20 s. SB and LB were also seen after stimulation of the alveus. 3. Variations of the membrane potential with injection of steady. DC current modified the shape of SB and LB. When microelectrodes filled with the lidocaine derivative QX-314 were used, the amplitudes of both SB and LB increased in a linear fashion during changes of the baseline membrane potential in the hyperpolarizing direction. The membrane input resistance, as measured by injecting brief square pulses of hyperpolarizing current, decreased by 65-80% during the long-lasting depolarizing plateau of LB. 4. A synchronous field potential and a transient increase in [K+]o accompanied the epileptiform responses. The extracellular counterpart of the SB was a burst of three to six population spikes and a small increase in [K+]o (less than or equal to 2 mM from a resting value of approximately 2.5 mM). The LB was associated with a large-amplitude, biphasic, negative field potential and a large increase in [K+]o (up to 12.4 mM above the resting value). Changes in [K+]o during the LB were largest at the border between S. oriens and S. pyramidale. This was also the site where the field potentials measured 2-5 s after the stimulus attained their maximal amplitude. Conversely, field potentials associated with the early component of the LB or with the SB displayed a maximal amplitude in the S. radiatum. 5. Spontaneous SBs and LBs were at times recorded in the CA1 and in the CA3 subfield.(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
  1. 在以等摩尔的羟乙基磺酸钠或甲磺酸钠替代氯化钠的人工脑脊液(ACSF,以下称为低氯ACSF)灌注大鼠海马脑片CA1亚区的过程中,进行了细胞外和细胞内记录以及细胞外游离钾离子浓度([K⁺]o)的测量。2. 用低氯ACSF灌注的CA1锥体细胞,对放射层(S.)中传递的正向单脉冲刺激产生细胞内癫痫样电位。低强度刺激诱发持续40 - 150毫秒的短暂癫痫样动作电位爆发(SB),随后是长时间的超极化。当刺激强度增加时,出现持续4 - 15秒的长时间癫痫样爆发(LB);它由类似于SB的动作电位早期放电组成,随后是长时间的大幅度去极化平台期。LB的不应期超过20秒。刺激海马槽后也可见SB和LB。3. 注入稳定直流电流时膜电位的变化改变了SB和LB的形状。当使用填充利多卡因衍生物QX - 314的微电极时,在超极化方向的基线膜电位变化期间,SB和LB的幅度均呈线性增加。通过注入超极化电流的短暂方波脉冲测量的膜输入电阻,在LB的长时间去极化平台期降低了65 - 80%。4. 癫痫样反应伴有同步场电位和[K⁺]o的短暂升高。SB的细胞外对应物是三到六个群体锋电位的爆发以及[K⁺]o的小幅升高(从约2.5 mM的静息值增加到小于或等于2 mM)。LB与大幅度的双相负场电位以及[K⁺]o的大幅升高(比静息值高至12.4 mM)相关。LB期间[K⁺]o的变化在原层(S. oriens)和锥体层(S. pyramidale)之间的边界处最大。这也是刺激后2 - 5秒测量的场电位达到最大幅度的部位。相反,与LB早期成分或SB相关的场电位在放射层显示最大幅度。5. 在CA1和CA3亚区有时会记录到自发性SB和LB。(摘要截断于400字)

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