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

Estimation of autospectra and coherence and phase spectra of seizure EEG, using the FFT technique, will cause "smearing" of the rapid dynamic changes which occur during the seizure. This is inherent to FFT spectral estimation, due to the averaging process which is necessary in order to get consistent spectral estimates. A different approach suggested in the present study is to carry out multivariate autoregressive modeling of the multichannel seizure EEG, combined with adaptive segmentation. In order to obtain good estimates in cases of short record length, the vectorial AR modeling was based on residual energy ratios. The method has been tested on multichannel seizure EEG recordings from rats with focal epilepsy, caused by intracerebral administration of Kainic acid, and in depth EEG recordings in patients with temporal lobe epilepsy.
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PMID:On the tracking of rapid dynamic changes in seizure EEG. 147 24

Changes in endogenous somatostatin after quinolinic and kainic acids were investigated by measuring somatostatin-like peaks by in vivo voltammetry and by assessing the distribution of somatostatin-positive neurons by immunocytochemistry. Kainic acid (0.19 nmol/0.5 microliter) or quinolinic acid (120 nmol/0.5 microliter) in doses inducing comparable electroencephalographic seizure patterns, were injected into the hippocampus of freely moving rats. Somatostatin-like peaks were measured every 6 min for 3 h by a carbon fiber electrode implanted in the proximity of the injection needle. Kainic acid kept somatostatin-like peaks significantly higher than saline from 48 min after the injection till the end of the recording. Somatostatin-like peaks were dramatically elevated by quinolinic acid, reaching a maximum of 482% 60 min after the injection. Three days later, administration of kainic acid resulted in selective degeneration of CA3 pyramidal neurons but did not affect the number of somatostatin-positive cells, while quinolinic acid induced cell loss in all pyramidal layers and complete degeneration of somatostatin-positive cells in the whole hippocampus. Thus, the quantitative difference in somatostatin release in response to doses of kainic and quinolinic acids inducing comparable electroencephalographic seizure patterns was reflected in a substantial difference in the neurodegenerative consequences. In both models, the release of somatostatin in response to seizures may be interpreted as a "defense" mechanism aimed at reducing the spread of excitation in the tissue.
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PMID:Functional and histological consequences of quinolinic and kainic acid-induced seizures on hippocampal somatostatin neurons. 167 38

Temporal lobe epilepsy is a common form of epilepsy in human adults and is associated with a unique pattern of damage in the hippocampus. The damage includes cell loss of the CA3 and CA4 areas and synaptic growth (sprouting) of mossy fibers in the supragranular layer of the dentate gyrus. Experimental evidence indicates that in adult rats the excitatory amino acid, kainic acid, induces a similar pattern of changes in hippocampal circuitry associated with alterations in perforant path excitation and inhibition. It has been suggested that, in humans, this type of damage may be a result of seizures early in life. In this study we examined the effects of kainic acid-induced status epilepticus on synaptic reorganization and paired-pulse electrophysiology in developing rats and adults. Kainic acid induced more severe seizures in 15-day-old rat pups than in adults. In contrast to adult rats, these seizures did not produce CA3/CA4 neuronal loss, mossy fiber sprouting or changes in paired-pulse excitation or inhibition in the hippocampus of rat pups tested 2-4 weeks after status epilepticus. Our results provide evidence that the immature hippocampus may be more resistant to seizure-induced changes than the mature hippocampus.
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PMID:Resistance of the immature hippocampus to seizure-induced synaptic reorganization. 171 81

Kainic acid was injected into the hippocampus of rats and glutamine synthetase was measured to determine whether astrocytes are involved in the early effects of this neurotoxic agent. Glutamine synthetase was reduced by 38%, 24 h after the stereotaxic application of 4 nmol of kainic acid to this region. The reduction in glutamine synthetase by kainic acid was not due to direct inhibition of the brain enzyme. This effect also was not due to seizure activity since rats peripherally injected with a convulsant dose of kainic acid were found to have normal hippocampal glutamine-synthetase activity. Exposure of astrocyte cultures to kainic acid for 24 h produced no evidence of gliotoxicity and no change in glutamine synthetase activity. The effect of intrahippocampal kainic acid on glutamine synthetase appears to be indirect, most likely produced secondarily to its neuronal effects. Several studies have shown that endogenous glutamate is involved in kainate neurotoxicity. A reduction in glutamine synthetase by kainic acid may impair the capacity for astrocytes to metabolize glutamate. Such an impairment could contribute to the glutamate-mediated cell death following kainic acid exposure.
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PMID:Intrahippocampal kainic acid reduces glutamine synthetase. 197 Jun 31

