Neurons in the deep layers of superior colliculus are a requisite component of the neuronal network for seizures during ethanol withdrawal.
Neurons in the deep layers of superior colliculus are a requisite component of the neuronal network for seizures during ethanol withdrawal.
复制标题
上丘深层的神经元是乙醇戒断期间癫痫发作的神经元网络的必要组成部分。
DOI：
10.1016/s0006-8993(01)03048-7
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发表时间：
2001
期刊：
影响因子：
2.9
通讯作者：
Faingold,CL
中科院分区：
文献类型：
--
作者：
Yang,L;Long,C;Faingold,CL
乙醇依赖动物和人类的乙醇戒断(ETX)常常导致癫痫易感性。上丘深层(DLSC)被认为参与了几种类型癫痫发作的神经元网络。在啮齿动物中，ETX导致对听源性癫痫(AGS)的易感性，DLSC被认为是AGS基因形式的癫痫网络的关键组成部分。乙醇抑制NMDA受体，在ETX过程中，这些受体的结合在某些大脑区域增加。因此，我们观察了DLSC内注射竞争性NMDA受体拮抗剂dl-2-氨基-7-膦庚酸(AP7)对ETX惊厥的影响。双侧DLSC内微量注射AP7(2和5nmol/侧)可抑制AGS，支持DLSC在ETX期间AGS网络中的关键作用。随后使用长期植入的微丝电极检测了行为大鼠DLSC神经元放电的变化。在乙醇中毒和ETX期间，声诱发的DLSC的放电明显受到抑制。然而，在AGs的狂奔行为开始之前，DLSC神经元就开始以1-2 S的方式进行强直放电。在发作后抑郁期间，听觉诱发的DLSC放电受到抑制，随着翻正反射的恢复，DLSC开始恢复。这些数据支持DLSC在ETX期间在AGS中发挥的必要作用。这些神经元放电的变化表明，DLSC神经元在ETX期间AGS野跑相的产生中起着重要作用，这可能是一种一般的病理生理机制，也是启动野跑的关键事件，因为以前在AGS的遗传形式中也发现了类似的模式。
Ethanol withdrawal (ETX) in ethanol-dependent animals and humans often results in seizure susceptibility. The deep layers of superior colliculus (DLSC) are proposed to be involved in the neuronal networks of several types of seizures. In rodents, ETX results in susceptibility to audiogenic seizures (AGS), and the DLSC are implicated as a critical component of the seizure network in a genetic form of AGS. Ethanol inhibits NMDA receptors, and the binding at these receptors is increased during ETX in certain brain regions. Therefore, the effect of focal microinjection into DLSC of a competitive NMDA receptor antagonist, dl-2-amino-7-phosphonoheptanoic acid (AP7) on ETX seizures was examined. AP7 (2 and 5 nmol/side) microinjected bilaterally into DLSC suppressed AGS, supporting a critical role of the DLSC in the AGS network during ETX. DLSC neuronal firing changes in behaving rats were subsequently examined, using chronically implanted microwire electrodes. Acoustically-evoked DLSC firing was significantly suppressed during ethanol intoxication and during ETX. However, DLSC neurons began firing tonically 1–2 s before the onset of the wild running behavior of AGS. Acoustically-evoked DLSC firing was suppressed during post-ictal depression with recovery beginning as the righting reflex returned. These data support a requisite role of the DLSC in AGS during ETX. These neuronal firing changes suggest an important role of DLSC neurons in generation of the wild running phase of AGS during ETX, which may be a general pathophysiological mechanism and a critical event in the initiation of wild running, since a similar pattern was seen previously in a genetic form of AGS.