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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study spatial interactions during low magnesium induced epileptiform activity, changes in extracellular potassium concentration ([K+]0) and associated slow field potentials (f.p.'s) were recorded in thin rat temporal cortex slices (400 microns) containing the neocortical temporal area 3 (Te3), the entorhinal cortex (EC) and the hippocampal formation with the dentate gyrus, area CA3 and CA1 and the subiculum (Sub). The epileptiform activity was characterized by short recurrent epileptiform discharges (40 to 80 ms, 20/min) in areas CA3 and CA1 and by interictal discharges and tonic and clonic seizure like events (SLE's) (13-88s) in the EC, Te3 and Sub. While interictal discharges occurred independent of each other in the different subfields, the three areas became synchronized during the course of a SLE. The EC, Te3 and Sub all could represent the "focus" for generation of the SLE's. This initiation site for SLE's sometimes changed from one area to another. The characteristics of the rises in [K+]0 and subsequent undershoots were comparable to previous observations in in vivo preparations. Interestingly, rises in [K+]0 could start before actual onset of seizure like activity in secondarily recruited areas. The epileptiform activity could change its characteristics to either a state of recurrent tonic discharge episodes or to a continuous clonic discharge state reminiscent of various forms of status epilepticus. We did not observe, in any of these states, active participation by area CA3 in the epileptiform activity of the EC in spite of clear projected activity to the dentate gyrus. Even after application of picrotoxin (20 microM), area CA3 did not actively participate in the SLE's generated in the entorhinal cortex. When baclofen (2 microM) was added to the picrotoxin containing medium, SLE's occurred both in the entorhinal cortex and in area CA3, suggesting that inhibition of inhibitory interneurons by baclofen could overcome the "filtering" of projected activity from the entorhinal cortex to the hippocampus.
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PMID:Regional and time dependent variations of low Mg2+ induced epileptiform activity in rat temporal cortex slices. 178 28

Extracellular amino acid levels in CA3 and CA1 fields of rat hippocampus, an area highly sensitive to seizures, were determined by intracranial microdialysis during seizures induced by systemic administration of soman (o-1,2,2-trimethylpropyl methylphosphonofluoridate), a potent inhibitor of acetylcholinesterase. The glutamate uptake level was determined on another series of animals in hippocampus homogenates. An early and transient increase in the extracellular glutamate level occurred in CA3 within 30 min of seizures, with correlated brief elevations of taurine, glycine and glutamine levels. The glutamate level increased early in CA1, declined and then became more sustained (after 50 min of seizures). Apparent elevations of taurine, glycine and glutamine levels in CA1 accompanied changes in glutamate concentrations. Changes of glutamate level correlated with an increase in the glutamate uptake which rapidly declined after 40 min of seizures. The role of the transient release of glutamate in CA3 and of the sustained release in CA1 in prolonged soman-induced seizures is considered. The correlation between glutamate and other amino acid release is studied.
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PMID:Effects of soman-induced seizures on different extracellular amino acid levels and on glutamate uptake in rat hippocampus. 178 36

The two forms of epileptic brain damage, that found in patients with chronic epilepsy (post-mortem or in an anterior temporal lobectomy specimen) and that occurring acutely after status epilepticus, have much in common but are not identical. Hippocampal lesions occurring acutely after status epilepticus show a high degree of selectivity for hilar interneurones, CA1 pyramidal neurones and CA3 pyramidal neurones. Hippocampal lesions in anterior temporal lobectomy specimens tend to involve the subfields less selectively with CA1 being only slightly more severely affected than dentate granule cells, CA3 and CA2 pyramidal neurones. The most severely damaged hippocampi may result from a combination of acute damage early in life (commonly from prolonged febrile convulsions) and cumulative damage associated with seizures. Less severe degrees of damage are probably a consequence of repeated seizures. The abnormal patterns of firing associated with epileptic activity are almost certainly responsible for cell death occurring acutely after status epilepticus; they may contribute to the progressive cell loss occurring in chronic epilepsy.
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PMID:Excitotoxicity and epileptic brain damage. 179 Jul 73

