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

Kainic acid-induced seizures produced early (2 hr) generalized edema and later (24 and 48 hr) necrotic edema in temporal cortex and hippocampus as measured by specific gravity changes. Mannitol given during the seizure partially protected against the early edema and prevented the necrotic edema indicating early edema may play a role in later brain damage. However, H2O intoxication, causing much greater generalized edema than the kainic acid-induced seizures, caused no necrotic edema in temporal cortex or hippocampus at 48 hr. Thus it appears that mannitol protection against kainic acid-induced brain damage may be by a mechanism in addition to dehydration.
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PMID:Role of early edema in the development of regional seizure-related brain damage. 311 Jun 40

Cerebral blood flow was sequentially determined (every 2-3 min) with helium clearance in two "vulnerable" structures: the hippocampus and the frontoparietal cortex during bicuculline (n = 11) and kainic acid (n = 9)-induced seizures in unanaesthetized, spontaneously breathing rats. Tissue partial pressures of oxygen and carbon dioxide were continuously and simultaneously evaluated in the same brain areas. All these variables were measured by mass spectrometry with a single gas sampling cannula previously implanted in each structure. The systemic variables, arterial blood pressure, arterial partial pressures of oxygen and carbon dioxide, pH, and bicarbonate concentration were also determined. Arterial and venous catheters were chronically implanted several days prior to the definitive experiments. Bicuculline induced short (about 15 min), recurrent, generalized seizures, with an abrupt rise in arterial blood pressure, an arterial metabolic acidosis and comparable blood flow increases (4-fold) in the hippocampus and the neocortex. A marked increase in tissue partial pressure of oxygen was always preceded by an increase in tissue partial pressure of carbon dioxide. After the seizures, in the 5 rats that survived, cerebral blood flow was significantly lowered; tissue partial pressure of oxygen and partial pressure of carbon dioxide also decreased, but to a lesser extent. Histological examination revealed two types of lesions: predominantly selective chromatolysis but also ischaemic cell change. Kainic acid first induced a decrease in arterial pressure and then hypertension during status epilepticus, with a return of arterial pressure towards basal levels during the recovery period (4 h after the injection). Respiratory alkalosis occurred throughout the experiment. Cerebral blood flow increased progressively to become maximal during status epilepticus. This vasodilatation was greater in the hippocampus (x 8) than in the neocortex (x 4). During recovery, cerebral blood flow tended to decrease but remained significantly elevated. In both structures, tissue partial pressure of oxygen was first lowered while tissue partial pressure of carbon dioxide was elevated; with the occurrence of the wet dog shakes, tissue partial pressure of O2 increased and tissue partial pressure of CO2 decreased. The changes in tissue gases were maximal during status epilepticus and tended to return to their basal levels thereafter, but no decrease in tissue partial pressure of O2 was observed, even 4 h after kainic acid administration. Histological analysis demonstrated ischaemic cell changes, particularly in the limbic system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Continuous determination of the cerebrovascular changes induced by bicuculline and kainic acid in unanaesthetized spontaneously breathing rats. 312 92

Kainic acid (KA) injections destroy hippocampal pyramidal cells, induce recurrent collateral sprouting of the hilar mossy fibers (MFs), and lead to chronic seizures. In the present study, rats were injected systemically with KA (14 mg/kg) to determine whether the subsequent occurrence of seizures was correlated with MF sprouting, as indicated by Timm's staining of proximal dendrites. At 4 weeks, 56% of the KA-treated rats had MF sprouting in the temporal (ventral) hippocampus, and 52% had shown seizures between 10 and 28 days. Both seizures and sprouting were seen in 32% of the treated animals. While Timm's staining of MFs in the inner molecular layer was not directly correlated with seizure scores, animals which exhibited chronic seizures had significantly more sprouting than animals which did not have seizures.
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PMID:Chronic seizures and collateral sprouting of dentate mossy fibers after kainic acid treatment in rats. 321 10

