SYNAPTIC AND MEMBRANE MECHANISMS UNDERLYING SYNCHRONIZED OSCILLATIONS IN THE FERRET LATERAL GENICULATE-NUCLEUS IN-VITRO
SYNAPTIC AND MEMBRANE MECHANISMS UNDERLYING SYNCHRONIZED OSCILLATIONS IN THE FERRET LATERAL GENICULATE-NUCLEUS IN-VITRO
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DOI：
10.1113/jphysiol.1995.sp020612
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发表时间：
1995-03-15
影响因子：
5.5
通讯作者：
MCCORMICK, DA
中科院分区：
文献类型：
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作者：
BAL, T;VONKROSIGK, M;MCCORMICK, DA
1. 采用细胞外和细胞内记录技术，在体外保存的雪貂背外侧膝状核（LGNd）切片中研究了纺锤波和类似失神发作的较慢同步振荡产生的细胞基础。2．体外 LGNd 中继细胞的细胞内记录显示，纺锤波每 3-30 秒发生一次，并与以 6-10 Hz 频率发生的抑制性突触后电位 (IPSP) 连串相关。这些 IPSP 导致在 2-4 Hz 处产生回弹低阈值 Ca2+ 尖峰，这是由于 LGNd 中继细胞在该频率范围内产生振荡爆发放电的固有倾向。这些动作电位的反弹爆发与局部多单元和单单元活动高度同步。3． LGNd 中继细胞中与纺锤波相关的 IPSP 表现出 -86 mV 的平均反转电位。通过使用充满 KCl 的微电极向细胞内注射 Cl-，这种反转电位被转变为更加去极化的膜电位。周膝状核（PGN）和 LGNd 的同时记录表明 IPSP 与 PGN 中爆发放电的发生是同步的。药理学阻断兴奋性氨基酸传递后，用局部电刺激对PGN神经元进行兴奋，导致中继神经元中出现荷包牡丹碱敏感的IPSP，其幅度和时程与纺锤波期间发生的相似。4． (-)-荷包牡丹碱的应用导致纺锤波相关的 IPSP 的消除或这些 IPSP 的上升速率减慢、幅度增加和延长；这导致了同步的 2-4 Hz 振荡，其中每个中继单元几乎在每个周期都强烈爆发，从而形成阵发性事件。 GABA(B) 受体拮抗剂 2-OH-saclofen 的浴应用可阻断这些减慢的振荡，表明它们是由 GABA(B) 受体激活介导的。相反，GABA(B)受体的药理拮抗作用并不能阻止正常纺锤波的产生。5．这些和其他结果表明，纺锤波在体外雪貂 LGNd 中产生，作为一种网络现象，通过 LGNd 的中继细胞和 PGN 的 GABA 能神经元之间的相互作用发生。我们提出 PGN 细胞中的爆发放电通过 GABA(A) 受体的激活使中继神经元超极化。这些 IPSP 导致 LGNd 细胞反弹爆发放电，然后刺激 PGN 神经元。 GABA(A) 受体的阻断导致纺锤波转变为类似于失神（棘波）癫痫发作的事件，通过增加 GABA(B) 受体的激活以及随后在每个振荡周期中发生的 IPSP 的持续时间和幅度的增加。
1. The cellular basis for generation of spindle waves and a slower synchronized oscillation resembling absence seizures was investigated with extracellular and intracellular recording techniques in slices of ferret dorsal lateral geniculate nucleus (LGNd) maintained in vitro.2. Intracellular recording from LGNd relay cells in vitro revealed that spindle waves occurred once every 3-30 s and were associated with barrages of inhibitory postsynaptic potentials (IPSPs) occurring at a frequency of 6-10 Hz. These IPSPs resulted in the generation of rebound low threshold Ca2+ spikes at 2-4 Hz, owing to the intrinsic propensity of LGNd relay cells to generate oscillatory burst firing in this frequency range. These rebound bursts of action potentials were highly synchronized with local multiunit and single unit activity.3. The spindle wave-associated IPSPs in LGNd relay cells exhibited a mean reversal potential of -86 mV. This reversal potential was shifted to more depolarized membrane potentials with the intracellular injection of Cl- through the use of KCl-filled microelectrodes. Simultaneous recording from the perigeniculate nucleus (PGN) and LGNd revealed the IPSPs to be synchronous with the occurrence of burst firing in the PGN. Excitation of PGN neurons with local electrical stimulation after pharmacological block of excitatory amino acid transmission resulted in bicuculline-sensitive IPSPs in relay neurons similar in amplitude and time course to those occurring during spindle waves.4. Application of (-)-bicuculline methiodide resulted in the abolition of spindle wave associated IPSPs or in the slowing of the rate of rise, an increase in amplitude and a prolongation of these IPSPs; this resulted in a synchronized 2-4 Hz oscillation, in which each relay cell strongly burst on nearly every cycle, thus forming a paroxysmal event. Bath application of the GABA(B) receptor antagonist 2-OH-saclofen blocked these slowed oscillations, indicating that they are mediated by the activation of GABA(B) receptors. In contrast, pharmacological antagonism of GABA(B) receptors did not block the generation of normal spindle waves.5. These and other results indicate that spindle waves are generated in the ferret LGNd in vitro as a network phenomenon occurring through an interaction between the relay cells of the LGNd and the GABAergic neurons of the PGN. We propose that burst firing in PGN cells hyperpolarizes relay neurons through activation of GABA(A) receptors. These IPSPs result in rebound burst firing in LGNd cells, which then excite PGN neurons. Block of GABA(A) receptors results in the transformation of spindle waves into events resembling those associated with absence (spike-and-wave) seizures through the increased activation of GABA(B) receptors and the subsequent increase in duration and amplitude of IPSPs occurring during each cycle of oscillation.