POTENTIATION OF AMYGDALOID KINDLING AND METRAZOL-INDUCED SEIZURES BY 6-HYDROXYDOPAMINE IN RATS
POTENTIATION OF AMYGDALOID KINDLING AND METRAZOL-INDUCED SEIZURES BY 6-HYDROXYDOPAMINE IN RATS
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DOI：
10.1016/0014-4886(74)90105-8
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发表时间：
1974-01-01
影响因子：
5.3
通讯作者：
WADA, JA
中科院分区：
文献类型：
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作者：
CORCORAN, ME;FIBIGER, HC;WADA, JA
完整对照组大鼠和脑室内注射6-羟基多巴胺（6-OHDA）预处理的大鼠接受惊厥剂量的戊四唑（Metrazol）。对照组大鼠对皮下注射Metrazol有反应，出现一次或多次短暂间歇性阵挛性惊厥。相比之下，用6-OHDA预处理的大鼠显示出显著更长的全身性癫痫发作，几乎所有的发作都包含后肢的强直性伸展。去甲肾上腺素（NE）和多巴胺（DA）大量耗竭的大鼠癫痫发作综合征的严重程度与NE优先耗竭的大鼠无显著差异，表明NE而不是DA耗竭是6-OHDA产生的Metrazol惊厥反应加剧的机制。在第二个实验中，对完整的和6-OHDA处理的大鼠进行点燃程序，其中最初亚惊厥的杏仁核的每日电刺激最终引起双侧阵挛性惊厥。大量消耗NE和DA的大鼠需要不到一半的刺激点燃癫痫发作的完整的大鼠或优先消耗NE的大鼠，他们继续显示显着更长的后放电近15天后，第一次点燃癫痫发作。这些数据表明，联合破坏去甲肾上腺素能和多巴胺能神经元，或破坏后者单独，是必要的，以促进点燃癫痫发作的发展。总之，这两个实验证实了早期的观察，即中央儿茶酚胺能系统往往抑制各种癫痫发作的现象。
Intact control rats and rats pretreated with an intraventricular injection of 6-hydroxydopamine (6-0HDA) received a convulsive dose of pentylenetetrazol (Metrazol). The control rats responded to the subcutaneous injection of Metrazol with one or more brief intermittent clonic convulsions. In contrast, the rats pretreated with 6-OHDA displayed significantly longer episodes of generalized seizures, nearly all of which contained episodes of tonic extension of the hindlimbs. The severity of the seizure syndrome in rats with substantial depletion of both norepinephrine (NE) and dopamine (DA) did not differ markedly from that in rats with preferential depletion of NE, suggesting that depletion of NE and not DA is the mechanism of the exacerbated convulsive response to Metrazol produced by 6-OHDA. In a second experiment, intact and 6-OHDA-treated rats were subjected to a kindling procedure, wherein daily electrical stimulation of the amygdala that was initially subconvulsive eventually came to elicit bilateral clonic convulsions. Rats with substantial depletion of both NE and DA required less than half as many stimulations to kindle seizures as did intact rats or rats with preferential depletion of NE, and they continued to display significantly longer afterdischarges for nearly 15 days after the first kindled seizure. These data suggest that combined destruction of noradrenergic and dopaminergic neurons, or destruction of the latter alone, is necessary to facilitate the development of kindled seizures. Together, the two experiments confirm earlier observations that central catecholaminergic systems tend to inhibit a variety of seizure phenomena.