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

Kainic acid (KA) injected focally into the amygdala induced spontaneous recurrent motor seizures. One to 6 hr after the injection of KA, the hippocampal ir-dynorphin (ir-DYN) was significantly lowered whereas 24 hr after the injection it increased. The hippocampal level of ir-alpha-neoendorphin decreased 6 hr after KA injection, and reached the control level 24 hr after the injection. Chlordiazepoxide (5 mg/kg) and phenobarbital (40 mg/kg) blocked convulsions as well as the increase in the ir-DYN content. Cycloheximide (500 micrograms icv) also antagonized the increase in the hippocampal ir-DYN. The above findings suggest that hippocampal dynorphin-related peptides are released during the seizures and that these peptides may play a physiological role in the seizure phenomena and limbic excitability.
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PMID:Changes in hippocampal immunoreactive dynorphin and neoendorphin content following intra-amygdalar kainic acid-induced seizures. 613 84

Electrical stimulation of the lateral septum results in a transient cardiodeceleration which may represent parasympathetic rebound to a brief sympathetic activation. Kainic acid (KA) is a potent neuronal excitant. Stimulation of the lateral septum by KA produced a short-latency tachycardia. Vehicle injections, as well as KA administration to adjacent structures, did not effect significant changes in heart rate. Intraventricular KA, however, did result in a significant tachycardia. Knife cuts of the fornix, interrupting the glutamatergic innervation of the septum, completely blocked the cardiovascular response to KA. Pharmacological treatments reducing sympathetic activity prevented or reversed KA-elicited tachycardia. Thus, it appears that septal administration of KA produces sympathetic activation. KA may serve as a useful tool in studies assessing central regulation of the autonomic nervous system, and the interrelationship between autonomic activity and seizure-induced neuronal loss.
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PMID:Kainic acid stimulation of the lateral septum elicits tachycardia. 614 75

Kainic acid (KA) is known as a powerful convulsant and neurotoxic agent. When intracerebrally administered it causes repetitive seizures for about 1 or 2 days and brain damage both locally and in several remote brain regions. In the present paper the long-term effects of intrahippocampal KA administration are reported. Doses from 0.1 to 3.0 micrograms of KA were injected in the right hippocampus of Wistar rats and both the behaviour and EEG were observed during a period of about 3 months. Following KA doses of 0.8-2.0 micrograms, 4 distinct phases were observed: (1) acute phase which lasted 1-2 days and corresponded to the pattern of repetitive seizures as already described; (2) silent phase (5-21 days) which was characterized by a progressive return to apparently normal EEG and behaviour except for some aggressive behaviour in those animals receiving the highest doses; (3) phase of spontaneous recurrent seizures (these seizures started 6-22 days after KA injections and were mostly triggered upon handling and recurred approximately 2 times by day for about 30 days; usually they resembled the amygdaloid kindled seizures); and (4) post-seizure phase where no more seizures were observed but significant spiking activity in the amygdala recordings could be seen. Animals receiving KA doses of 0.1-0.4 microgram did not evolve beyond the acute phase whereas those receiving 3.0 micrograms died during this first phase. Neuropathological examination revealed dose-dependent alterations. These serial events offer a new method to induce spontaneous recurrent seizures with brain damage.
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PMID:Long-term effects of intrahippocampal kainic acid injection in rats: a method for inducing spontaneous recurrent seizures. 617 3

Kainic acid (KA) is a potent convulsant which, when administered subcutaneously, induces sustained limbic seizures and a pattern of limbic brain damage that is thought to be seizure-mediated. Diazepam suppresses and morphine enhances both the seizures and brain damage induced by KA. Here we show that morphine enhancement of KA neurotoxicity is blocked in a dose-dependent manner by subcutaneous pretreatment with naloxone. Theses and related findings support the hypothesis that morphine enhances the seizure-linked neurotoxicity of KA by an opiate specific action at certain limbic receptor sites where opiates suppress GABAergic activity, thereby lowering the threshold for propagation of seizure activity in limbic circuits.
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PMID:Naloxone blocks morphine enhancement of kainic acid neurotoxicity. 628 30

