Inferior colliculus neuronal response abnormalities in genetically epilepsy-prone rats: evidence for a deficit of inhibition.
Inferior colliculus neuronal response abnormalities in genetically epilepsy-prone rats: evidence for a deficit of inhibition.
复制标题
遗传性癫痫易感大鼠的下丘神经元反应异常：抑制缺陷的证据。
DOI：
10.1016/0024-3205(86)90368-1
复制
发表时间：
1986
期刊：
影响因子：
6.1
通讯作者：
Caspary,DM
中科院分区：
文献类型：
--
作者：
Faingold,CL;Gehlbach,G;Travis,MA;Caspary,DM
遗传性癫痫易感大鼠(GEPR)对声刺激诱发癫痫异常敏感。下丘(IC)对听源性惊厥的敏感性至关重要。与其他纯音频率相比，GEPR在12 kHz时更容易诱发听源性癫痫发作。GEPR中的IC神经元表现出明显高于正常的反应阈值和更宽的调谐特性。这些发现以及之前的神经生理学和解剖学数据表明，GEPR存在听力障碍。GEPR中的IC神经元表现出一种反应模式的发生率显著增加，在刺激的开始和结束时活动达到峰值，即开始-抵消反应。这种响应模式出现在12 kHz和高刺激强度的特征频率上，可能代表后放电现象。起始-偏移模式可能是中枢机制的一种表现，该中枢机制的发展是为了补偿似乎与GEPR听力障碍有关的减少的外周听觉输入。这种代偿机制可能涉及脑干听觉核团神经递质活动的改变。GABA被认为是IC中的一种抑制性递质。与正常大鼠相比，离子导入应用GABA或苯二氮卓类药物对GEPR内IC神经元的抑制作用明显减弱。在GEPR的IC神经元中，内源性声音诱导的(双耳)抑制也显着减少，这被认为是由GABA介导的。GABA受体拮抗剂荷包牡丹碱的离子导入可将IC的正常反应模式转变为GEPR IC神经元中常见的起搏-偏置反应，提示GABA效应的降低可能导致起搏-偏置的流行。这种抑制效果的降低可能无法补偿在GEPR中高强度声刺激期间IC中假定的兴奋性递质天冬氨酸的上升。这些改变的递质作用可能是导致遗传性癫痫易感大鼠听源性癫痫发作的重要机制。
The genetically epilepsy-prone rat (GEPR) is abnormally susceptible to induction of seizures by acoustic stimulation. The inferior colliculus (IC) is critically important to audiogenic seizure susceptibility. The GEPR is more susceptible to induction of audiogenic seizures at 12 kHz than at other pure tone frequencies. IC neurons in the GEPR exhibit significantly elevated response thresholds and broader tuning characteristics than normal. These findings along with previous neurophysiological and anatomical data suggest that a hearing deficit occurs in the GEPR. IC neurons in the GEPR exhibit a significantly elevated incidence of a response pattern with a peak of activity at the beginning and end of the stimulus, the onset-offset response. This response pattern occurs at 12 kHz and at characteristic frequency with high stimulus intensities and may represent an afterdischarge phenomenon. The onset-offset pattern may be a manifestation of central mechanisms developed to compensate for reduced peripheral auditory input that appears to be involved in the hearing deficit of the GEPR. Such compensatory mechanisms may involve alterations of the actions of neurotransmitters of the brain-stem auditory nuclei. GABA is implicated as an inhibitory transmitter in the IC. Iontophoretic application of GABA or a benzodiazepine produces significantly less inhibition of IC neurons of the GEPR than of the normal rat. Endogenous sound-induced (binaural) inhibition which is suggested to be GABA-mediated is also significantly reduced in IC neurons of the GEPR. Iontophoresis of the GABAAantagonist, bicuculline, often converts normal response patterns in the IC to onset-offset responses seen with high incidence in GEPR IC neurons, suggesting that the decreased effectiveness of GABA may lead to the onset-offset prevalence. This reduced effectiveness of inhibition may be unable to compensate for the rise in the putative excitatory transmitter, aspartate, in IC during high intensity acoustic stimulation in the GEPR. These altered transmitter actions may be important mechanisms subserving initiation of audiogenic seizures in the genetically epilepsy-prone rat.