Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 168-nucleotide exon, found in alternatively spliced amyloid precursor protein (APP) mRNAs, encodes a Kunitz protease inhibitor (KPI) domain. Kainic acid (ip) caused a selective increase of KPI mRNA in rat hippocampus. By in situ hybridization, KPI mRNA was induced in the neuronal layers of the hippocampus 11-12 h after the onset of kainate-induced seizures. The kainate-induced elevation of the KPI-containing APP-770 mRNA was blocked by pretreatment with the anticonvulsant pentobarbital. These data suggest that kainate-induced seizures cause alterations in APP RNA stability and/or processing in rat hippocampal neurons.
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PMID:Amyloid precursor protein mRNA encoding the Kunitz protease inhibitor domain is increased by kainic acid-induced seizures in rat hippocampus. 130 90

It was shown in the experiments on rats that intracerebroventricular administration of kainic acid (0.01, 0.05 microgram) after brain trauma, resulted in the occurrence of behavioral and electrographic convulsive disturbances; maximal expression of epileptic activity was obtained in entorhinal cortex and ventral hippocampus. Kainic acid induced epileptic reactions in nontraumatized rats only if injected in dose 0.1 microgram. Brain trauma did not lead to changes in seizures intensity induced by systemic picrotoxin administration. It is concluded that the formation of generator of pathologically enhanced excitation in limbic structures via increase of excitor glutamatergic neurotransmission is the important mechanism of traumatic epilepsy.
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PMID:[Role of limbic structures in the mechanisms of post-traumatic epilepsy]. 133 70

We have investigated by in situ hybridization changes in the content of mRNAs encoding for chromogranin B, secretogranin II, synaptin/synaptophysin and p65 after kainic acid-induced seizures and pentylenetetrazol kindling. Kainic acid seizures resulted in marked but transient increases in secretogranin II mRNA concentrations in the granule cell layer and throughout the pyramidal cell layers of the hippocampus (by 100-500%) as well as in various areas of the cerebral cortex (by up to 900%) and the thalamus (up to 300%) 12 h after injection of the toxin. Chromogranin B mRNA concentrations were persistently increased in granule cells (but not in pyramidal cells) of the hippocampus (suprapyramidal blade, 450%) and in cortical areas (250%) at all time intervals after kainic acid injection (12 h to 60 days). Accordingly chromogranin B immunoreactivity was enhanced in the terminal field of mossy fibers and in the inner part of the molecular layer 30 days after kainic acid. Secretogranin II immunoreactivity was also markedly increased in CA1, the paraventricular thalamic nucleus and in the central amygdala. In rats kindled with pentylenetetrazol only chromogranin B (by 200%) but not secretogranin II mRNA was increased in dentate granule cells. In contrast to the mRNAs of these secretory proteins concentrations of mRNAs encoding synaptin/synaptophysin and p65, two membrane proteins of synaptic vesicles, were not altered in any of these brain structures. These data demonstrate that in brain the biosynthesis of chromogranin B and secretogranin II is regulated like that of neuropeptides which is consistent with a role of these secretory polypeptides as precursors of functional peptides. Activation of neurons induces an increased synthesis of neuropeptides but not a concomitant synthesis of membrane proteins of synaptic vesicle. This might lead to an increased quantal content available for transmission.
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PMID:Temporal lobe epilepsy of the rat: differential expression of mRNAs of chromogranin B, secretogranin II, synaptin/synaptophysin and p65 in subfield of the hippocampus. 133 87

Kainic acid-induced seizure activity in adult rats produces an impairment of long-term potentiation induction in hippocampal slices. As the consequences of seizure activity are different in adult and juvenile rats, we tested the ability of hippocampal slices prepared from kainate-treated juvenile rats to exhibit long-term potentiation. Long-term potentiation was induced by theta-burst stimulation and was not significantly different in slices prepared from control or kainate-injected juvenile rats (16-18 postnatal days). Short-term potentiation, however, was reduced in the kainate-treated juveniles. Calpain inhibitor I has been shown to prevent long-term potentiation formation in adult hippocampal slices, and we evaluated its effect on long-term potentiation in hippocampal slices from juvenile rats. Calpain inhibitor I produced a significant reduction in the degree of long-term potentiation induced by theta-burst stimulation in hippocampal slices prepared from 14-20 postnatal day-old animals. The results are consistent with the notion that, although similar mechanisms participate in the formation of long-term potentiation in juvenile and adult animals, juvenile animals are much more resistant than adult animals to the consequences of seizure activity.
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PMID:Effect of seizure activity and calpain inhibitor I on LTP in juvenile hippocampal slices. 138 74

