Neuronal aggregate formation underlies spatiotemporal dynamics of nonsynaptic seizure initiation
Neuronal aggregate formation underlies spatiotemporal dynamics of nonsynaptic seizure initiation
复制标题
DOI：
10.1152/jn.00764.2002
复制
发表时间：
2003-04-01
影响因子：
2.5
通讯作者：
Jefferys, JGR
中科院分区：
文献类型：
--
作者：
Bikson, M;Fox, JE;Jefferys, JGR
高频活动通常先于癫痫发作。我们发现，使用低 Ca2+ 模型在体外诱导的电图癫痫发作以高频（>150 Hz）活动开始，然后频率降低，幅度增加。多通道和单元记录表明，这种转变的机制是逐渐形成更大的神经元聚集体。因此，癫痫发作时明显的高频活动可以反映几个较慢放电聚合体的同时记录。通过降低渗透压可以加速聚集体形成速率。由于当细胞外 Ca2+ 减少时，突触传递被阻断，因此非突触机制（间隙连接、场效应）必须足以形成聚集体和募集。
High-frequency activity often precedes seizure onset. We found that electrographic seizures, induced in vitro using the low-Ca2+ model, start with high-frequency (>150 Hz) activity that then decreases in frequency while increasing in amplitude. Multichannel and unit recordings showed that the mechanism of this transition was the progressive formation of larger neuronal aggregates. Thus the apparent high-frequency activity, at seizure onset, can reflect the simultaneous recording of several slower firing aggregates. Aggregate formation rate can be accelerated by reducing osmolarity. Because synaptic transmission is blocked when extracellular Ca2+ is reduced, nonsynaptic mechanisms (gap junctions, field effects) must be sufficient for aggregate formation and recruitment.