Aminooxyacetic acid (AOAA), a potent yet nonspecific transaminase inhibitor, is known to cause convulsions when administered at high doses to experimental animals. The present study was designed to explore the mechanism(s) underlying the epileptogenic properties of AOAA. To this end, the drug was injected into the hippocampus of unanesthetized rats. Injection of 1.8 to 450 nmol AOAA produced dose-dependent EEG abnormalities including, at the higher doses, limbic seizures. Coadministration of the selective NMDA receptor antagonist D-2-amino-7-phosphonoheptanoic acid (APH) at doses of 45 and 225 nmol caused an almost complete inhibition of seizures produced by 225 nmol AOAA. At 225 and 450 nmol, AOAA also caused selective neuronal damage, which was restricted to the CA1 region at the lower dose and also affected the CA3/CA4 area in two of six rats injected with the higher dose. Co-injection of 225 nmol APH completely protected the hippocampus from AOAA-induced damage. In separate experiments, microiontophoretic application of AOAA to CA1 pyramidal neurons failed to increase the firing rate of each of the 10 cells tested, thus indicating that the drug does not directly activate NMDA receptors. These experiments suggest that seizures and neurotoxicity produced by AOAA are mediated indirectly via NMDA receptor activation.
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PMID:Focal injection of aminooxyacetic acid produces seizures and lesions in rat hippocampus: evidence for mediation by NMDA receptors. 183 21

The mammalian central nervous system (CNS) contains an abundance of the transition metal zinc, which is highly localized in the neuronal parenchyma. Zinc is actively taken up and stored in synaptic vesicles in nerve terminals, and stimulation of nerve fibre tracts that contain large amounts of zinc, such as the hippocampal mossy fibre system, can induce its release, suggesting that it may act as a neuromodulator. The known interaction of zinc with the major excitatory and inhibitory amino-acid neurotransmitter receptors in the CNS supports this notion. That zinc has a role in CNS synaptic transmission, however, has so far not been shown. Here we report a physiological role for zinc in the young rat hippocampus (postnatal, P3-P14 days). Our results indicate that naturally occurring spontaneous giant depolarizing synaptic potentials (GDPs) in young CA3 pyramidal neurones, mediated by the release of GABA (gamma-aminobutyric acid), are induced by endogenously released zinc. These synaptic potentials are inhibited by specific zinc-chelating agents. GDPs are apparently generated by an inhibitory action of zinc on both pre- and postsynaptic GABAB receptors in the hippocampus. Our study implies that zinc modulates synaptic transmission in the immature hippocampus, a finding that may have implications for understanding benign postnatal seizures in young children suffering with acute zinc deficiency.
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PMID:A physiological role for endogenous zinc in rat hippocampal synaptic neurotransmission. 184 46

Hippocampal mossy fiber zinc was examined in mice selectively bred for differences in susceptibility to handling-induced convulsions during ethanol withdrawal. The density of mossy fiber zinc in the CA3 stratum lucidum was significantly decreased in the duplicate lines of untreated withdrawal seizure prone (WSP) mice compared to untreated withdrawal seizure resistant (WSR) mice. Mossy fiber zinc densities in randomly bred control lines of mice (WSC) were intermediate to WSP and WSR mice. Serum, whole brain and whole hippocampal zinc were not significantly different between WSP and WSR mice, indicating that the reduction in the chelatable pool of hippocampal mossy fiber zinc was not a consequence of deficits in brain or whole body zinc nutrition. A highly significant correlation between hippocampal mossy fiber zinc density and handling-induced convulsion indices suggests that a reduction in mossy fiber zinc may be one contributing factor in the expression of seizure susceptibility in WSP mice.
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PMID:Hippocampal mossy fiber zinc deficit in mice genetically selected for ethanol withdrawal seizure susceptibility. 186 62