This study was conducted to assess the functional integrity of the kainate receptor-mediated seizure response in aged rats. Kainic acid was administered systemically to aged female Long-Evans (LE) rats and aged male F344 rats and the proconvulsant actions of kainic acid was compared to adult controls. The effects of kainic acid on brain regional content of monoamines and amino acids was also determined in the aged female LE and adult control rats. The latency to full clonic-tonic seizures was significantly reduced in aged female LE rats, and the number of seizures was significantly increased above that of the controls. There was increased mortality and a reduction in the latency to exhibit wet dog shakes in the aged F344 rats. Studies were also conducted to evaluate the role of ovarian hormones, route of administration, and dose of kainic acid in mediating the enhanced proconvulsant actions of kainic acid in aged rats. The neurochemical studies suggested that kainic acid significantly enhanced the release of ASP, GLU, and norepinephrine (NE) in the aged rats exhibiting clonic-tonic seizures. The adult rats given the same dose of kainic acid (15 mg/kg, IP) did not exhibit any significant change in brain content of monoamines or amino acids except for a reduction in mediobasal hypothalamic NE. An in vitro study was also conducted using brain slices from adult and aged F344 and it was found that aged rats released significantly more ASP than adults in response to kainic acid. These neurochemical findings were discussed in relation to previous studies of age-related alterations in excitatory amino acids (EAAs) and the role of EAA and NE in modulating limbic seizures. This study has clearly demonstrated that aged rats may be more susceptible to the excitotoxic action of EEAs acting through kainetic receptors.
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PMID:Kainic acid-induced seizures in aged rats: neurochemical correlates. 139 17

In a previous study we investigated the intraspecific defensive reactions evoked by excitation of neurons in the intermediate third of the midbrain periaqueductal gray matter (PAG) of the rat. Experiments revealed that activation of neurons in this region of the PAG mediated: (i) backward defensive behavior, characterized by upright postures and backward movements, and (ii) reactive immobility ("freezing"), in which the rat remained immobile, but reacted with backward defensive behavior to investigative, non-aggressive contact initiated by the partner. In the present study, we aimed to extend our understanding of PAG mediation of defensive behavior by observing: (i) in a non-aggressive social interaction test, the behavioral effects of microinjections of low doses of kainic acid (40 pmol in 200 nl) made in the caudal third of the PAG; and (ii) the behavioral and cardiovascular effects of microinjections of D,L-homocysteic acid (5-10 nmol in 50-100 nl) made in the PAG of the unanesthetized decerebrate rat. Kainic acid injections into the area lateral to the midbrain aqueduct in the caudal third of the PAG evoked: (i) forward avoidance behavior, characterized by forward locomotion and occasional hop/jumps; (ii) reactive immobility ("freezing"), in which the rat remained immobile, but reacted with forward avoidance behavior to investigative, non-aggressive contact initiated by the partner; and (iii) 22-28 kHz ultrasonic vocalizations. These injections also evoked a dramatic increase in defensive responsiveness to tactile stimuli on the half of the body contralateral, but not ipsilateral, to the site of injection. Electroencephalographic measurements indicated that none of these effects were secondary to seizure activity. In the decerebrate rat, D,L-homocysteic acid injections in the caudal third of the PAG evoked forward running movements along with increased blood pressure and heart rate, the strongest effects being evoked from the region lateral to the midbrain aqueduct. More rostrally, sites in the intermediate PAG evoked backward "defensive" movements, which were also associated with increased blood pressure and heart rate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Longitudinal neuronal organization of defensive reactions in the midbrain periaqueductal gray region of the rat. 139 45

