ROLE OF THE FERRET PERIGENICULATE NUCLEUS IN THE GENERATION OF SYNCHRONIZED OSCILLATIONS IN-VITRO
ROLE OF THE FERRET PERIGENICULATE NUCLEUS IN THE GENERATION OF SYNCHRONIZED OSCILLATIONS IN-VITRO
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DOI：
10.1113/jphysiol.1995.sp020613
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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. 利用体外保存的雪貂孕周核（PGN）细胞内和细胞外记录技术，研究了其神经元参与纺锤波产生和减缓缺失癫痫样振荡的细胞机制。在纺锤波产生过程中，PGN神经元产生重复的（2- 9hz）高频（高达500hz）突发放电，这是由兴奋性突触后电位（EPSPs）的到来激活低阈值Ca2+峰值介导的。在大多数处于静息膜电位（-60 ~ -70 mV）的PGN细胞中，梭形波与进行性超极化相关，并在超极化后持续很长时间。在PGN细胞中发生的EPSPs与相邻膝状核背外侧（LGNd）的爆发放电高度同步，并与短时间抑制性突触后电位（IPSPs）混合。gaba能受体阻滞后，纺锤波产生过程中产生的EPSPs在0 mV左右极性反转。此外，这些epsp被非nmda受体拮抗剂6-氰-7-硝基喹啉-2,3-二酮（CNQX）完全阻断，PGN和lcnd中的纺锤波也被阻断。通过阻断GABA(A)受体，将轴内频率降低至2-4 Hz，导致PGN细胞的突发放电强度显著增加，每次突发的动作电位数量从最多13个增加到最多60个。GABA(A)受体的阻滞也导致在缓慢振荡的产生过程中，从中继层到达的EPSP波的振幅和持续时间显著增加。这些发现表明，在体外培养的雪貂LGNd中，纺锤波是通过PGN的gaba能神经元和中继神经元之间的相互作用产生的，因此中继神经元的突发放电激活了epsp的弹幕和随后PGN细胞中的低阈值Ca2+峰值。PGN神经元的这种激活抑制了大量的中继细胞，其中一些在IPSP后反弹破裂，从而再次开始循环。GABA(A)受体的阻断导致PGN细胞的活性显著增强，通过增加中继细胞的兴奋和邻近PGN细胞的去抑制。PGN神经元活动的增加导致中继神经元中GABA(B)受体的激活显著增强，随后产生的发作性活动类似于与失神发作相关的活动。
1. The cellular mechanisms by which neurons of the ferret perigeniculate nucleus (PGN) participate in the generation of spindle waves and slowed absence seizure-like oscillations were investigated with intracellular and extracellular recording techniques in geniculate slices maintained in vitro.2. During spindle wave generation, PGN neurons generated repetitive (2-9 Hz) high frequency (up to 500 Hz) burst discharges mediated by the activation of a low threshold Ca2+ spike by the arrival of barrages of excitatory postsynaptic potentials (EPSPs). In most PGN cells at resting membrane potentials (-60 to -70 mV) spindle waves were associated with a progressive hyperpolarization that persisted as a prolonged after-hyperpolarization.3. The EPSPs occurring in PGN cells were highly synchronized with burst firing in the neighbouring portion of the dorsal lateral geniculate nucleus (LGNd) and were intermixed with short duration inhibitory postsynaptic potentials (IPSPs). After block of GABAergic receptors, the EPSPs occurring during the generation of spindle waves reversed polarity at around 0 mV. In addition, these EPSPs were completely blocked with the bath application of the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), as was spindle wave generation in both the PGN and LCNd.4. Slowing the intraspindle frequency to 2-4 Hz with pharmacological block of GABA(A) receptors resulted in a marked increase in the intensity of burst firing by PGN cells such that the number of action potentials per burst increased from a maximum of thirteen to a maximum of sixty. Block of GABA(A) receptors also resulted in a marked increase in the amplitude and duration of the EPSP barrages arriving from the relay laminae during generation of the slowed oscillation.5. These findings indicate that spindle waves are generated in the ferret LGNd in vitro through an interaction between the GABAergic neurons of the PGN and relay neurons, such that burst firing in relay neurons activates a barrage of EPSPs and a subsequent low threshold Ca2+ spike in PGN cells. This activation of PGN neurons inhibits a substantial number of relay cells, a few of which rebound burst after this IPSP, thus starting the cycle again. Block of GABA(A) receptors results in a marked enhancement of activity in PGN cells through increased excitation from relay cells and disinhibition from neighbouring PGN cells. This increased activity in PGN neurons results in a markedly enhanced activation of GABA(B) receptors in relay neurons and the subsequent generation of paroxysmal activity that is similar to that associated with absence seizures.