Hirsch E, Danober L, Simler S, Pereira de Vasconcelos A, Maton B, Nehlig A, Marescaux C, Vergnes M
INSERM U 398, Faculté de Médecine, Strasbourg, France.
Neuroscience. 1997 Apr;77(4):975-84. doi: 10.1016/s0306-4522(96)00503-9.
Audiogenic seizures, a model of brainstem epilepsy, are characterized by a tonic phase (sustained muscular contraction fixing the limbs in a flexed or extended position) associated with a short cortical electroencephalogram flattening. When sound-susceptible rats are exposed to repeated acoustic stimulations, kindled audiogenic seizures, characterized by a clonic phase (facial and forelimb repetitive jerks) associated with cortical spike-waves, progressively appear, suggesting that repetition of brainstem seizures causes a propagation of the epileptic discharge toward the forebrain. In order to determine the structures through which this propagation occurs, four kinds of experiments were performed in non-epileptic rats and in sound-susceptible rats exposed to single or repeated sound stimulations. The following results were obtained: (I) Electrical amygdalar kindling was similar in non-epileptic and naive-susceptible rats, but was facilitated in sound-susceptible rats submitted to 40 acoustic stimulations and presenting kindled audiogenic seizures. (2) Audiogenic seizures induced an increase in [(14)C]2-deoxyglucose concentration in the amygdala after a single seizure, and in the amygdala, hippocampus and perirhinal and piriform cortices after a kindled audiogenic seizure. (3) A single audiogenic seizure induced the expression of c-Fos protein mainly in the auditory nuclei. A few cells were stained in the amygdala. After 5-10 audiogenic seizures, a clear staining appeared in the amygdala, and perirhinal and piriform cortices. The hippocampus expressed c-Fos later, after 40 audiogenic seizures. (4) Injection of lidocaine into the amygdala did not modify single audiogenic seizures, but suppressed myoclonias and cortical spike-waves of kindled audiogenic seizures. Similar deactivation of the hippocampus failed to modify kindled audiogenic seizures. Taken together, these data indicate a critical role for the amygdala in the spread of audiogenic seizures from brainstem to forebrain.
听源性癫痫发作是脑干癫痫的一种模型,其特征为强直期(持续的肌肉收缩,使肢体固定于屈曲或伸展位置),伴有短暂的皮质脑电图平坦化。当对声音敏感的大鼠反复进行声音刺激时,会逐渐出现点燃性听源性癫痫发作,其特征为阵挛期(面部和前肢重复性抽搐),伴有皮质棘波,这表明脑干癫痫发作的重复会导致癫痫放电向前脑传播。为了确定这种传播发生所经过的结构,我们对非癫痫大鼠以及接受单次或重复声音刺激的声音敏感大鼠进行了四类实验。得到了以下结果:(I)非癫痫大鼠和未致敏的声音敏感大鼠的电杏仁核点燃情况相似,但在接受40次声音刺激并出现点燃性听源性癫痫发作的声音敏感大鼠中,电杏仁核点燃情况得到促进。(2)单次听源性癫痫发作后,杏仁核中[(14)C]2-脱氧葡萄糖浓度升高,点燃性听源性癫痫发作后,杏仁核、海马体、嗅周皮质和梨状皮质中[(14)C]2-脱氧葡萄糖浓度升高。(3)单次听源性癫痫发作主要诱导听觉核团中c-Fos蛋白表达。杏仁核中有少量细胞被染色。5-10次听源性癫痫发作后,杏仁核、嗅周皮质和梨状皮质中出现明显染色。海马体在40次听源性癫痫发作后较晚表达c-Fos。(4)向杏仁核注射利多卡因并未改变单次听源性癫痫发作,但抑制了点燃性听源性癫痫发作的肌阵挛和皮质棘波。对海马体进行类似的失活处理未能改变点燃性听源性癫痫发作。综上所述,这些数据表明杏仁核在听源性癫痫发作从脑干向前脑的传播中起关键作用。