The influence of anticonvulsant treatment upon (1) chronically increased seizure susceptibility, (2) on late increases in peptide levels and (3) on seizure-induced brain damage was investigated during various stages of acute kainic acid (10 mg/kg i.p.)-induced seizures. The seizures were interrupted at various stages of the syndrome (50 min to 24 h after injection of the toxin) by injecting thiopental (50 mg/kg i.p.) or the excitatory amino acid antagonist, MK-801 (10 mg/kg i.p.). The increase in neuropeptide Y and somatostatin levels in the frontal cortex could be prevented by early injection of either anticonvulsant (up to 180 min after kainic acid). No protection against the increase in peptide levels was observed when the anticonvulsants were applied later. Kainic acid-induced neuronal damage in the amygdala, with glutamate decarboxylase as a neurochemical marker, was entirely prevented by interrupting seizures up to 2 h after kainic acid. Partial protection (about 40-50%) was even found when the anticonvulsant treatment was applied after the acute syndrome, as late as 8 h after kainic acid injection. Chronically increased seizure susceptibility induced by kainic acid was not prevented, even by early injection (90 min after kainic acid) of the anticonvulsant drugs. The data indicate that (1) the late increase in seizure susceptibility may be initiated early after injection of kainic acid. (2) the late increase in peptide levels may be related to the frequency of acute seizures rather than to a change in seizure threshold or brain damage and (3) even late anticonvulsant therapy may antagonize seizure-induced brain damage in the amygdala.
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PMID:Effect of anticonvulsant treatment on kainic acid-induced increases in peptide levels. 197 15

Experimental epilepsy was induced in developing normal, undernourished and subsequently rehabilitated rats by locally injecting graded doses of Kainic acid (KA) in the right frontal cortex. Frequency and power spectral analysis of EEG was carried out to assess the progressive changes in EEG during KA-epileptogenesis. Undernourished animals were highly susceptible to seizure discharge. They exhibited generalized tonic-clonic discharge and had episodes of clinical seizures even after temporary neuronal recovery. Increase in power of delta, theta and decrease in alpha power was observed in the compressed spectral array (CSA) of undernourished animals. Delayed neuronal recovery with reduced background EEG and marked electrosilence in response to intra-rectal sodium valproate was observed in undernourished animals. Rehabilitated animals exhibited partial recovery which was related to the body weight gain. Spike frequency, spike amplitude and neuronal recovery time were not significantly differet between normal and undernourished animals at lower doses of KA (7.5-60 ng) whereas at higher doses (120-500 ng) marked differences were observed in these parameters. In KA treated undernourished rats 3H-glycine incorporation was significantly higher than normal in the hippocampus and spinal cord and lower in the cerebellum.
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PMID:Kainic acid induced epileptogenesis in developing normal & undernourished rats--a computerised EEG analysis. 207 64

Kainic acid (KA) is a potent neuroexcitatory drug widely used in the experimental study of seizure activity. Subcutaneous injection of KA into rats (10 mg/kg in saline 10 mg/ml; pH 7.0) induced longlasting status epilepticus followed by damage of CNS tissue in the entorhinal/pyriform cortex and in the hippocampus. The studies covered by this report demonstrated the formation of cytotoxic brain edema characterized by massive swelling of perineuronal and perivascular astroglia with microcirculation disturbance after KA injection, resulting in parenchymal necrosis of the affected region; furthermore perivenous hemorrhages and necroses corresponding to herniation lesions of the brain appear. Tracer studies with Na-fluorescein, Evans blue, albumin, and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. Treatment of brain edema with dexamethasone did not influence the incidence and severity of edematous brain damage. Treatment with mannitol, however, completely prevented the lesion in 54% of animals injected with KA. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic KA intoxication. It is suggested that in this model brain edema develops due to massive ionic imbalance caused by KA induced persistent neuronal excitation. In addition the model demonstrates the possible pathogenetic role of selective astrocytic swelling in the production of local hippocampal ischemia followed by herniation and its sequels. Such pathology originating from astrocytes probably may occur also in closed brain injury.
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PMID:Some mechanisms of brain edema studied in a kainic acid model. 213 Jun 48

