Velísek L, Moshé S L, Stanton P K
Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Neurosci Lett. 1996 Apr 5;207(3):143-6. doi: 10.1016/0304-3940(96)12515-5.
Brain pH is thought to be an influential factor in determining susceptibility to seizures. We compared the susceptibility of brain slices from carbonic anhydrase II (CA II)-deficient mice to epileptiform activity induced by low extracellular [Mg2+], with slices from normal littermates, both bathed in artificial cerebrospinal fluid at pH 7.3. In both entorhinal cortex and hippocampal field CA1, epileptiform activity started earlier in CA II-deficient slices. Raising extracellular [CO2] (20%; extracellular pH, 6.7) reversibly blocked the epileptiform activity in normal, but not in CA II-deficient, slices. The data, combined with previous in vivo findings showing an increased resistance of mutants to seizures, suggest the presence of in vivo anticonvulsant acidosis with long-term compensatory changes that lead to in vitro 'proconvulsant' behavior in CA II-deficient slices clamped at pH 7.3.
脑内pH值被认为是决定癫痫易感性的一个影响因素。我们将碳酸酐酶II（CA II）缺陷小鼠的脑片对低细胞外[Mg2+]诱导的癫痫样活动的易感性，与正常同窝小鼠的脑片进行了比较，二者均浸泡在pH值为7.3的人工脑脊液中。在内嗅皮层和海马CA1区，CA II缺陷脑片中的癫痫样活动开始得更早。提高细胞外[CO2]（20%；细胞外pH值为6.7）可使正常脑片中的癫痫样活动可逆性阻断，但对CA II缺陷脑片无效。这些数据，结合之前的体内研究结果显示突变体对癫痫发作的抵抗力增加，表明体内存在抗惊厥性酸中毒，并伴有长期的代偿性变化，这导致在pH值为7.3的条件下钳制的CA II缺陷脑片出现体外“促惊厥”行为。
