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

Kainic acid (KA) was injected into the amygdala (AM) complex of the rat and its effect on the cholinergic enzymes, choline acetyltransferase (CAT) and acetylcholinesterase (AChE), and the binding of the muscarinic ligand, [3H]quinuclidinyl-benzilate (QNB) and the nicotinic ligand [125I]alpha-bungarotoxin (aBuTX) was investigated. Ka produced a loss of approximately 35% of the CAT activity in the AM. However, no effect on AChE activity was observed. A 30--50% decrease in the number of muscarinic and nicotinic receptor sites was also found. CAT, AChE and QNB binding in the AM contralateral to the injection did not change. However, the binding of aBuTX was found to decrease by approximately 40%. The present results suggest that the loss of CAT activity in the AM after treatment with KA is due to the destruction of cholinergic neurons within the AM. The lack of effect on AChE suggests that the major cholinergic input to the AM is not affected by KA. In addition, the loss of nicotinic receptors in the contralateral AM may reflect anterograde degeneration of terminals that have nicotinic sites located on them, or may be secondary to the elicitation of intense seizure activity evoked by the KA.
 ...
PMID:The effect of kainic acid on cholinergic enzymes and receptors in the amygdala complex of the rat. 740 18

The neuroprotective effect of acidic fibroblast growth factor (aFGF) has been analysed in a rat model of seizures-associated brain damage. We report that after treatment with a convulsivant dose of Kainic acid, systemically administered aFGF prevents neuronal degeneration in specific brain areas, mainly in the hippocampal formation. Our findings extend the potential pharmacological use of fibroblast growth factors and afford new data to understand the neurophysiology of these proteins.
 ...
PMID:Neuroprotective effect of acidic fibroblast growth factor on seizure-associated brain damage. 753 8

Kainic acid-induced seizures in the rat brain cause severe brain damage that is thought to result, in part, from oxidative stress. In this study, we examine the consequences of systemic administration of kainic acid on expression of several genes that encode proteins thought to play roles in protection from oxidative stress, including metallothionein-I, and -III. Kainic acid causes an increase in metallothionein-I and heme oxygenase-I mRNAs, as well as an increase in c-fos, heat shock protein-70, and interleukin-1 beta mRNAs. The induction of these mRNAs is seizure dependent, and is greater in brain areas with extensive damage (e.g. piriform cortex) than in areas with minimal damage (e.g. frontal cortex and cerebellum). In contrast, little or no change in mRNA for metallothionein-III, manganese superoxide dismutase, copper-zinc superoxide dismutase, glutathione-s-transferase ya subunit or glutathione peroxidase occur. The prolonged and robust concordant induction of the metallothionein-I and heme oxygenase-I genes may reflect the oxidative stress produced by kainic acid-induced seizures. In addition, the induction of interleukin-1 beta gene expression suggests an inflammatory response in brain regions damaged by kainic acid-induced seizures. Delineating the regulation of genes associated with oxidative and inflammatory responses can contribute to a fuller understanding of seizures and associated brain damage.
 ...
PMID:Temporalspatial patterns of expression of metallothionein-I and -III and other stress related genes in rat brain after kainic acid-induced seizures. 765 48

Kainic acid (KA)-induced seizures in adult rats have been reported to cause sprouting of mossy fibres in the inner molecular layer (IML) of the dentate gyrus. In the present study, using electron microscopic immunostaining for GAP-43 we found that 3 months after KA treatment, several GAP-43 positive terminals in the IML showed structural characteristics of mossy fibre boutons. No GAP-43-positive mossy fibre terminals were found in the normal projection areas of granule cells, thus indicating that newly synthesized GAP-43 is transported predominantly in the axonal branches actively undergoing remodelling. These results provide evidence of the involvement of GAP-43 in the structural remodelling of mossy fibres, and suggest a role of this protein in the functional activity of the sprouted mossy fibres as a consequence of KA-induced seizures.
 ...
PMID:Ultrastructural immunolocalization of GAP-43 in the sprouted mossy fibres of kainic acid lesioned rats. 769 23

Status epilepticus (SE) produced by excitatory amino acids is a well established model in adult rodents. Limbic neuronal degeneration and synaptic reorganization observed after, for example, kainic acid-induced SE are considered relevant to human epilepsy. Kainic acid also produces severe seizures in infant rats, but neuronal injury and sprouting have not been demonstrated. The results of the present study show that corticotropin releasing hormone (CRH)-induced SE causes limbic neuronal death and reorganization in infant rats. In adults, CRH produced seizures at much higher doses, and no neuronal degeneration. As a modulator of the CNS stress response, CRH is activated in various 'stressful' circumstances. Its age-dependent ability to kill neurons represents a unique form of cell death potentially important in human medicine.
 ...
PMID:Peptide-induced infant status epilepticus causes neuronal death and synaptic reorganization. 775 9

Kainic acid microinjection into unilateral sensori-motor cortex induced focal seizure status and secondarily generalized seizure status for about 4 hours. After these seizure status, focal myoclonic jerkings were induced for about 2 days. EEG demonstrated generalized synchronous periodic spikes with these myoclonic jerkings. This phenomenon was very similar to those symptoms of epilepsia partialis continua in man. During focal seizure status, autoradiographic study with 14C-deoxyglucose demonstrated increased local cerebral glucose utilizations in the injected site of the sensori-motor cortex, ipsilateral caudate nucleus, globus pallidus, substantia nigra and thalamic nuclei. The result suggested that subcortical pathways played an important roles in the seizure propagation from the cortical epileptogenic focus.
 ...
PMID:[Jacksonian seizure model induced by a kainic acid microinjection into unilateral sensori-motor cortex]. 778 24