The aim of the present study was to investigate whether the hippocampus exerts a modulatory effect on the activity of the hypothalamic-pituitary-adrenal (HPA) axis. Kainic acid was stereotaxically injected into the CA1 pyramidal cell layer of the dorsal hippocampus, causing histological and behavioural changes typical of kainic acid toxicity. The CA3 pyramidal cells of the dorsal hippocampus were selectively lesioned. Rats treated with kainic acid were hyperactive, executed clockwise rotatory movements and displayed epileptic seizures. The acute excitatory effect of kainic acid on glutamatergic receptors in the hippocampus resulted in an elevation in plasma corticosterone levels, suggesting a stimulation of HPA axis activity. Direct or indirect stimulation of the CA1 pyramidal cells of the dorsal hippocampus appeared to have caused the increase in corticosterone secretion.
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PMID:The effect of intrahippocampal injection of kainic acid on corticosterone release in rats. 216 46

Kainic acid (KA), microinjected unilaterally into the rat prepiriform cortex (PC), produces generalized motor seizures in a dose-dependent manner. The adenosine agonist N-ethylcarboxamidoadenosine (NECA), when co-injected with KA, protects against seizures in a dose-dependent and highly potent manner: ED50 = 25.6 +/- 2.1 pmol/rat. The seizure-suppressing effects of NECA are completely abolished by co-administration of the adenosine receptor antagonist 8-(p-sulfophenyl)theophylline (8-pSPT), suggesting that adenosine receptor activation underlies the efficacy of NECA against KA seizures. Moreover, dilazep, an effective blocker of adenosine uptake, when co-administered with KA, provides significant protection against seizures. Together, these findings suggest that adenosine receptors may play an important role in the regulation of the inhibitory neuronal circuitry of this paleocortical brain area.
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PMID:Anticonvulsant effect of N-ethylcarboxamidoadenosine against kainic acid-induced behavioral seizures in the rat prepiriform cortex. 240 43

Three days after systemic administration of kainic acid (15 mg/kg, s.c.), selected cholinergic markers (choline acetyltransferase, acetylcholinesterase, muscarinic acetylcholine receptor, and high-affinity choline uptake) and GABAergic parameters [benzodiazepine and gamma-aminobutyric acid (GABA) receptors] were studied in the frontal and piriform cortex, dorsal hippocampus, amygdaloid complex, and nucleus basalis. Kainic acid treatment resulted in a significant reduction of choline acetyltransferase activity in the piriform cortex (by 20%), amygdala (by 19%), and nucleus basalis (by 31%) in comparison with vehicle-injected control rats. A lower activity of acetylcholinesterase was also determined in the piriform cortex following parenteral kainic acid administration. [3H]Quinuclidinyl benzilate binding to muscarinic acetylcholine receptors was significantly decreased in the piriform cortex (by 33%), amygdala (by 39%), and nucleus basalis (by 33%) in the group treated with kainic acid, whereas such binding in the hippocampus and frontal cortex was not affected by kainic acid. Sodium-dependent high-affinity choline uptake into cholinergic nerve terminals was decreased in the piriform cortex (by 25%) and amygdala (by 24%) after kainic acid treatment. In contrast, [3H]flunitrazepam binding to benzodiazepine receptors and [3H]muscimol binding to GABA receptors were not affected 3 days after parenteral kainic acid application in any of the brain regions studied. The data indicate that kainic acid-induced limbic seizures result in a loss of cholinergic cells in the nucleus basalis that is paralleled by degeneration of cholinergic fibers and cholinoceptive structures in the piriform cortex and amygdala, a finding emphasizing the important role of cholinergic mechanisms in generating and/or maintaining seizure activity.
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PMID:Changes in cholinergic but not in GABAergic markers in amygdala, piriform cortex, and nucleus basalis of the rat brain following systemic administration of kainic acid. 254 59


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