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冷却可消除大鼠海马切片中的神经网络同步。

Cooling abolishes neuronal network synchronization in rat hippocampal slices.

作者信息

Javedan Sam P, Fisher Robert S, Eder Hans G, Smith Kris, Wu Jie

机构信息

Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona 85013, USA.

出版信息

Epilepsia. 2002 Jun;43(6):574-80. doi: 10.1046/j.1528-1157.2002.40101.x.

Abstract

PURPOSE

We sought to determine whether cooling brain tissue from 34 to 21 degrees C could abolish tetany-induced neuronal network synchronization (gamma oscillations) without blocking normal synaptic transmission.

METHODS

Intracellular and extracellular electrodes recorded activity in transverse hippocampal slices (450-500 microm) from Sprague-Dawley male rats, maintained in an air-fluid interface chamber. Gamma oscillations were evoked by afferent stimulation at 100 Hz for 200 ms. Baseline temperature in the recording chamber was 34 degrees C, reduced to 21 degrees C within 20 min.

RESULTS

Suprathreshold tetanic stimuli evoked membrane potential oscillations in the 40-Hz frequency range (n = 21). Gamma oscillations induced by tetanic stimulation were blocked by bicuculline, a gamma-aminobutyric acid (GABA)A-receptor antagonist. Cooling from 34 to 21 degrees C reversibly abolished gamma oscillations in all slices tested. Short, low-frequency discharges persisted after cooling in six of 14 slices. Single-pulse-evoked potentials, however, were preserved after cooling in all cases. Latency between stimulus and onset of gamma oscillation was increased with cooling. Frequency of oscillation was correlated with chamber cooling temperature (r = 0.77). Tetanic stimulation at high intensity elicited not only gamma oscillation, but also epileptiform bursts. Cooling dramatically attenuated gamma oscillation and abolished epileptiform bursts in a reversible manner.

CONCLUSIONS

Tetany-induced neuronal network synchronization by GABAA-sensitive gamma oscillations is abolished reversibly by cooling to temperatures that do not block excitatory synaptic transmission. Cooling also suppresses transition from gamma oscillation to ictal bursting at higher stimulus intensities. These findings suggest that cooling may disrupt network synchrony necessary for epileptiform activity.

摘要

目的

我们试图确定将脑组织温度从34℃降至21℃是否能消除强直刺激诱导的神经网络同步化(γ振荡),同时不阻断正常的突触传递。

方法

采用细胞内和细胞外电极记录处于气液界面槽中的Sprague-Dawley雄性大鼠横向海马切片(450 - 500微米)的活动。通过100Hz的传入刺激持续200毫秒诱发γ振荡。记录槽中的基线温度为34℃,在20分钟内降至2l℃。

结果

阈上强直刺激诱发40Hz频率范围内的膜电位振荡(n = 21)。强直刺激诱导的γ振荡被γ-氨基丁酸(GABA)A受体拮抗剂荷包牡丹碱阻断。从34℃冷却至21℃可使所有测试切片中的γ振荡可逆性消失。在14个切片中的6个切片冷却后,短的低频放电持续存在。然而,在所有情况下冷却后单脉冲诱发电位均得以保留。冷却后刺激与γ振荡起始之间的潜伏期延长。振荡频率与槽冷却温度相关(r = 0.77)。高强度强直刺激不仅诱发γ振荡,还诱发癫痫样爆发。冷却显著减弱γ振荡并以可逆方式消除癫痫样爆发。

结论

通过冷却至不阻断兴奋性突触传递的温度,可使由GABAA敏感的γ振荡介导的强直刺激诱导的神经网络同步化可逆性消失。冷却还可抑制在较高刺激强度下从γ振荡向发作性爆发的转变。这些发现提示冷却可能破坏癫痫样活动所需的网络同步性。

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