beta-Kainic acid, and the glycine and amino-methylphosphonate derivatives of alpha- and beta-kainic acid, have been injected intracerebroventricularly in DBA/2 mice, that show sound-induced seizure responses. An anticonvulsant effect is observed with marked protection against the tonic and clonic phases of the seizure response. ED50 values against clonus are (in mumol): beta-kainic acid, 0.09; beta-kainylglycine, 0.11; alpha-kainylglycine, 0.28; alpha-kainylaminomethylphosphonate, 0.31; beta-kainylaminomethylphosphonate, greater than 1.5. In addition a direct convulsant effect occurs after the alpha-kainyl derivatives.
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PMID:Kainic acid derivatives with anticonvulsant activity. 652 64

The substantia innominata complex (SI) is the major source of cholinergic innervation to the amygdala, entorhinal and pyriform cortices, and the neocortex. Immunohistochemical studies using both monoclonal and polyclonal antibodies to choline acetyltransferase (ChAT) have clearly identified that the large size neurons of this area are cholinergic. We have lesioned this area by three methods: electrocoagulation, kainic acid (KA) injection and folic acid (FA) injection. Biochemical (GAD, ChAT and QNB binding) and histological studies of the SI and its known target areas as well as the hippocampus, thalamus and striatum were undertaken. Histologically, electrolytic and KA (2 nmol) lesions produced extensive local damage, but local damage was minimal with FA (100-250 nmol). Electrolytic lesions produced no remote neuronal damage. KA injections produced mild to moderate damage in the amygdala and cortex, while FA produced severe damage in the amygdala and pyriform cortex, with less severe damage in the entorhinal cortex and neocortex. Biochemically, electrolytic lesions produced drops in ChAT only in remote areas. Kainic acid produced moderate drops in ChAT, GAD and QNB binding. FA, on the other hand, produced only a minimal change in ChAT, but very heavy reductions in GAD and QNB binding. Thus, GABA neurons of the cortex were damaged. They may also be the cholinoceptive neurons that were damaged. The remote damage following KA and, particularly, FA, is presumed to be due to the epileptiform activity induced by the local injection of these agents. Reduction in both seizures and remote damage was brought about by pre-treatment of the animals with valium (20 mg/kg) or scopolamine (50 mg/kg). Injection of FA into the amygdala or striatum produced some remote damage but it was much less in magnitude than after SI injection.
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PMID:A possible relationship between folic acid neurotoxicity and cholinergic receptors in the pyriform cortex and amygdala. 657 18

Kainic acid (KA), a heterocyclic structural analog of the putative excitatory neurotransmitter, glutamate (Glu), powerfully mimics many of the neuroexcitatory and neurotoxic properties of Glu. KA differs from Glu and its straight chain "excitotoxic" analogs, however, in inducing a limbic seizure-brain damage syndrome when administered subcutaneously (12 mg/kg) to adult rats. This syndrome consists of sustained seizures, resembling amygdaloid kindled seizures, and acute destruction of neural elements in limbic brain regions (amygdala, olfactory cortex, hippocampus, lateral septum and several thalamic nuclei). Early changes consist of massive edematous swelling of glia and neuronal dendrites and either swelling or dark cell changes in neuronal somata, with subsequent necrosis of many of the neurons involved. Elsewhere we demonstrated that pretreatment with morphine markedly enhances both the convulsant and brain damaging actions of KA. Here we report that pretreatment with 2 anticonvulsants (diazepam or phenobarbital) markedly reduces both athe seizure and brain damaging actions of KA, whereas, two other anticonvulsants (phenytoin or valproic acid) fail to suppress either phenomenon. Our findings suggest that a seizure mechanism underlies much of the limbic brain damage induced by systemic KA and that the toxic mechanism may have two mutually reinforcing components--a glutamergic excitatory component and a GABAergic disinhibitory component.
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PMID:Only certain anticonvulsants protect against kainate neurotoxicity. 679 81

