Wasterlain C G, Liu H, Mazarati A M, Baldwin R A, Shirasaka Y, Katsumori H, Thompson K W, Sankar R, Pereira de Vasconselos A, Nehlig A
Department of Neurology, VA Greater Los Angeles Health Care System, California 90073, USA.
Epilepsia. 2000;41 Suppl 6:S134-43. doi: 10.1111/j.1528-1157.2000.tb01572.x.
We describe a model of self-sustaining status epilepticus (SSSE) induced by stimulation of the perforant path in free-running rats. In this model, seizures can be transiently suppressed by intrahippocampal injection of a blocker of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/ kainate synapses but return in the absence of further stimulation when the drug ceases to act. However, seizures are irreversibly abolished by blockers of N-methyl-D-aspartate receptors given locally or systemically. SSSE is enhanced by substance P and its agonists and blocked by its antagonists. SSSE induces novel expression of substance P-like immunoreactivity in hippocampal principal cells. These changes and those in other limbic peptides may contribute to the maintenance of SSSE and to the modulation of hippocampal excitability during epileptic seizures. NMDA
我们描述了一种在自由活动大鼠中通过刺激穿通通路诱导的自我维持性癫痫持续状态（SSSE）模型。在该模型中，海马内注射α-氨基-3-羟基-5-甲基异恶唑-4-丙酸/海人藻酸突触阻滞剂可短暂抑制癫痫发作，但当药物作用消失且无进一步刺激时，癫痫发作会再次出现。然而，局部或全身给予N-甲基-D-天冬氨酸受体阻滞剂可不可逆地消除癫痫发作。P物质及其激动剂可增强SSSE，而其拮抗剂则可阻断SSSE。SSSE可诱导海马主细胞中P物质样免疫反应性的新表达。这些变化以及其他边缘肽的变化可能有助于SSSE的维持以及癫痫发作期间海马兴奋性的调节。NMDA
