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

Perforant path stimulation for 24 h evoked hippocampal granule cell spikes and epileptiform discharges throughout the stimulation period. After stimulation, hippocampal neurons that receive granule cell output were irreversibly damaged and the stimulated hippocampus of each rat revealed a selective loss of Timm stain in the mossy fiber pathway. These results provide evidence in vivo for a role for synaptic zinc in neurotransmission and/or seizure mechanisms.
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PMID:A selective loss of hippocampal mossy fiber Timm stain accompanies granule cell seizure activity induced by perforant path stimulation. 285 83

Zinc ions, which are unevenly distributed in the CNS and can be released from nerve terminals, have been implicated as causative agents in epileptogenesis. The present study has shown that intraventricular administration to anesthetized rats causes seizure activity of the ECOG and convulsions. Since the manner in which zinc influences neuronal activity and triggers convulsions is unclear, studies were also made of its effect on spontaneous and evoked activity in the rat forebrain. It was found that iontophoretic application of zinc to cortical neurons causes slow and often prolonged increases in firing rate, usually accompanied by bursts of high frequency discharge in just under half the studies. Another cation, barium, evoked excitatory responses of a similar type and a reduction in potassium permeability may underlie the effects of both cations. In contrast, calcium, magnesium, manganese and cerium caused short duration depressant effects. The depression induced by calcium, but not by the other cations, could be blocked by zinc. Similarly, in the hippocampus zinc depressed calcium-dependent potentiation in subfield CA3 evoked by paired-pulse stimulation of mossy fibers; excitatory effects (namely an increase in spike amplitude and appearance of multiple population spikes) were seen at higher zinc concentrations. The depressant effects of an enkephalin analog on cortical firing rate were also blocked by zinc, consistent with studies from another laboratory suggesting enkephalin/zinc interactions. In contrast, the depressant effect of GABA could not be blocked by zinc, although an antagonism has been reported in the lobster muscle. Firm conclusions regarding the mechanism(s) underlying the triggering of seizure activity by zinc cannot yet be drawn, but the results of these studies would be consistent with an interference with calcium and/or potassium ion activity rather than with GABA binding sites.
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PMID:Effect of zinc on neuronal activity in the rat forebrain. 302 63

The effect of long-term treatment with valproic acid (VPA) on zinc (Zn) metabolism was studied in 15 children with absence seizures. During treatment with VPA the erythrocyte Zn content was significantly lower than that found in controls matched for sex and age. Plasma and urine values of Zn and of copper were within normal limits. It is suggested that the anticonvulsive action of VPA may be mediated through its effect on the metabolism of Zn in the brain and the concomitant changes in the activity of the enzymes glutamic acid decarboxylase and carbonic anhydrase.
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PMID:Effect of valproic acid therapy on zinc metabolism in children with primary epilepsy. 310 54

Fourty-nine patients were examined with epileptic seizures and values of serum and erythrocyte magnesium (sMg, RBC Mg) and serum zinc (sZn) were determined. Chronic deficiency in RBC Mg and sZn were confirmed. The percentage of patients with decreased RBC Mg increased with the time of antiepileptic treatment; significant lowering occurs after 5 years of treatment for RBC Mg and within 5 years for sZn. Various antiepileptics and their combinations have different effects on the degree of the lowering. The therapy of magnesium lactate produces significantly higher RBC Mg and sZn. The clinical, electroencephalographical and biochemical findings are improved.
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PMID:Metabolism of magnesium and zinc in patients treated with antiepileptic drugs and with magnesium lactate. 312 21

A quinoline fluorescence method for staining zinc in axonal boutons was used to study the effects of kainic acid (KA) induced seizures upon zinc in the boutons of hippocampal mossy fibers. Compared to untreated rats, rats given KA (10-12 mg/kg) and undergoing sustained seizures showed a marked loss of zinc fluorescence in the mossy fiber regions. The reduced fluorescence was detectable within 3 h of KA administration, was most pronounced at 12-24 h, and was still noticeable up to 48 h after KA. The findings suggest that zinc is released rapidly from mossy fiber boutons during seizures.
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PMID:Loss of zinc staining from hippocampal mossy fibers during kainic acid induced seizures: a histofluorescence study. 337 Apr 96