Subtractive library construction and differential screening were used to identify a cDNA for a cell type-specific immediate early gene induced in rat PC12 pheochromocytoma cells. Sequencing identified the protein product of this gene as rat synaptotagmin IV (SytIV). Synaptotagmins are synaptic vesicle proteins thought to play a role in depolarization-induced, calcium-mediated exocytosis and neurotransmitter release. SytIV mRNA accumulation is transiently induced in PC12 cells by potassium depolarization, calcium ionophore, ATP, and forskolin. In contrast, growth factors and phorbol 12-myristate 13-acetate induce little or no SytIV mRNA accumulation. Kainic acid-induced seizures in rats are followed by accumulation of SytIV message in the hippocampus and piriform cortex. The SytIV gene may provide a direct link between depolarization-induced neuronal gene expression and subsequent modulation of synaptic structure and function.
 ...
PMID:Synaptotagmin IV is an immediate early gene induced by depolarization in PC12 cells and in brain. 789 40

In young rats, systemic or local administration of kainic acid (KA) elicits scratching as the prevailing automatism whereas in adult rats, wet dog shakes (WDS) are usually recorded. We tested the effects of the alpha 2-adrenergic agonist clonidine (0.25 mg/kg, IP; also acting, however, on imidazoline receptors), which has been reported to block KA-induced WDS in adult rats and the 5-HT2 antagonist ritanserin (20 mg/kg, IP) in rats aged 7, 12, 18, 25, and 90 days treated IP with doses of KA that induce maximum number of automatisms with minimal early lethal effects (i.e., 4, 6, 8, 10, and 14 mg/kg, respectively). Both WDS and scratching were frequently recorded together in one animal. Neither ritanserin nor its solvent had significant effects on the total number of automatisms or on their distribution between WDS and scratching. In contrast, clonidine suppressed automatisms throughout the development studied. In 90-day-old (adult) rats clonidine decreased the incidence of both WDS and scratching, whereas it usually attenuated scratching at younger ages. Kainic acid-induced seizures were also recorded because of reported incompatibility between tonic-clonic seizures and WDS in adult rats. In 18-90-day-old rats, tonic-clonic seizures and WDS were found incompatible. In 7-18-day-old pups, scratching and KA-induced tonic-clonic seizures occurred together. Moreover, in 7-day-old rats, clonidine was anticonvulsant. We have demonstrated that KA-induced automatisms develop from scratching in pups to prevailing WDS in adult rats, whereas the incidence of scratching rather decreases during development.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Clonidine, but not ritanserin, suppresses kainic acid-induced automatisms in developing rats. 802 8

To investigate the potential role of drug therapy in preventing or exacerbating seizure-related brain injury in the prepubescent brain, we administered kainic acid to rats at postnatal day 35. Therapy with daily phenobarbital was started directly before or 1 day after kainic acid was administered, and was continued through postnatal day 153. Rats receiving phenobarbital had therapeutic concentrations during most of the 24-hour dosing period, but also experienced supratherapeutic peak concentrations. The animals were subsequently tested using the water maze (a measure of visuospatial memory), open field (a measure of activity level), and handling tests (a measure of emotionality). The frequency of spontaneous recurrent seizures was monitored during and after phenobarbital therapy. Kainic acid resulted in status epilepticus on postnatal day 35 in all the rats that received it but those receiving phenobarbital first manifested a shorter and less severe status epilepticus as compared to the rats given kainic acid alone. Rats starting phenobarbital immediately before kainic acid was administered did not differ from control rats on behavioral testing and had no subsequent spontaneous recurrent seizures and no histological lesions. Rats receiving kainic acid alone performed significantly poorer than did control rats in the water maze, were more aggressive, had histological lesions, and manifested spontaneous recurrent seizures. As compared to the group treated only with kainic acid, rats receiving kainic acid followed by phenobarbital at postnatal days 36 to 153 manifested similar aggressiveness and histological lesions, similar frequency of spontaneous recurrent seizures after phenobarbital taper, and even greater disturbances in memory, learning, and activity level.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Phenobarbital modifies seizure-related brain injury in the developing brain. 808 Feb 50

The present study was directed at evaluating the possible involvement of protein synthesis in excitotoxin-induced neuronal damage and prolonged expression of the proto-oncogene, c-fos. Kainic acid-induced seizure activity elicited varying degrees of neuronal damage and cell loss in selectively vulnerable regions of the adult rat limbic system. Pretreatment with cycloheximide, a protein synthesis inhibitor, did not alter behavioral seizure characteristics, but markedly attenuated damage to susceptible neuronal populations. A prolonged increase in c-fos mRNA was observed by in situ hybridization up to 16 h after the onset of seizures in regions exhibiting neuronal death. Pretreatment with cycloheximide did not affect the transient induction of c-fos observed in numerous structures, but significantly reduced the prolonged expression of c-fos mRNA in kainate-vulnerable regions. Despite producing massive seizure activity, systemic kainic acid administration during the early postnatal period did not induce any neuronal death, and did not result in prolonged c-fos expression in any brain structures. The developmental onset of selective neuronal vulnerability coincided with that of prolonged c-fos expression in susceptible neuronal populations. In adult rats, seizure activity induced by pentylenetetrazole did not produce neuronal damage nor did it produce prolonged c-fos expression. These results not only demonstrate that kainate-induced neurotoxicity and the prolonged expression of c-fos are both prevented by cycloheximide, but also strengthen idea that prolonged c-fos expression is a marker of neuronal death.
 ...
PMID:Cycloheximide prevents kainate-induced neuronal death and c-fos expression in adult rat brain. 829 88


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>