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Kindling induced changes in EEG recorded during stimulation from the site of stimulation: collapse of GABA-mediated inhibition and onset of rhythmic synchronous burst.

作者信息

Morimoto K, Goddard G V

出版信息

Exp Neurol. 1986 Dec;94(3):571-84. doi: 10.1016/0014-4886(86)90238-4.

DOI:10.1016/0014-4886(86)90238-4
PMID:3780908
Abstract

As a new approach to the functional alteration of kindled epileptogenic foci, we have demonstrated electroencephalographic (EEG) changes at the site of stimulation at the times when the kindling stimulation is applied in freely moving rats. In the kindled amygdala, three components of response were observed: an initial evoked potential, a subsequent EEG suppression, and an eventual burst of rhythmic spiking. The three components were a common feature also in the kindled hippocampus and prepyriform region. The duration of component 2, EEG suppression, progressively increased with each day of kindling (40 to 50 days), but dramatically shortened again after a rest period of 1 month. It was sensitive to pharmacological manipulations of gamma-aminobutyric acid (GABA). The amplitude of component 3, rhythmic spiking, increased during kindling, and was relatively insensitive to current intensities. The increased amplitude was long-lasting, independent of GABAergic, monoaminergic, and cholinergic manipulations, but sensitive to a benzodiazepine. It is suggested that component 3 is the outbreak of synchronous excitatory action which may be related to the basic mechanism of kindling.

摘要

相似文献

1
Kindling induced changes in EEG recorded during stimulation from the site of stimulation: collapse of GABA-mediated inhibition and onset of rhythmic synchronous burst.
Exp Neurol. 1986 Dec;94(3):571-84. doi: 10.1016/0014-4886(86)90238-4.
2
Kindling-induced changes in EEG recorded during stimulation from the site of stimulation. III. Direct pharmacological manipulations of the kindled amygdala.点燃诱导的在刺激部位刺激期间记录的脑电图变化。III. 对点燃杏仁核的直接药理学操作。
Exp Neurol. 1987 Jul;97(1):17-34. doi: 10.1016/0014-4886(87)90279-2.
3
Deep prepyriform cortex kindling and its relation to amygdala kindling in the rat.
Exp Neurol. 1986 Dec;94(3):637-48. doi: 10.1016/0014-4886(86)90243-8.
4
Kindling-induced changes in the EEG recorded during stimulation from the site of stimulation. II. Comparison between spontaneous and evoked potentials.点燃效应诱导的脑电图变化,记录于刺激部位的刺激过程中。II. 自发电位与诱发电位的比较。
Exp Neurol. 1987 Jul;97(1):1-16. doi: 10.1016/0014-4886(87)90278-0.
5
Kindling-induced long-lasting changes in synaptic transmission in the basolateral amygdala.点燃诱导的基底外侧杏仁核突触传递的长期变化。
J Neurophysiol. 1992 Feb;67(2):443-54. doi: 10.1152/jn.1992.67.2.443.
6
Mechanisms underlying the enhancement of excitatory synaptic transmission in basolateral amygdala neurons of the kindling rat.点燃大鼠基底外侧杏仁核神经元兴奋性突触传递增强的潜在机制。
J Neurophysiol. 1998 Aug;80(2):638-46. doi: 10.1152/jn.1998.80.2.638.
7
Seizure-triggering mechanisms in the kindling model of epilepsy: collapse of GABA-mediated inhibition and activation of NMDA receptors.
Neurosci Biobehav Rev. 1989 Winter;13(4):253-60.
8
Amygdala-kindling induces a lasting reduction of GABA-immunoreactive neurons in a discrete area of the ipsilateral piriform cortex.杏仁核点燃诱导同侧梨状皮质离散区域中γ-氨基丁酸免疫反应性神经元的持续减少。
Synapse. 1998 Aug;29(4):299-309. doi: 10.1002/(SICI)1098-2396(199808)29:4<299::AID-SYN2>3.0.CO;2-0.
9
The substantia nigra is an important site for the containment of seizure generalization in the kindling model of epilepsy.在癫痫点燃模型中,黑质是抑制癫痫发作泛化的重要部位。
Epilepsia. 1987 Jan-Feb;28(1):1-10. doi: 10.1111/j.1528-1157.1987.tb03613.x.
10
Abnormal neuronal excitability in hippocampal slices from kindled rats.点燃大鼠海马切片中神经元兴奋性异常。
J Neurophysiol. 1985 Nov;54(5):1295-304. doi: 10.1152/jn.1985.54.5.1295.

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Different phases of afterdischarge during rapid kindling procedure in mice.小鼠快速点燃过程中后放电的不同阶段。
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High doses of memantine (1-amino-3,5-dimethyladamantane) induce seizures in kindled but not in non-kindled rats.高剂量的美金刚(1-氨基-3,5-二甲基金刚烷)可诱发点燃大鼠的癫痫发作,但对未点燃大鼠则无此作用。
Naunyn Schmiedebergs Arch Pharmacol. 1990 May;341(5):476-81. doi: 10.1007/BF00176343.
5
A review of evidence for GABergic predominance/glutamatergic deficit as a common etiological factor in both schizophrenia and affective psychoses: more support for a continuum hypothesis of "functional" psychosis.关于γ-氨基丁酸能占优势/谷氨酸能缺陷作为精神分裂症和情感性精神病共同病因因素的证据综述:对“功能性”精神病连续体假说的更多支持
Neurochem Res. 1991 Oct;16(10):1099-111. doi: 10.1007/BF00966587.