In the present study, zinc content was determined in discrete hippocampal and amygdaloid areas of 3 strains of mice (El, ddY and CBA) using an atomic absorption spectrophotometer. Zinc content was significantly lower in the dentate area of El strain compared to ddY and CBA strains. The El mouse is considered an animal model for epilepsy and the seizures in this mouse appear to originate in the hippocampus. The results suggest the possible involvement of hippocampal zinc in the pathophysiology of convulsive seizures in the epileptic mouse.
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PMID:Zinc content in discrete hippocampal and amygdaloid areas of the epilepsy (El) mouse and normal mice. 340 88

The reported convulsant properties of zinc and its association with hippocampal function prompted investigation of zinc levels during the induction and maintenance of kindling. Rats were fed zinc adequate diets during kindling, incited by daily amygdalar stimulation. The concentration of zinc in hippocampus was unperturbed during 3 stages of kindling induction when compared to either naive, sham surgery, or electroshock controls. In contrast, cortical zinc increased during kindling induction but returned to control levels in fully kindled animals. Two weeks after full kindling was established, the concentration of zinc in the hippocampus and overlying cortex increased significantly, in the absence of further electrical stimulation. The effect was restricted to the central nervous system inasmuch as zinc levels were unaffected in liver and other extracerebral tissues. Moreover, the zinc concentration was relatively unchanged during the 24 h period following a single electroconvulsive seizure, implying that the observed changes were not simply a postictal phenomenon. The results of this study suggest that long-lasting elevations in zinc are present after kindling is established. Whether this finding is related to the perpetuation of abnormal neuronal excitability or represents a compensatory response remains to be elucidated.
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PMID:Amygdalar kindling is associated with elevated zinc concentration in the cortex and hippocampus of rats. 350 98

Seizure produced by intrahippocampal injection of zinc sulfate in rabbits is a new chronic model of experimental epilepsy. In this model, the clinical manifestations are easily observed and are expressed not only as partial clonic seizures, but also by secondary generalized seizures. The electrohippocampalogram (EHG) and electrocorticogram (ECoG) discharges change correspondingly during both types of seizures, and last for weeks. The mechanism for induced seizures may be partly related to the inhibitory effect of zinc sulfate injections on the acetylcholinesterase (AchE) activity in the hippocampus. The commonly used antiepileptic drugs, such as phenobarbital and phenytoin, afforded protection against the zinc-induced secondary generalized clonic seizures and alleviated the partial clonic seizures but had no influence on the EHG- and ECoG-monitored periodic bursts of spike discharges. Nitrazepam was found to antagonize both types of seizures and also transiently restored the EHG and ECoG to normal. D-penicillamine, a metal chelator, may be the most effective agent for the treatment of zinc-induced seizures; the agent, in addition to affording protection against both types of seizures, also caused the periodic burst spike discharges in EHG and ECoG to disappear.
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PMID:Features of seizures and behavioral changes induced by intrahippocampal injection of zinc sulfate in the rabbit: a new experimental model of epilepsy. 369 33

Amygdala kindling stimulation produced significant changes in plasma zinc levels in cats otherwise unaffected by zinc loading or deprivation. While a normal diet had no effect, moderate zinc loading was accompanied by a marked increase in plasma zinc during kindling. Conversely, plasma zinc sharply declined in animals fed a zinc-deficient diet. Corresponding differences were obtained in the development of generalized seizures with kindling such that loading delayed and deprivation accelerated this process.
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PMID:Kindled seizure induction alters and is altered by zinc absorption. 376 4

Hippocampal calcium and zinc content was determined using atomic absorption spectrophotometry in control and commissural-kindled rats. In animals exhibiting 5-10 consecutive motor seizures hippocampal calcium was slightly elevated (356.7 parts per million (ppm), dry weight) but not significantly different from controls (329.8 ppm), whereas the amount of zinc was significantly higher (101.6 ppm) than in nonstimulated animals (88.3 ppm). These results are indicative of certain pathophysiological changes in kindled hippocampi, most likely localized to the granule cells of the dentate gyrus where the bulk of hippocampal zinc is confined.
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PMID:Levels of hippocampal calcium and zinc following kindling-induced epilepsy. 398 99


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