Cottrell G A, Robertson H A
Brain Res. 1987 May 26;412(1):161-4. doi: 10.1016/0006-8993(87)91453-3.
In kindled rats, the administration of cysteamine (CSH, 200 mg/kg, i.p.) 4 h prior to a kindled seizure leads to long-term (up to 10 days) inhibition of kindled seizures. CSH (200 mg/kg, i.p.) also induces myoclonic seizures in kindled rats. We suggest that the long-term inhibition of kindled seizures might be the result of the myoclonus, not the somatostatin depletion as previously suggested. Prior administration of the short-acting benzodiazepine midazolam (5 mg/kg, i.p.) eliminated the CSH-induced myoclonus and prevented the long-term inhibition of kindled seizures. These results suggest that the CSH-induced long-term inhibition of kindled seizures is the result of an interaction between the myoclonic seizure and a subsequent kindled seizure.
在点燃大鼠中，在点燃性癫痫发作前4小时腹腔注射半胱胺（CSH，200mg/kg）可导致点燃性癫痫发作的长期（长达10天）抑制。CSH（200mg/kg，腹腔注射）也可在点燃大鼠中诱发肌阵挛性癫痫发作。我们认为，点燃性癫痫发作的长期抑制可能是肌阵挛的结果，而非如先前所认为的生长抑素耗竭的结果。预先给予短效苯二氮䓬类咪达唑仑（5mg/kg，腹腔注射）可消除CSH诱导的肌阵挛，并防止点燃性癫痫发作的长期抑制。这些结果表明，CSH诱导的点燃性癫痫发作的长期抑制是肌阵挛性癫痫发作与随后的点燃性癫痫发作之间相互作用的结果。
