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

The hallmark of brain tissue is its electrical activity. However, few techniques are available to directly monitor voltage changes in neural tissue, especially in whole brain preparation. A technique has been developed using a fluorescent voltage-sensitive dye and digital image analysis to produce a high spatial resolution map of the voltage changes induced by seizures in the hippocampus. Eight different anatomical regions within the septal hippocampus of the rat were analyzed. Seizures were produced in vivo by methods which use entirely different mechanisms and produce electrographically and behaviorally different types of seizures. Kainic acid produced depolarization during the seizure, whereas bicuculline produced hyperpolarization. The results provide experimental evidence that all seizures do not induce a depolarized state in the brain.
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PMID:Regional voltage map of the hippocampus during seizures. 266 49

To characterize further the hypoglycemic effect of intrathecally (i.t.) administered morphine, species and drug specificity, effects of morphine-induced tolerance and pentobarbital-induced anesthesia and effects on liver glycogen were studied in nonfasted animals. In rats, morphine (125 micrograms i.t.) produced the same behavioral toxicity (scratching, biting, seizures) and hypoglycemia as previously reported in mice. In mice, the glycine antagonist strychnine (5 micrograms i.t.) and the morphine metabolite morphine-3-glucuronide (2 micrograms i.t.) mimicked the behavioral, but not the hypoglycemic, effects of high-dose i.t. morphine. Kainic acid (0.1 micrograms i.t.), which caused high-frequency hindlimb movements, also did not cause hypoglycemia. Naltrexone (1 mg/kg/ s.c.) or the s.c. implantation of morphine pellets for 3 days attenuated the hypoglycemic effect, but not the behavioral effects, of morphine (40 micrograms i.t.). The hyperglycemic effect of s.c. morphine(20 mg/kg) was blocked by i.t. morphine. Anesthesia with pentobarbital (75 mg/kg i.p.) attenuated the hypoglycemic effect of morphine (40 micrograms i.t.). Morphine i.t. also caused a time- and dose-dependent decrease in liver glycogen levels and was more potent in causing glycogenolysis (30 min ED50 = 19 micrograms) than in causing hypoglycemia (30 min ED50 = 30 micrograms). It is concluded that the hypoglycemic effect of i.t. morphine appears to be independent of its behavioral effects, displays tolerance and is accompanied by hepatic glycogen depletion.
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PMID:Studies on the mechanism of hypoglycemia induced by intrathecal morphine: dissociation from behavioral effects, effects of tolerance and depletion of liver glycogen. 273 44

Kainic acid (KA, 8-15 ng) was injected into the amygdala of conscious freely moving rats via chronically implanted fused silica cannulas. At 15-25 min after the injection, most rats suffered a limbic seizure attack of short duration, consisting of mastication, forelimb clonus, and raising on hind limbs, behaviorally indistinguishable from kindled seizures. Typically, the attack was followed by stereotypies, intense exploration, and by 1 or 2 more attacks. About 60 min after the injection, most rats appeared normal again and histopathological changes in their brains did not exceed those seen in vehicle-injected rats. In 3 cases, however, recurrent seizures culminated in behavioral status epilepticus 60-90 min after the injection. The status epilepticus was stopped by i.p. injection of diazepam (10 mg/kg) after a duration of 10 min (1 case) and 30 min (2 cases), respectively. After 10 min status epilepticus, we observed marginal neuronal damage with slight gliosis in both hippocampi (CA3 and CA1); after 30 min, hippocampal histopathology was more pronounced, with additional necrosis of the ipsilateral piriform cortex. After 0.8 microgram KA, a hundredfold higher dose, the incidence of limbic seizures during the first 40 min was not significantly higher (9/12) than after the lower KA doses (13/19). However, a significantly higher proportion of rats exhibited long-lasting seizure activity, associated with confluent destruction of CA3 pyramidal cells and additional seizure-related brain damage. Our results show that limbic motor seizures do not inevitably lead to histopathological changes in the brain, provided they do not culminate in a state of permanent seizure activity.
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PMID:Limbic seizures without brain damage after injection of low doses of kainic acid into the amygdala of freely moving rats. 274 56

The effect of kainic acid on extracellular [K+], [Ca2+], and [Na+] in the rat piriform cortex and hippocampus was studied by means of intracranial microdialysis. Either a dialysis fiber loop or horizontal Vita fiber were stereotaxically implanted within the piriform cortex or hippocampus, respectively. About 24 h later, fibers were perfused (1 ml/min) with Krebs-Ringer bicarbonate solution. Effluent samples were collected before (four at 30 min intervals), and after (six at 30 min intervals) administration of kainic acid (16 mg/kg, i.p.) or kainic acid vehicle. Kainic acid induced sequential signs of lethargy, staring, "wet-dog shakes," forepaw clonus, and tonic-clonic convulsions. In these awake free-moving rats, kainic acid induced a rapid and prolonged increase in extracellular [K+] and an apparent, but not statistically significant, decrease in extracellular [Ca2+] within the hippocampus. In the piriform cortex, kainic acid induced increases in extracellular [K+] and [Na+], which were associated with early pre-convulsive signs. In contrast to the pronounced ion changes commonly seen when the brain is activated by factors such as local application of excitatory substances or when the brain is made ischemic or hypoxic, extracellular ion concentrations are relatively well maintained during parenteral kainic acid-induced seizures.
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PMID:Kainic acid-induced seizures: changes in brain extracellular ions as assessed by intracranial microdialysis. 277 Apr 22

