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点燃拮抗作用的进一步特征分析。

Further characterization of kindling antagonism.

作者信息

Kirkby R D, Gilbert T H, Westcott M C, Corcoran M E

机构信息

Department of Psychology, University of Victoria, B.C., Canada.

出版信息

Epilepsy Res. 1995 Jun;21(2):115-24. doi: 10.1016/0920-1211(95)00019-7.

Abstract

Alternating stimulation of two sites in the forebrain culminates in typical kindling of generalized seizures from one site (dominant), whereas the other site (suppressed) supports only nongeneralized seizures for as long as stimulation of the dominant site continues, a phenomenon referred to as kindling antagonism. With the termination of stimulation of the dominant site, however, seizures provoked from the suppressed site eventually generalize, a progression thought to reflect the resumption of kindling from a previous point of arrest. To further assess the nature of kindling antagonism, we established antagonism between the amygdala and the septal area and subsequently evaluated the development of seizures provoked by stimulation of sites distal to the dominant site (always the amygdala). In Experiment 1, a 30-d stimulation-free period imposed after the establishment of antagonism failed to result in immediate generalization of seizures provoked from the suppressed site (septal area) in seven of eight rats. Although these results suggest that antagonism reflects an actual arrest of kindling rather than a transient inhibition of seizures, they are not entirely unambiguous: Rats exposed to the prolonged stimulation-free period required only half the number of septal stimulations for the expression of a generalized seizure as compared to rats receiving septal stimulation immediately after the establishment of antagonism. The latter finding is suggestive of a transient component of antagonism. In Experiment 2, development of generalized seizures from the previously naive right amygdala was virtually identical in rats previously kindled from the left amygdala and in rats expressing antagonism between the septal area and left amygdala. Development of generalized seizures from the right amygdala was faster than from the left amygdala in both groups of rats, however, suggesting that the expression of seizures provoked from the suppressed site after the establishment of antagonism does not involve a general impairment or enhancement of transfer. Experiment 3 revealed that radio-frequency lesions of the dominant site (amygdala) after the establishment of antagonism did not alter the subsequent development of generalized seizures from the suppressed site (septal area). This suggests that the expression of generalized seizures from the suppressed site after the establishment of kindling antagonism is not dictated by the functional state of the dominant site.

摘要

在前脑两个部位进行交替刺激,最终会导致其中一个部位(占主导地位)引发典型的全身性癫痫发作点燃,而另一个部位(受抑制部位)在对占主导地位部位的刺激持续期间,仅支持非全身性癫痫发作,这种现象被称为点燃拮抗作用。然而,随着对占主导地位部位刺激的终止,受抑制部位引发的癫痫发作最终会全身性发作,这一进展被认为反映了从先前的停滞点重新开始点燃。为了进一步评估点燃拮抗作用的本质,我们在杏仁核和隔区之间建立了拮抗作用,随后评估了对占主导地位部位(始终是杏仁核)远端部位进行刺激所引发的癫痫发作的发展情况。在实验1中,在建立拮抗作用后施加30天的无刺激期,8只大鼠中有7只受抑制部位(隔区)引发的癫痫发作并未立即全身性发作。尽管这些结果表明拮抗作用反映的是点燃的实际停滞而非癫痫发作的短暂抑制,但结果并非完全明确:与在建立拮抗作用后立即接受隔区刺激的大鼠相比,经历长时间无刺激期的大鼠在表达全身性癫痫发作时所需的隔区刺激次数仅为一半。后一发现提示拮抗作用存在短暂成分。在实验2中,先前从未接受过刺激的右侧杏仁核引发全身性癫痫发作的发展情况,在先前从左侧杏仁核点燃的大鼠和在隔区与左侧杏仁核之间表现出拮抗作用的大鼠中几乎相同。然而,两组大鼠中右侧杏仁核引发全身性癫痫发作的速度都比左侧杏仁核快,这表明建立拮抗作用后受抑制部位引发的癫痫发作的表达并不涉及传递的普遍受损或增强。实验3表明,建立拮抗作用后对占主导地位部位(杏仁核)进行射频损伤,并未改变受抑制部位(隔区)随后全身性癫痫发作的发展情况。这表明建立点燃拮抗作用后受抑制部位全身性癫痫发作的表达不受占主导地位部位功能状态的支配。

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