Electrolytic lesions of the lateral hypothalamus (LH) are known to produce severe and chronic behavioral and electrographic abnormalities. In order to assess the effects of damage to LH cells vs damage to fibers of passage in the LH, a comparison was made of the effects of electrolytic lesions and microinjections of the neurotoxin kainic acid (kainate) in the LH. Behavior and neocortical and hippocampal electroencephalographic (EEG) activity were studied before, immediately after, and for 25 days after the lesions were made. Electrolytic-lesioned rats were aphagic and adipsic, showed an absence of normal atropine-resistant EEG activity, and a release of atropine-sensitive EEG activity in the hippocampus and neocortex. Kainic acid-lesioned rats showed some similar behavioral impairments but the kainate lesions produced different EEG abnormalities, including chronic slow-wave and seizure activity in both the neocortex and hippocampus. Following extended recovery hippocampal EEG was normal despite extensive cellular loss in areas CA3 and CA4. Understanding of the differences in EEG between the electrolytic and kainate effects was compounded by widespread cellular damage in areas outside the hypothalamus in the rats with kainate lesions. Thus, the kainate-produced abnormalities precluded a simple analysis of the contribution that cell damage alone makes to LH lesion-induced behavioral and EEG changes.
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PMID:Effects of kainic acid lesions in the lateral hypothalamus on behavior and hippocampal and neocortical electroencephalographic (EEG) activity in the rat. 723 51

Kainic acid (KA), a powerful neurotoxic analogue of glutamate, has been extensively used as a tool for selectively lesioning neuronal cell bodies; however, axons or nerve terminals are spared from damage in the area injected with kainic acid. Injections of this neurotoxin in various brain regions were successfully used to locate cell bodies of neurones containing substance P, enkephalin and other putative neurotransmitters. While attempting to locate the cell bodies of the enkephalin containing neurones present in hippocampus using KA injections, we found that a few days after intracerebral injections of KA a drastic increase in the Met-enkephalin (ME) content of hippocampus occurs. We now describe the delayed increase in hippocampal ME content elicited by intracerebral KA injections and examine the possible mechanism that is operative in causing this increase. Moreover, we provide some evidence suggesting that the increase in ME content elicited by intracerebral injections of KA may be related to the recurrent motor seizures elicited by intracerebral injections of KA.
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PMID:Changes of hippocampal Met-enkephalin content after recurrent motor seizures. 737 75

Kainic acid (KA) was injected systemically, intracerebroventricularly (i.c.v.) and focally in the amygdala and other deep brain structures in the rat. EEG and behavioral changes were studied in relation to the neuropathology which developed subsequently. Following intra-amygdaloid KA injection, diazepam blocked the epileptic events induced by the toxin, and abolished the neuronal loss usually seen in the lateral septum, claustrum, and contralateral cortex and hippocampus. The lesions in medial thalamic structures and ipsilateral hippocampus were also reduced by diazepam. Prior transection of the perforant path ipsilateral to the KA injection also decreased the severity of the electrographic and motor effects of the toxin and similarly reduced the extent of distant ("remote") pathological brain damage. Neither diazepam nor perforant path transection reduced the damage at the site of KA injection. Kainic acid (0.4-2 microgram) injected into the bed nucleus of the stria terminalis (BST) or the medial septum produced seizures with a longer latency and little brain damage outside the injection site. In contrast, intrastriatal KA injections were followed by ipsilateral hippocampal lesions. i.c.v. Injection of KA (0.4-1.6 microgram) produced a complex syndrome which included bilateral exophthalmos, mydriasis, foaming, tremor of the vibrissae, and paw and body tremor. The pattern of brain damage resembled that seen following intra-amygdaloid administration of the toxin. In addition, however, there was a bilateral necrosis of the pyriform and prepyriform cortices up to the rhinal fissure. Systemic administration of diazepam (i.p.) reduced the extent of the damage and in particular completely prevented the cortical damage. Systemic administration of KA (9-15 mg/kg i.p.) readily produced motor and EEG seizures similar to those seen after intra-amygdaloid injection of the toxin. The pattern of brain damage was however more symmetrical than that which followed focal i.c.v. injection of the toxin and included necrosis of the pyriform cortex. It is concluded that spread of seizure activity from the injection site plays a crucial role in the induction of "remote" brain damage after focal intracerebral injections.
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PMID:The role of epileptic activity in hippocampal and "remote" cerebral lesions induced by kainic acid. 737 61


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