EPILEPTIFORM ACTIVITY INDUCED BY CHANGES IN EXTRACELLULAR POTASSIUM IN HIPPOCAMPUS

EPILEPTIFORM ACTIVITY INDUCED BY CHANGES IN EXTRACELLULAR POTASSIUM IN HIPPOCAMPUS
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DOI:
10.1152/jn.1985.54.5.1363
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发表时间:
1985-01-01
影响因子:
2.5
通讯作者:
JOHNSTON, D
JOHNSTON, D
中科院分区:
医学3区
文献类型:
--
作者:
RUTECKI, PA;LEBEDA, FJ;JOHNSTON, D

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使用细胞外和细胞内记录技术,我们研究了细胞外钾([K+]o)浓度变化产生的自发性癫痫样活动的诱导和频率调制。本文描述了 [K+]o 与自发发生癫痫样事件的频率之间的定量关系。从大鼠体外海马切片制备的 CA3 亚区进行记录。细胞内微电极充满 2 M Cs2SO4,并连接到 3 kHz、分时、单电极电流和电压钳装置。自发性癫痫样(发作间期)放电的频率根据细胞外记录确定为 [K+]o 的函数。使用电流钳和电压钳技术来表征这些癫痫样事件的细胞内相关性。荷包牡丹碱诱发的自发性癫痫样放电的频率取决于[K+]o。低于 4 mM [K+]o,在 10 µM 荷包牡丹碱存在的情况下,偶尔会发生自发放电。 [K+]o 从 5 mM 增加到 10 mM 导致自发放电率增加五倍。当 [K+]o 增加到 6.5 mM 以上时,在没有荷包牡丹碱的情况下也会发生自发性癫痫样放电。这些放电的速率取决于[K+]o,其方式与荷包牡丹碱引起的放电大致相同。然而,对于任何给定的大于 6.5 mM 的 [K+]o 浓度,所得的放电速率比沐浴溶液中存在荷包牡丹碱时获得的放电速率更快。细胞内和细胞外的同时记录显示,自发的高[K+]o诱导的发作间期放电伴随着膜电位的大量去极化,这与其他惊厥患者所见的阵发性去极化转变(PDS)相似。细胞内记录的事件满足突触介导的 PDS 的标准。 PDS 的波形很复杂并且取决于膜电位。当膜电位保持在 0 mV 时,在 PDS 间间隔期间注意到自发发生的超极化电位。这些事件被印防己毒素或荷包牡丹碱阻断,并且可能是自发的抑制性突触后电位。 PDS 波形的复杂性表明,不止一种突触电导参与了 PDS 的生成。去极化相的平均测量反转电位为-10.7 mV。电压钳技术用于测量高[K+]o 诱导的PDS 去极化相下的电导。平均测量电导为 51.5 nS,反转电位为 -7.9 mV。(摘要截断为 400 字)
Using extra- and intracellular recording techniques, we investigated the induction and frequency modulation of spontaneous epileptiform activity produced by changes in the concentration of extracellular potassium ([K+]o). This paper describes a quantitative relationship between [K+]o and the frequency of spontaneously occurring epileptiform events. Recordings were made from the CA3 subfield of the rat in vitro hippocampal slice preparation. Intracellular microelectrodes were filled with 2 M Cs2SO4 and connected to a 3-kHz, time-share, single-electrode current- and voltage-clamp device. The frequency of spontaneous epileptiform (interictal) discharges was determined from extracellular recordings as a function of [K+]o. Current- and voltage-clamp techniques were used to characterize the intracellular correlate of these epileptiform events. The frequency of bicuculline-induced spontaneous epileptiform discharges was dependent on [K+]o. Below 4 mM [K+]o, spontaneous discharges occurred sporadically in the presence of 10 microM bicuculline. Increasing [K+]o from 5 to 10 mM caused a fivefold increase in the rate of spontaneous discharges. Spontaneous epileptiform discharges also occurred in the absence of bicuculline when [K+]o was increased above 6.5 mM. The rate of these discharges was dependent on [K+]o in much the same way as the discharges induced by bicuculline. For any given [K+]o concentration greater than 6.5 mM, however, the resultant discharge rate was faster than that obtained when bicuculline was present in the bathing solution. Simultaneous intra- and extracellular recordings revealed that the spontaneous high-[K+]o-induced interictal discharge was accompanied by a large depolarization of the membrane potential that appeared similar to the paroxysmal depolarizing shift (PDS) seen with other convulsants. The intracellularly recorded event fulfilled the criteria for a synaptically mediated PDS. The waveform of the PDS was complex and dependent on the membrane potential. When the membrane potential was held at 0 mV, spontaneously occurring hyperpolarizing potentials were noted during the inter-PDS interval. These events were blocked by picrotoxin or bicuculline and were probably spontaneous inhibitory postsynaptic potentials. The complexity of the PDS waveform suggested that more than one synaptic conductance was involved in the generation of the PDS. The mean measured reversal potential of the depolarizing phase was -10.7 mV. Voltage-clamp techniques were used to measure the conductance underlying the depolarizing phase of the high-[K+]o-induced PDS. The mean measured conductance was 51.5 nS, with a reversal potential of -7.9 mV.(ABSTRACT TRUNCATED AT 400 WORDS)