Mechanisms of long lasting hyperpolarizations underlying slow sleep oscillations in cat corticothalamic networks
Mechanisms of long lasting hyperpolarizations underlying slow sleep oscillations in cat corticothalamic networks
复制标题
DOI：
10.1113/jphysiol.1996.sp021488
复制
发表时间：
1996-07-01
影响因子：
5.5
通讯作者：
Steriade, M
中科院分区：
文献类型：
--
作者：
Contreras, D;Timofeev, I;Steriade, M
1. 为了探索体内皮质丘脑回路缓慢振荡特征的持久超极化的性质，在氯胺酮-甲苯噻嗪麻醉下，从猫的前交叉运动皮层的皮质 (Cx) 细胞、来自鼻外侧区的丘脑网状 (RE) 细胞和来自腹外侧 (VL) 核的丘脑皮质 (TC) 细胞获得细胞内记录。2.三种细胞类型的测量结果显示，在对应于皮质脑电图深度正波的长期超极化期间，输入电阻 (R(in)) 最高。 R(in)在高振幅深度负EEG波的早期阶段最低，此后增加，直到下一个慢振荡周期。3．将自发的持久超极化与背侧丘脑刺激引起的超极化进行比较。电压与电流 (V-I) 图显示，Cx 和 RE 细胞中自发超极化和诱发超极化的膜电位 (V-m) 范围和斜率相似。 TC 细胞的 V-I 图具有相似的斜率，但诱发超极化期间的 V-m 向更负的值移动。4．向Cx细胞内注入恒定的超极化电流，使慢振荡去极化平台起始部分的振幅增大，而去极化平台最后部分的振幅减小。5．这些结果表明，在自发性长期超极化过程中，功能失调是皮质和丘脑细胞膜的主要机制，它形成并同步了皮质丘脑网络中的缓慢振荡。在 Cx 和 RE 细胞中，丘脑诱发的持久超极化具有相同的机制。相比之下，TC 细胞中的诱发反应显示出强大的额外超极化因子。我们提出 GABA(B) 过程在 TC 中比在 Cx 神经元中更强，从而通过增强丘脑反弹能力使丘脑更容易成为失神型癫痫现象的目标。
1. To explore the nature of the long-lasting hyperpolarizations that characterize slow oscillations in corticothalamic circuits in vivo, intracellular recordings were obtained under ketamine-xylazine anaesthesia from cortical (Cx) cells of the cat precruciate motor cortex, thalamic reticular (RE) cells from the rostrolateral sector, and thalamocortical (TC) cells from the ventrolateral (VL) nucleus.2. Measurements in the three cell types showed input resistance (R(in)) to be highest during the long-lasting hyperpolarizations that correspond to depth-positive waves of the cortical EEG. R(in) was lowest during the early phase of high-amplitude depth-negative EEG waves and increased thereafter until the next cycle of the slow oscillation.3. Spontaneous long-lasting hyperpolarizations were compared with those evoked by dorsal thalamic stimulation. Voltage versus current (V-I) plots showed similar membrane potential (V-m) ranges and slopes for spontaneous and evoked hyperpolarizations in both Cx and RE cells. V-I plots from TC cells had similar slopes, but V-m during evoked hyperpolarizations was displaced towards more negative values.4. Intracellular injection of constant hyperpolarizing current in Cx cells increased the amplitude of the initial part of the depolarizing plateau of the slow oscillation, but decreased the amplitude of the last part.5. These results suggest disfacilitation to be the dominant mechanism in the membrane of cortical and thalamic cells during the spontaneous long-lasting hyperpolarizations, which shape and synchronize slow oscillations in corticothalamic networks. In Cx and RE cells, the same mechanism underlies thalamically evoked long-lasting hyperpolarizations. By contrast, evoked responses in TC cells show a strong additional hyperpolarizing factor. We propose that GABA(B), processes are stronger in TC than in Cx neurones, thus rendering the thalamus an easier target for absence-type epileptic phenomena through potentiation of thalamic rebound capabilities.