The short and long-term effects of systemic administration of kainic acid to immature animals were studied in rats. Kainic acid was administered systemically to rats of 1-30 days of age. The rats were monitored for both behavioral and EEG changes. To study the effects of kainic acid on seizure susceptibility, status epilepticus was induced in 12-, 18-, and 27-day-old rats by systemic administration of kainic acid. Seizure susceptibility was assessed 3 days later using the kindling technique. In addition, another group of 27-day-old rats that developed status epilepticus following systemic administration of kainic acid were kindled as adults. Young rats (1 day of age) developed behavioral status epilepticus after kainic acid and ictal electroencephalographic changes were seen beginning at age 6 days. The 15- and 21-day-old rats kindled 3 days after kainic acid administration kindled at the same rate as controls. However, 30-day-old rats that received kainic acid at age 27 days kindled more quickly to stage-5 seizures than controls. Rats that received kainic acid at age 27 days and maintained until adulthood developed spontaneous recurrent seizures and kindled faster as adults than controls. These results demonstrate that the effect of kainic acid on seizure susceptibility is an age-dependent phenomenon.
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PMID:Effects of kainic acid on seizure susceptibility in the developing brain. 335 30

Kainic acid (KA) is a powerful convulsant and neurotoxic agent. In the present paper the acute and long term effects of intrahippocampal KA administration on estrous cycle and on serum concentrations of progesterone were studied in adult female rats. Following KA injection, 3 distinct periods were observed: 1) acute period (24-48 h), 2) silent period (21-30 days), and 3) chronic period, characterized by the appearance of spontaneous recurrent seizures (30-45 days). KA administration did not affect progesterone levels during the acute period. In contrast, during the silent period, KA-treated animals exhibited irregular estrous cycling and decreased progesterone levels. These results are of interest in view of a possible link between epileptic phenomena and hormone secretion.
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PMID:Effects of intrahippocampal injection of kainic acid on estrous cycle in rats. 345 64

The pro-convulsant actions of theophylline and caffeine have been investigated using the hippocampal slice preparation and rats administered kainic acid or Metrazol. Both theophylline and caffeine induced the generation of epileptiform activity in the CA3 region of the hippocampal slice with convulsive dose50 (CD50) values of 3 microM respectively. Kainic acid-induced bursting in hippocampal slices was enhanced by theophylline (0.3-30 microM) and caffeine (1-100 microM). Theophylline induced burst firing in response to electrical stimulation in hippocampal area CA3 but not area CA1. Theophylline (50 mg/kg) strongly potentiated the effect of the limbic convulsant kainic acid in vivo whilst a dose of 200 mg/kg was necessary to significantly lower the threshold dose of Metrazol required to induce generalized convulsions. We conclude that alkylxanthines, probably by antagonizing the effect of endogenous adenosine, exert a pro-convulsant action in the hippocampus which preferentially promotes limbic seizures.
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PMID:Pro-convulsant actions of theophylline and caffeine in the hippocampus: implications for the management of temporal lobe epilepsy. 369 Mar 22

It is well established that the putative excitatory neurotransmitters, glutamate (Glu) and aspartate (Asp), are neurotoxins that have the potential of destroying central neurons by an excitatory mechanism. Kainic acid (KA), a rigid structural analog of Glu, powerfully reproduces the excitatory neurotoxic (excitotoxic) action of Glu on central neurons and, in addition, causes sustained limbic seizures and a pattern of seizure-linked brain damage in rats that closely resembles that observed in human epilepsy. In the course of studying the seizure-related brain damage syndrome induced by KA, we observed that a similar type of brain damage occurs as a consequence of sustained seizure activity induced by any of a variety of methods. These included intraamygdaloid or supradural administration of known convulsants such as bicuculline, picrotoxin and folic acid, or systemic administration of lithium and cholinergic agonists or cholinesterase inhibitors that have not commonly been viewed as convulsants. We have further observed that this type of brain damage can be reproduced in the hippocampus by persistent electrical stimulation of the perforant path, a major excitatory input to the hippocampus that is thought to use Glu as transmitter. It is a common feature of all such neurotoxic processes that the acute cytopathology resembles the excitotoxic type of damage induced by Glu or Asp, which is acute swelling of dendrites and vacuolar degeneration of neuronal soma, without acute changes in axons or axon terminals. We have found that the seizure-brain damage syndrome induced by cholinergic agents can be prevented by pretreatment with atropine and that the syndrome induced by any of the above methods, cholinergic or noncholinergic, can be either prevented or aborted respectively by either pre-or posttreatment with diazepam. Our findings in experimental animals may be summarized in terms of their potential relevance to human epilepsy as follows. Sustained complex partial seizure activity consistently results in cellular damage if allowed to continue for longer than 1 hr. Hippocampal, or Ammon's horn, sclerosis is the primary pathological result. It may be a priority goal, therefore, in the management of human epilepsy to control such seizure activity within very narrow limits. This proposal is discussed in terms of three major transmitter systems that may be involved; cholinergic, GABAergic, and glutamergic/aspartergic. The cholinergic system may play a role in generating or maintaining this type of seizure activity, and anticholinergics may protect against it provided they are given prior to commencement of behavioral seizures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Excitotoxic mechanisms of epileptic brain damage. 370 27

