Sohal Vikaas S, Pangratz-Fuehrer Susanne, Rudolph Uwe, Huguenard John R
Department of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford, California 94305-5122, USA.
J Neurosci. 2006 Apr 19;26(16):4247-55. doi: 10.1523/JNEUROSCI.3812-05.2006.
Rhythmic inhibition entrains the firing of excitatory neurons during oscillations throughout the brain. Previous work has suggested that the strength and duration of inhibitory input determines the synchrony and period, respectively, of these oscillations. In particular, sleep spindles result from a cycle of events including rhythmic inhibition and rebound bursts in thalamocortical (TC) neurons, and slowing and strengthening this inhibitory input may transform spindles into spike-wave discharges characteristic of absence epilepsy. Here, we used dynamic clamp to inject TC neurons with spindle-like trains of IPSCs and studied how modest changes in the amplitude and/or duration of these IPSCs affected the responses of the TC neurons. Contrary to our expectations, we found that prolonging IPSCs accelerates postinhibitory rebound (PIR) in TC neurons, and that increasing either the amplitude or duration of IPSCs desynchronizes PIR activity in a population of TC cells. Tonic injection of hyperpolarizing or depolarizing current dramatically alters the timing and synchrony of PIR. These results demonstrate that rhythmic PIR activity is an emergent property of interactions between intrinsic and synaptic currents, not just a passive reflection of incoming synaptic inhibition.
节律性抑制在全脑振荡过程中调节兴奋性神经元的放电。先前的研究表明，抑制性输入的强度和持续时间分别决定了这些振荡的同步性和周期。特别是，睡眠纺锤波源于一系列事件，包括丘脑皮质（TC）神经元的节律性抑制和反弹爆发，减慢并增强这种抑制性输入可能会将纺锤波转变为失神癫痫特有的棘波放电。在这里，我们使用动态钳位向TC神经元注入类似纺锤波的抑制性突触后电流（IPSC）序列，并研究这些IPSC的幅度和/或持续时间的适度变化如何影响TC神经元的反应。与我们的预期相反，我们发现延长IPSC会加速TC神经元的抑制后反弹（PIR），并且增加IPSC的幅度或持续时间会使一群TC细胞中的PIR活动去同步化。持续注入超极化或去极化电流会显著改变PIR的时间和同步性。这些结果表明，节律性PIR活动是内在电流和突触电流之间相互作用的一种涌现特性，而不仅仅是传入突触抑制的被动反映。
