Steriade M, Amzica F
Laboratoire de Neurophysiologie, Faculté de Médicine, Université Laval, Quebec, Canada G1K 7P4.
J Neurophysiol. 1999 Dec;82(6):3108-22. doi: 10.1152/jn.1999.82.6.3108.
The excitability of neocortical neurons from cat association areas 5-7 was investigated during spontaneously occurring seizures with spike-wave (SW) complexes at 2-3 Hz. We tested the antidromic and orthodromic responsiveness of neocortical neurons during the "spike" and "wave" components of SW complexes, and we placed emphasis on the dynamics of excitability changes from sleeplike patterns to seizures. At the resting membrane potential, an overwhelming majority of neurons displayed seizures over a depolarizing envelope. Cortical as well as thalamic stimuli triggered isolated paroxysmal depolarizing shifts (PDSs) that eventually developed into SW seizures. PDSs could also be elicited by cortical or thalamic volleys during the wave-related hyperpolarization of neurons, but not during the spike-related depolarization. The latencies of evoked excitatory postsynaptic potentials (EPSPs) progressively decreased, and their slope and depolarization surface increased, from the control period preceding the seizure to the climax of paroxysm. Before the occurrence of full-blown seizures, thalamic stimuli evoked PDSs arising from the postinhibitory rebound excitation, whereas cortical stimuli triggered PDSs immediately after the early EPSP. These data shed light on the differential excitability of cortical neurons during the spike and wave components of SW seizures, and on the differential effects of cortical and thalamic volleys leading to such paroxysms. We conclude that the wave-related hyperpolarization does not represent GABA-mediated inhibitory postsynaptic potentials (IPSPs), and we suggest that it is a mixture of disfacilitation and Ca(2+)-dependent K(+) currents, similar to the prolonged hyperpolarization of the slow sleep oscillation.
在猫5-7联合区新皮质神经元出现2-3Hz棘波-慢波（SW）复合波的自发性癫痫发作期间，对其兴奋性进行了研究。我们测试了新皮质神经元在SW复合波的“棘波”和“慢波”成分期间的逆向和顺向反应性，并着重研究了从睡眠样模式到癫痫发作时兴奋性变化的动态过程。在静息膜电位时，绝大多数神经元在去极化包络上出现癫痫发作。皮质和丘脑刺激均可引发孤立的阵发性去极化偏移（PDSs），最终发展为SW癫痫发作。在神经元与慢波相关的超极化期间，皮质或丘脑的电刺激也可引发PDSs，但在与棘波相关的去极化期间则不会。从癫痫发作前的对照期到发作高潮，诱发的兴奋性突触后电位（EPSPs）的潜伏期逐渐缩短，其斜率和去极化面积增大。在全面癫痫发作发生之前，丘脑刺激诱发的PDSs源于抑制后反弹兴奋，而皮质刺激在早期EPSP之后立即引发PDSs。这些数据揭示了SW癫痫发作的棘波和慢波成分期间皮质神经元的不同兴奋性，以及导致此类发作的皮质和丘脑电刺激的不同作用。我们得出结论，与慢波相关的超极化并不代表GABA介导的抑制性突触后电位（IPSPs），我们认为它是去易化和钙依赖性钾电流的混合，类似于慢睡眠振荡的延长超极化。