In acute experiments on cats the effect of kainic acid microinjected into the raphe dorsal nucleus on the EEG activity recorded from various brain structures was investigated. Kainic acid in doses of 0.2 to 32.0 nmol was injected by glass micropipets and an air-pressure system. The analysis of the EEG and the EEG power analysis in the usual frequency bands (delta, theta, alpha, and beta) revealed an activating to hyperexcitatory effect of kainic acid. This hyperexcitatory effect was manifested by the appearance of paroxysmal EEG patterns of different types which developed in some cases into seizure episodes or an epileptic state. Abnormal EEG changes occurred first in the thalamus and mesencephalic reticular formation. A dose-response relationship existed: the duration of the EEG with pathological patterns increased whereas the latency of their appearance decreased with increase of the dose of kainic acid. Five to seven hours after the injection there were no severe histopathologic changes in the region of the raphe dorsal nucleus. The hyperexcitatory effect of kainic acid on brain excitability might be a result of the excitatory action of kainic acid and of triggering of circuits of neuronal hyperactivity in structures connected with the raphe dorsal nucleus.
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PMID:Intraraphedorsal kainic acid induces paroxysmal electroencephalographic changes in some brain structures of cats. 373 69

Kainic acid (KA) was injected intraperitoneally into rats at a dose (9 mg/kg) which produced status epilepticus in approximately 50% of the animals. Rats were categorized into groups that displayed status epilepticus, partial seizures or no effect in the 4 hr following kainic acid injection. Behavioral and morphological changes were characterized for each group. Rats that were not affected by kainic acid were indistinguishable from a saline-injected control group. When sacrificed 4 hr after treatment, rats displaying partial seizures showed morphological changes similar to, but less severe than, those exhibiting status epilepticus. Additional groups were tested and sacrificed 7 days (d) after treatment. Rats from the limited seizure group showed little behavioral or morphological response, while animals from the status epilepticus group had marked behavioral deficits and severe lesions. The tissue damage and its distribution were similar to lesions observed after seizures induced by other convulsants, and in spontaneously epileptic dogs. These results suggest that the extent of damage resulting from systemic administration of KA is dependent on the extent of seizure activity, which may in turn be related to the influence of kainic acid and other excitatory amino acids on the limbic system.
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PMID:Damage induced by systemic kainic acid in rats is dependent upon seizure activity--a behavioral and morphological study. 382 60

The histopathological alterations developing in the hippocampus, piriform cortex and thalamus of the rat brain, the blood-brain barrier damage, and the effects of dexamethasone pretreatment on the brain edema were investigated 4 h following intraperitoneal kainic acid administration. The most pronounced Evans Blue extravasation accompanied by increases in the water and sodium contents and a decrease in the potassium content, were observed in the thalamus. Dexamethasone, injected in a dose of 5 mg/kg 2 h before kainic acid administration, reduced considerably the vasogenic edema and neuronal damage in the thalamus, but the cytotoxic edema of the hippocampus and piriform cortex remained unaltered. Kainic acid-induced seizures lead to the development of vasogenic brain edema mainly in the thalamus, as well as to cytotoxic edema in the hippocampus and piriform cortex. The vasogenic edema seems to contribute to the cell damage in the thalamus. Dexamethasone reduces the vasogenic edema and cell damage in the thalamus, possibly by inducing the synthesis of certain protein(s) with antiphospholipase A2 activity.
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PMID:Effects of dexamethasone on brain edema induced by kainic acid seizures. 396 Mar 7


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