The effect of an intermittent administration of kainic acid on the KA-induced behavior, scratching, wet-dog shakes and limbic seizures was studied in the rat. Nine mg/kg kainic acid was injected i.p. at 3, 7, 14 or 21 days after the priming with the same dose of kainic acid at 25 days of age. There was no significant effect of KA-priming on the onset time of scratching. The frequency of wet-dog shakes decreased significantly in all the KA-primed rats. Fourteen day-priming of kainic acid was most effective for reducing the wet-dog shakes response. The onset time of limbic seizures tended to be shorter in all the KA-primed groups; seven day-priming resulted in a significant decrease. Histological findings showed a delay in the formation of dendritic processes of pyramidal cells in the CA3 area of the hippocampus. The results indicated that an intermittent administration of kainic acid with an interval of 3 to 21 days induces a marked tolerance in the wet-dog shakes response to kainic acid in juvenile rats, while no change in the scratching and an acceleration of the onset of limbic seizures were shown, implying that different neuronal systems are involved in these three behaviors induced by kainic acid.
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PMID:[A decrease in the wet-dog shakes response to the second administration of kainic acid in juvenile rats]. 187 60

Domoic acid, in increasing doses (10-300 pmol), was microinjected into the hippocampal CA3 region of rats. All rats consistently exhibited generalized bilateral electrical seizure discharge activity at 100 pmol of domoic acid. Seizure latency varied inversely with the dose of domoic acid in the range tested. Local hippocampal administration of gamma-aminobutyric acid (GABA) resulted in neuronal recovery from domoic acid-induced seizures. The seizure activity of domoic acid might be the result of decreased GABAergic inhibition.
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PMID:Domoic acid induced seizure activity in rats. 188 31

We evaluated the ability of preoperative radiologic imaging to detect hippocampal sclerosis in 31 patients who underwent surgery for intractable epilepsy. Hippocampal sclerosis is commonly associated with surgically treatable temporal lobe epilepsy. It is pathologically described as neuronal cell loss with associated gliosis in the hippocampus. While previous reports have correlated imaging results with clinical or qualitative histologic findings, this study used quantitative pathologic criteria (neuronal cell density) to diagnosis hippocampal sclerosis. We focused our study on the 11 patients with cryptogenic temporal lobe epilepsy. Of these, nine had hippocampal sclerosis by pathologic criteria. MR findings included unilateral hippocampal atrophy, an increased signal in the hippocampus on long TR scans, and atrophy in the adjacent white matter and temporal lobe. Hippocampal atrophy was most frequently seen in the red nucleus plane on coronal scans, corresponding to the body of the hippocampus. We also compared hippocampal size on MR with neuronal density in surgical specimens of the 11 patients with cryptogenic temporal lobe epilepsy. A statistically significant correlation was found between MR size and neuronal density in CA3 and CA4 of the cornu ammonis and the granular cell layer of the hippocampus. Since temporal lobectomy eliminated seizures in seven of nine patients with hippocampal sclerosis, preoperative diagnosis by MR has important therapeutic consequences.
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PMID:Imaging findings in hippocampal sclerosis: correlation with pathology. 195 Sep 25

We investigated time-dependent changes in low magnesium-induced epileptiform activity in combined rat entorhinal cortex/hippocampal slices with extracellular recording techniques. While in area CA3 short interictal discharges are generated without any major changes in activity during prolonged recording periods, initial tonic clonic ictaform events in the entorhinal cortex may change with time. We observed often a transition into a state of recurrent tonic activity without any clonic afterdischarges. Alternatively, seizures could stay in the clonic discharge mode for the rest of the experiment. These different seizure states were not equally affected by the anticonvulsant valproic acid. While the early clonic tonic discharges in the entorhinal cortex and the interictal like activity in area CA3 were effectively suppressed by valproic acid (VPA) the late recurrent tonic seizure discharge state was unaffected by the drug. It was, however, still sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist 2-aminophosphonovalerate. These findings point to seizure-induced changes in neuronal interaction in rat entorhinal cortex.
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PMID:Late low magnesium-induced epileptiform activity in rat entorhinal cortex slices becomes insensitive to the anticonvulsant valproic acid. 198 61


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