A NOVEL SLOW (LESS-THAN-1 HZ) OSCILLATION OF NEOCORTICAL NEURONS IN-VIVO - DEPOLARIZING AND HYPERPOLARIZING COMPONENTS
A NOVEL SLOW (LESS-THAN-1 HZ) OSCILLATION OF NEOCORTICAL NEURONS IN-VIVO - DEPOLARIZING AND HYPERPOLARIZING COMPONENTS
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DOI：
10.1523/jneurosci.13-08-03252.1993
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发表时间：
1993-08-01
影响因子：
5.3
通讯作者：
AMZICA, F
中科院分区：
文献类型：
--
作者：
STERIADE, M;NUNEZ, A;AMZICA, F
我们描述了一种新的缓慢振荡的细胞内记录从皮层联合区5和7，运动区4和6，和视觉区17和18的猫在各种麻醉剂。记录的神经元（n = 254）被逆向和orthodromically确定为皮质丘脑或胼胝体的元素，从适当的丘脑核团以及从对侧皮质的同源灶接收投影。记录了两种主要类型的细胞：规则尖峰（主要是慢适应，但也有快速适应）神经元和内在爆发细胞。一组慢振荡神经元（n = 21）细胞内染色显示，在Ⅲ ~ Ⅵ层细胞呈杯状，基底树突发达，88%的神经元出现慢节律。它由缓慢去极化信封（持续0.81。5秒）与叠加的全动作电位或假定的树突棘波，随后是持久的超极化。这种序列以低于1 Hz的频率有节奏地重复出现，在67%的麻醉动物中，主要振荡在0.3和0.4 Hz之间。（几乎等于70%）叠加在缓慢去极化上的重复尖峰被轻微的DC超极化完全阻断，发现30%的细胞显示相对小（3-12 mV），快速，完全动作电位消失后的全或无电位。在V（m）比-90 mV更负的情况下，这些快速尖峰以全或无的方式被抑制。在-90至-100 mV的V（m）下，慢节律的去极化包络被降低或抑制，并且其持续时间通过给予NMDA阻断剂氯胺酮而大大缩短。在氯胺酮和一氧化氮或氯胺酮和甲苯噻嗪麻醉的动物中，大多数（56%）神经元在较高频率下显示缓慢振荡（0.6-1 Hz）比乌拉坦麻醉下在18%的振荡细胞中，慢节律主要由重复性的节律组成（15-30 Hz），相对较短（15-25 msec）的IPSP，可以通过使V（m）处于比-70 mV更正值来揭示。在静息V（m）下观察到慢振荡的持久（几乎等于1秒）超极化相，并在约-100 mV时降低。同时记录另一个细胞跨膜表现出同步抑制期在两个神经元。Cl-或Cs+的细胞内扩散降低了周期性长持续超极化的幅度和/或持续时间。（感觉、运动和关联）皮质区，由形态学和生理学上鉴定的锥体细胞显示，但似乎也涉及局部回路抑制细胞，如从神经元型神经元中重复IPSP的节律（0.3 Hz）序列推断的。然后，我们处理一个大规模的人口事件，也表明了缓慢的细胞和脑电图振荡之间的密切相关性。如以下两篇配套文章所示（Steriade等人，1993 a，B），缓慢的皮质振荡在投射到记录的皮质神经元的丘脑核周体的全部损伤中存活，并且在0.3 Hz节律内分组其他睡眠振荡（例如纺锤波（7- 1 - 4 Hz）和δ波（1-4 Hz））中起关键作用。出现了一个新的观点睡眠振荡，与各种脑节律所产生的固有的电生理特性的丘脑和皮层神经元和复杂的皮质-丘脑-皮质网络中的突触相互作用。
We describe a novel slow oscillation in intracellular recordings from cortical association areas 5 and 7, motor areas 4 and 6, and visual areas 17 and 18 of cats under various anesthetics. The recorded neurons (n = 254) were antidromically and orthodromically identified as corticothalamic or callosal elements receiving projections from appropriate thalamic nuclei as well as from homotopic foci in the contralateral cortex. Two major types of cells were recorded: regular-spiking (mainly slow-adapting, but also fast-adapting) neurons and intrinsically bursting cells. A group of slowly oscillating neurons (n = 21) were intracellularly stained and found to be pyramidal-shaped cells in layers III-VI, with luxuriant basal dendritic arbors.The slow rhythm appeared in 88% of recorded neurons. It consisted of slow depolarizing envelopes (lasting for 0.81. 5 sec) with superimposed full action potentials or presumed dendritic spikes, followed by long-lasting hyperpolarizations. Such sequences recurred rhythmically at less than 1 Hz, with a prevailing oscillation between 0.3 and 0.4 Hz in 67% of urethane-anesthetized animals.While in most neurons (almost-equal-to 70%) the repetitive spikes superimposed on the slow depolarization were completely blocked by slight DC hyperpolarization, 30% of cells were found to display relatively small (3-12 mV), rapid, all-or-none potentials after obliteration of full action potentials. These fast spikes were suppressed in an all-or-none fashion at V(m) more negative than -90 mV. The depolarizing envelope of the slow rhythm was reduced or suppressed at a V(m) of -90 to -100 mV and its duration was greatly reduced by administration of the NMDA blocker ketamine. In keeping with this action, most (56%) neurons recorded in animals under ketamine and nitrous oxide or ketamine and xylazine anesthesia displayed the slow oscillation at higher frequencies (0.6-1 Hz) than under urethane anesthesia (0.3-0.4 Hz).In 18% of the oscillating cells, the slow rhythm mainly consisted of repetitive (15-30 Hz), relatively short-lasting (15-25 msec) IPSPs that could be revealed by bringing the V(m) at more positive values than -70 mV. The long-lasting (almost-equal-to 1 sec) hyperpolarizing phase of the slow oscillation was best observed at the resting V(m) and was reduced at about -100 mV. Simultaneous recording of another cell across the membrane demonstrated synchronous inhibitory periods in both neurons. Intracellular diffusion of Cl- or Cs+ reduced the amplitude and/or duration of cyclic long-lasting hyperpolarizations.Thus, the newly described oscillation is present in all investigated (sensory, motor, and associational) cortical areas, is displayed by morphologically and physiologically identified pyramidal cells, but does also seemingly involve local-circuit inhibitory cells as inferred from the rhythmic (0.3 Hz) sequences of repetitive IPSPs in pyramidal-type neurons. We then deal with a massive population event, as also indicated by the close correlation between the slow cellular and EEG oscillation. As shown in the following two companion articles (Steriade et al., 1993a,b), the slow cortical oscillation survives total lesions of thalamic perikarya projecting to the recorded cortical neurons and plays a pivotal role in grouping within the 0.3 Hz rhythm other sleep oscillations, such as spindle (7-14 Hz) and delta (1-4 Hz) waves. A new view of sleep oscillations emerges, with various cerebral rhythms generated by intrinsic electrophysiological properties of thalamic and cortical neurons and by synaptic interactions in complex corticothalamocortical networks.