Kainic acid, an analog of the excitatory amino acid L-glutamate, induces acute hyperexcitability and permanent structural alterations in the hippocampal formation of the adult rat. Administration of kainic acid is followed by acute seizures in hippocampal pathways, neuronal loss in CA3 and the hilus of the dentate gyrus, and reorganization of the synaptic connections of the mossy fiber pathway. Rats with these hippocampal structural alterations have increased susceptibility to kindling. To evaluate the role of the acute seizures and associated hippocampal structural alterations in the development of this long-lasting susceptibility, rats that received intraventricular kainic acid were cotreated with phenobarbital (60 mg/kg, s.c., once daily). Treatment with this dose for 5 d after administration of kainic acid suppressed acute seizure activity, protected against excitotoxic damage in the dentate gyrus, reduced mossy fiber sprouting, and completely abolished the increased susceptibility to kindling associated with kainic acid. Brief treatment with phenobarbital modified the pattern of damage and synaptic reorganization in the dentate gyrus in response to seizure-induced injury, and altered the long-lasting functional effects associated with hippocampal damage. As phenobarbital treatment did not protect against neuronal damage in CA3 or other regions of the hippocampus, the circuitry of the dentate gyrus was implicated as a locus of cellular alterations that influenced the development of kindling. These observations are evidence that pharmacological intervention can prevent the development of epilepsy in association with acquired structural lesions, and suggest that pharmacological modification of cellular responses to injury can favorably alter long-term functional effects of CNS damage.
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PMID:Alteration of long-lasting structural and functional effects of kainic acid in the hippocampus by brief treatment with phenobarbital. 143 95

Kainic acid (KA 4-14 mg/kg) administered intraperitoneally (i.p.) produces automatisms (scratching until third postnatal week, "wet dog" shakes thereafter), and clonic and tonic-clonic seizures in rats aged 7, 12, 18, 25, and 90 days. Administration of carbamazepine (CBZ) i.p. (25 or 50 mg/kg), phenobarbital (PB 20-80 mg/kg), clonazepam (CZP 0.2 or 1 mg/kg), or valproate (VPA 200 mg/kg) influenced neither incidence nor latency of automatisms. Clonic seizures that are regularly observed after the third postnatal week in controls were either abolished or substantially suppressed by any of the aforementioned antiepileptic drugs (AEDs). Tonic-clonic seizures observed in the first 3 postnatal weeks were suppressed only by solvent [including propyleneglycol (PEG), ethanol, and water]; the effect of AEDs on tonic-clonic seizures was proconvulsant instead. The automatisms were most resistant to AED therapy. These results induce some doubts about the adequacy of the KA model for identifying AEDs effective against complex partial seizures, but forthcoming AEDs that suppress automatisms in the KA rat model might also be active against human complex partial seizures.
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PMID:Action of antiepileptic drugs against kainic acid-induced seizures and automatisms during ontogenesis in rats. 146 81

The voltage-sensitive dye diO-C2-5 was used to produce an in vivo map of the membrane potential in two types of seizures. Mild limbic seizures were induced in rats with kainic acid; clonic convulsive seizures were induced with bicuculline. Kainic acid animals showed various levels of neural depolarization during their seizures in limbic, thalamic, cortical, and brainstem sites. The bicuculline animals showed uniformly greater levels of neural depolarization during their seizures. The magnitude of these changes relative to controls varied across seizure models and reflected the different underlying neural mechanisms for each model. The ability of the technique to capture local electrical events provides a new tool in which to explore brain activity.
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PMID:In vivo mapping of drug-induced seizures with voltage-sensitive dye. 146 62

Kainic acid (KA), in various concentrations, was applied iontophoretically into the central nucleus of the amygdala. Microlesions with this cell specific neurotoxin caused body weight loss, hypo- or aphagia and hypo- or adipsia in a dose-dependent manner. EEG-examinations proved that even low doses of KA produced seizure activity; however, these epileptiform symptoms disappeared within the first 48 h after the operations. Thus, the lasting feeding disturbances produced by iontophoretic KA applications to the central nucleus of the amygdala (i.e., even these fine microlesions) were not related causally to the pathological EEG activity changes. Our findings, along with previous data, indicated that the body weight loss and feeding deficits were due to the KA-induced impairment of complex regulatory mechanisms.
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PMID:Feeding disturbances and EEG activity changes after amygdaloid kainate lesions in the rat. 147 23


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