Takazawa A, Bilkey D K
Department of Psychology, University of Otago, Dunedin, New Zealand.
Brain Res. 1988 Nov 8;473(1):99-106. doi: 10.1016/0006-8993(88)90320-4.
The effect of the somatostatin depleting substance, cysteamine (100 mg/kg, i.p.), on cortical and amygdaloid kindled seizures was investigated. Cysteamine was tested after the establishment of amygdaloid kindling (AM group) and at two different developmental stages of cortical kindling, namely 'focal-cortical' (FC group) and 'cortico-generalized' seizures (CG group). In control, non-kindled, sham operated animals, cysteamine did not induce any spike activity or myoclonus. However, in all kindled groups clustered spike bursting appeared in the cortex within 5-15 min of the injection. The kindled bursting appeared in the cortex within 5-15 min of the injection. The kindled rats exhibited myoclonic jerks at 10 to 30 min after cysteamine injection, which coincided with the cortical spikes, and continued for about 40 min. In contrast, relatively small amounts of spiking were observed in the amygdala and this did not correlate with the myoclonus. At 4 h after cysteamine injection, the motor seizure and afterdischarge durations of the kindled seizure were prolonged in all kindled groups compared with preinjection levels. However, 24 h later the motor seizure duration and the afterdischarge duration were markedly reduced from the preinjection level in the AM and the CG groups and the tonic seizure component was suppressed in the FC group. This inhibitory effect on seizure activity lasted several days and gradually disappeared. These modifying effects of cysteamine were more marked in cortical kindled, than in amygdaloid kindled animals. The results suggest that the cortex is more sensitive to the effect of cysteamine on kindled seizures involves two phases. The first of these effect of cysteamine on kindled seizures involves two phases.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了生长抑素耗竭物质半胱胺（100毫克/千克，腹腔注射）对皮层和杏仁核点燃性癫痫发作的影响。在杏仁核点燃建立后（AM组）以及皮层点燃的两个不同发育阶段，即“局灶性皮层”（FC组）和“皮层全身性”癫痫发作（CG组）对半胱胺进行了测试。在对照、未点燃、假手术动物中，半胱胺未诱发任何棘波活动或肌阵挛。然而，在所有点燃组中，注射后5至15分钟内皮层出现成簇的棘波爆发。点燃性爆发在注射后5至15分钟内出现在皮层。点燃的大鼠在注射半胱胺后10至30分钟出现肌阵挛性抽搐，这与皮层棘波同时出现，并持续约40分钟。相比之下，杏仁核中观察到的棘波数量相对较少，且这与肌阵挛无关。注射半胱胺4小时后，与注射前水平相比，所有点燃组点燃性癫痫发作的运动性癫痫发作和放电后持续时间均延长。然而，24小时后，AM组和CG组的运动性癫痫发作持续时间和放电后持续时间与注射前水平相比明显缩短，FC组的强直性癫痫发作成分受到抑制。这种对癫痫活动的抑制作用持续数天并逐渐消失。半胱胺对点燃性癫痫发作的这些调节作用在皮层点燃的动物中比在杏仁核点燃的动物中更明显。结果表明，皮层对半胱胺对点燃性癫痫发作的影响更敏感，半胱胺对点燃性癫痫发作的影响涉及两个阶段。其中第一个阶段……（摘要截断于250字）
