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中脑和脑桥被盖部损伤对遗传性癫痫易感性大鼠听源性惊厥的影响。

Effect of midbrain and pontine tegmental lesions on audiogenic seizures in genetically epilepsy-prone rats.

作者信息

Browning R A, Nelson D K, Mogharreban N, Jobe P C, Laird H E

出版信息

Epilepsia. 1985 Mar-Apr;26(2):175-83. doi: 10.1111/j.1528-1157.1985.tb05402.x.

Abstract

A bilateral mechanical lesion of the midbrain and pontine tegmentum was found to abolish completely the tonic components of sound-induced seizures in genetically epilepsy-prone rats (GEPR) that display tonic-clonic seizures. Correlations between varied lesions placements and effects on maximal audiogenic seizures provided evidence that damage to the nucleus reticularis pontis oralis (RPO) of the midbrain and pontine reticular formation (RF) was responsible for the seizure-attenuating effects. Moreover, electrolytic lesions of the pontine RF involving the RPO nucleus were found to abolish the tonic components of the maximal audiogenic seizure. Additionally, bilateral mechanical lesions involving the RPO nucleus were found to attenuate the clonic components of sound-induced seizures in GEPR that display only running seizures and clonus. These findings are consistent with previous studies showing that pontine tegmental lesions attenuate the tonic components of maximal electroshock- and pentylenetetrazol-induced seizures, and lend further support to the hypothesis that all generalized tonic seizures share a common neural substrate. The role of the brainstem RF in tonic versus clonic convulsions is discussed in light of the present findings.

摘要

在表现为强直阵挛性癫痫发作的遗传性癫痫易感大鼠(GEPR)中,发现中脑和脑桥被盖的双侧机械性损伤可完全消除声音诱发癫痫发作的强直成分。不同损伤部位与对最大听源性癫痫发作的影响之间的相关性提供了证据,表明中脑脑桥网状结构(RF)的脑桥口网状核(RPO)受损是癫痫发作减弱效应的原因。此外,发现涉及RPO核的脑桥RF的电解损伤可消除最大听源性癫痫发作的强直成分。此外,发现涉及RPO核的双侧机械性损伤可减弱仅表现为奔跑性癫痫发作和阵挛的GEPR中声音诱发癫痫发作的阵挛成分。这些发现与先前的研究一致,即脑桥被盖损伤可减弱最大电休克和戊四氮诱发癫痫发作的强直成分,并进一步支持了所有全身性强直癫痫发作共享共同神经基质的假说。根据目前的发现,讨论了脑干RF在强直与阵挛性惊厥中的作用。

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