Abstract:
:Neuron loss in layer III of the entorhinal cortex (EC) occurs in patients with temporal lobe epilepsy and in several animal models of the disease and may play a role in the development of spontaneously recurring seizures. This damage can be reproduced in rats by a focal microinjection of the indirect excitotoxin aminooxyacetic acid into the EC (Neurosci. Lett., 147: 185, 1992). We have now examined a similar but approximately 20 times more potent toxin, gamma-acetylenic GABA (GAG), for its ability to produce seizures and neurodegeneration in the rat EC. EEG activity was recorded continuously for 48 h after a focal injection of 4 micrograms GAG into the rat EC. Seizure episodes, spiking, and other irregularities occurred with a latency of 150 min. Behavioral abnormalities were observed in all animals and were always accompanied by EEG seizures. The behavioral changes subsided gradually, but EEG seizures continued up to 24 h after GAG treatment. Nissl and silver-stained tissue sections obtained 2-3 days after the injection of 4 micrograms GAG revealed neuron loss which preferentially affected the medial part of layer III of the EC, and caused a modest lesion in the hilar region of the ventral hippocampus. The neurodegenerative potency of GAG, in contrast to the effects of aminooxyacetic acid, was not influenced by the depth of anesthesia during surgery. A slight increase in the dose of GAG (to 5 micrograms) resulted in more severe behavioral seizures, causing generalized convulsions with salivation and loss of righting posture in 3 of 13 rats. These animals also showed a marked enlargement of the lesioned area, with substantial neuronal loss occurring in layer III of the EC, in the hilus of the dentate gyrus, and occasionally also in homotopic structures of the contralateral hemisphere. Seizure activity and lesions induced by 4 micrograms GAG were prevented by the NMDA receptor antagonist Dizolcipine (MK-801) (4 mg/kg, i.p., 10 min before and 12 h after GAG). These data support the notion of a close correlation between the occurrence of seizures and neuronal loss in layer III of the EC. Taken together, the study suggests that intraentorhinal injections of GAG may provide an advantageous model for the study of epileptogenic and epileptic mechanisms.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Wu HQ,Schwarcz Rdoi
10.1006/exnr.1998.6908subject
Has Abstractpub_date
1998-10-01 00:00:00pages
203-13issue
2eissn
0014-4886issn
1090-2430pii
S0014-4886(98)96908-4journal_volume
153pub_type
杂志文章abstract::Cats were kindled in the amygdala. After completion of kindling, their EEG was monitored almost continuously by a computer system which allowed the detection of spontaneous seizures and the quantification of interictal spikes. The relationships between seizures triggered by stimulation, spontaneous seizures, and inter...
journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 临床试验,杂志文章,多中心研究
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pub_type: 杂志文章
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doi:10.1016/j.expneurol.2013.04.003
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doi:10.1016/j.expneurol.2007.05.011
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pub_type: 杂志文章
doi:10.1016/j.expneurol.2011.02.013
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1995.1028
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1998.6784
更新日期:1998-05-01 00:00:00
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abstract:RATIONALE:Neurofibromatosis type 1 (NF1) is associated with higher rates of epilepsy compared to the general population. Some NF1 patients with epilepsy do not have intracranial lesions, suggesting the genetic mutation itself may contribute to higher rates of epilepsy in these patients. We have recently demonstrated in...
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