Schwartzkroin P A, Prince D A
Brain Res. 1978 May 19;147(1):117-30. doi: 10.1016/0006-8993(78)90776-x.
Epileptogenic activity was induced in hippocampal slices by addition of penicillin (2.0mM) to the bathing medium. Field potential epileptiform events were recorded and single cell bursts studied with intracellular electrodes. Epileptogenic activity was seen in areas CA1 and CA3 of the slice, with bursts in CA3 always leading CA1 bursts; a cut between CA1 and CA3 abolished spontaneous bursting in CA1 but not in CA3. Increased (Mg2+) and decreased (Ca2+) abolished epileptiform discharge, thus demonstrating its dependence on synaptic activity; burst occurrence was also sensitive to (K+). Measurements of single cell resting potentials, resistance, and time constant in CA1 cells revealed no difference between cells in normal medium and cells made epileptogenic by penicillin. Depolarization shifts in CA1 neurons during epileptogenesis did not behave like 'giant EPSPs' but rather were complexes to which depolarizing spike after-potentials, fast prepotentials, and underlying slow depolarizing events all contributed.
通过向灌流介质中添加青霉素(2.0 mM)在海马切片中诱导致痫活性。记录场电位癫痫样事件,并用细胞内电极研究单细胞爆发。在切片的CA1和CA3区域观察到致痫活性,CA3中的爆发总是先于CA1爆发;CA1和CA3之间的切口消除了CA1中的自发性爆发,但未消除CA3中的爆发。增加(Mg2+)和降低(Ca2+)消除了癫痫样放电,从而证明其对突触活动的依赖性;爆发的发生对(K+)也敏感。对CA1细胞的单细胞静息电位、电阻和时间常数的测量显示,正常介质中的细胞与青霉素诱导致痫的细胞之间没有差异。癫痫发生期间CA1神经元的去极化变化不像“巨大兴奋性突触后电位”,而是由去极化尖峰后电位、快速预电位和潜在的缓慢去极化事件共同构成的复合体。