Depaulis A
Laboratoire de Neurophysiologie et Biologie des Comportements, Centre de Neurochimie du CNRS, Strasbourg, France.
J Neural Transm Suppl. 1992;35:125-39. doi: 10.1007/978-3-7091-9206-1_9.
A system exerting inhibitory control over generalized epilepsies and involving neurons from the substantia nigra has been described by several authors in experimental models of convulsive seizures. In the present study, the existence of such a control system governing absence epilepsy was investigated using models of non-convulsive seizures in the rat. Activation of the GABAergic neurotransmission within the substantia nigra by local injection of GABA agonists (muscimol, THIP) or an inhibitor of GABA degradation (gamma-vinyl GABA) suppresses generalized non convulsive seizures, whether they are genetically determined or induced by systemic injections of gamma-butyrolactone (100 and 200 mg/kg), pentylenetetrazole (20 mg/kg) or THIP (7.5 mg/kg). The ascending dopaminergic nigral output or the GABAergic fibres to the ventromedial thalamus are not critically involved in this control system. By contrast, the GABAergic nigro-collicular pathway appears crucial: bilateral lesion of the superior colliculus abolishes the anti-epileptic effects of intranigral injection of muscimol and blockade of the GABAergic transmission within the superior colliculus results in a suppression of generalized non-convulsive seizures. Finally, activation of collicular cell bodies by low doses of kainic acid significantly suppresses absence seizures. These results suggest the existence of a control system inhibiting generalized non-convulsive seizures which is activated by the release of the tonic inhibition exerted by the nigral GABAergic fibres on collicular neurons. The similarities between this system and the control system described for convulsive seizures are discussed.
几位作者在惊厥性癫痫发作的实验模型中描述了一个对全身性癫痫发挥抑制性控制作用且涉及黑质神经元的系统。在本研究中，利用大鼠非惊厥性癫痫发作模型研究了这样一个控制失神癫痫的系统的存在情况。通过局部注射GABA激动剂（蝇蕈醇、4,5,6,7-四氢异噁唑[5,4-c]吡啶-3-醇）或GABA降解抑制剂（γ-乙烯基-GABA）激活黑质内的GABA能神经传递，可抑制全身性非惊厥性癫痫发作，无论这些发作是由基因决定的，还是由全身注射γ-丁内酯（100和200mg/kg）、戊四氮（20mg/kg）或4,5,6,7-四氢异噁唑[5,4-c]吡啶-3-醇（7.5mg/kg）诱发的。黑质上行多巴胺能输出或至腹内侧丘脑的GABA能纤维在该控制系统中并非关键因素。相比之下，GABA能黑质-上丘通路似乎至关重要：上丘双侧损伤会消除黑质内注射蝇蕈醇的抗癫痫作用，而上丘内GABA能神经传递的阻断会导致全身性非惊厥性癫痫发作受到抑制。最后，低剂量 kainic 酸激活上丘细胞体会显著抑制失神发作。这些结果表明存在一个抑制全身性非惊厥性癫痫发作的控制系统，该系统由黑质GABA能纤维对丘神经元施加的紧张性抑制的释放所激活。讨论了该系统与针对惊厥性癫痫发作所描述的控制系统之间的相似性。
