Halonen T, Miettinen R, Toppinen A, Tuunanen J, Kotti T, Riekkinen P J
Department of Neurology, University of Kuopio, Finland.
Neurosci Lett. 1995 Jul 28;195(1):13-6. doi: 10.1016/0304-3940(95)11766-p.
We studied the neuroprotective effect of vigabatrin (gamma-vinyl GABA, VGB) in the rat hippocampus after status epilepticus (SE) induced by kainic acid (KA). Rats were treated with VGB (500 or 1000 mg/kg, i.p.) 24 h before KA injection (9 mg/kg, i.p.). The lower dose of VGB had no effect on the generation or severity of convulsions. However, VGB decreased neuronal damage in the CA3a (P < 0.05) and CA1 (P < 0.01) subfields of the hippocampus. The higher dose of VGB attenuated the severity of convulsions (P < 0.05) but had no effect on the development or generalization of convulsions. This finding may have clinical implications in the prevention of neuronal damage induced by drug refractory seizures or SE.
我们研究了氨己烯酸(γ-乙烯基氨基丁酸,VGB)对由海藻酸(KA)诱导的癫痫持续状态(SE)后大鼠海马体的神经保护作用。在注射KA(9mg/kg,腹腔注射)前24小时,用VGB(500或1000mg/kg,腹腔注射)处理大鼠。较低剂量的VGB对惊厥的发生或严重程度没有影响。然而,VGB减少了海马体CA3a(P<0.05)和CA1(P<0.01)亚区的神经元损伤。较高剂量的VGB减轻了惊厥的严重程度(P<0.05),但对惊厥的发展或扩散没有影响。这一发现可能对预防药物难治性癫痫发作或SE诱导的神经元损伤具有临床意义。