The substantia innominata (SI) contains a lot of cholinergic neurons and mainly project their fibers to the cerebral cortex and to the amygdala. Degenerative lesions were made in the bilateral SI and influences of these lesions upon kainic acid-induced limbic seizure were studied. Eleven adult cats were stereotaxically implanted and 2.5 micrograms of ibotenic acid (IBO) was injected into the bilateral SI in 6 cats (IBO group) and 1 microliter of phosphate buffer (PB) in 5 cats (PB group). All animals were given freedom at least 8 days to recover from the operation. Kainic acid microinjection was made into the left amygdala and electroclinical observation was done. In PB group, the limbic status was elicited and these seizures persisted for about 3 days after the KA injection. Seizures were subsided but interictal discharges were observed at the injected site of the amygdala. Then, limbic seizures reappeared within 10 days and a slowly progressive development of limbic seizure was observed. These seizures developed further. Occasionally, these limbic seizures successively developed and secondarily generalized seizures occurred once or twice a week. Otherwise, their clinical behaviors were normal during the interictal periods. In IBO group, the limbic status were elicited and lasted for about 3 days after the KA injection. Although interictal discharges reappeared at the injected site of the amygdala, successive development of the limbic seizure was not observed. The secondarily generalized seizure never occurred in the IBO group. Histopathological studies revealed circumscribed degenerative changes in the bilateral SI. The KA microinjection into the amygdala resulted stereotyped amygdaloid degenerative lesions in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Limbic seizure and ibotenic acid-induced lesions of substantia innominata in cats]. 281 6

Electroencephalographic techniques were used to study generalized convulsive status epilepticus induced by administration of subconvulsive doses of cholinomimetics (e.g., pilocarpine) to rats pretreated with lithium chloride. Status epilepticus induced by this treatment was compared with status epilepticus induced by kainic acid. Lithium/pilocarpine-induced status epilepticus developed within 10 min of initial paroxysmal spike activity, 24 +/- 1 min (N = 20) after administration of pilocarpine, and continued uninterrupted for more than 3 h. Kainic acid (10 mg/kg)-induced status epilepticus developed approximately 60 min after initial spike activity, 96 +/- 3 min (N = 7) after kainate administration, and continued for 0.5 h. Thus, the interval of intermittent seizure activity and the duration of status epilepticus differed markedly between these two models. The potentiation by lithium (3 meq/kg) of the convulsant effect of cholinergic agonists was found to be 10 to 13-fold for two direct-acting cholinomimetics, pilocarpine and arecoline, whereas the convulsant effect of the indirect-acting agonist, physostigmine, was potentiated by 50%. The full proconvulsant effect of lithium lasted from 2 to 24 h after a single acute treatment (3 meq/kg). The dose response of the proconvulsant effect of lithium was determined and the EC50 of lithium was approximately 1.5 meq/kg when pilocarpine (30 mg/kg) was administered 20 h later. Chronic treatment with lithium for 4 weeks potentiated the convulsant effect of pilocarpine by more than 26-fold. These results demonstrated that both acute and chronic administration of lithium enhance cholinergic function in vivo. Potentiation of cholinergic function by lithium may play a role in the therapeutic action of lithium in affective disorders.
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PMID:Status epilepticus is produced by administration of cholinergic agonists to lithium-treated rats: comparison with kainic acid. 282 29

An effect of the beta-stereoisomer of kainic acid on seizures produced by intracerebroventricular injections of excitatory amino acids was tested in mice. beta-Kainic acid preferentially antagonizes myoclonic seizures induced by N-methyl-D-aspartate and quinolinate, has less pronounced anticonvulsant action against alpha-kainate, D-homocysteinesulphinate and quisqualate, and no effect on convulsions induced by L-glutamate. The anticonvulsant activity of beta-kainic acid matches that of 2-amino-7-phosphonoheptanoic and kynurenic acids, both preferential N-methyl-D-aspartate receptor antagonists, and differs considerably from the profile of anticonvulsant action of gamma-D-glutamylaminomethylsulphonic acid, a preferential kainate/quisqualate antagonist.
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PMID:Anticonvulsant action of beta-kainic acid in mice. Is beta-kainic acid an N-methyl-D-aspartate antagonist? 286 Sep 49

Kainic acid (KA), an excitatory neurotoxin, was used as a tool to study the metabolism of hippocampal opioid peptides and their functional role in the expression of wet-dog shakes (WDS). A single intracerebral injection of KA (1 microgram/rat) caused recurrent motor seizures lasting 3-6 h. During the convulsive period, native Met5-enkephalin-like (ME-LI) and dynorphin A(1-8)-like (DYN-LI) immunoreactivities in hippocampus decreased by 31 and 63%, respectively. By 24 h after dosing, the hippocampal opioid peptides had returned to control levels, and by 48 h ME-LI had increased 270% and DYN-LI 150%. Immunocytochemical analysis revealed that ME-LI and Leu5-enkephalin-like (LE-LI) immunostaining in the mossy fibers of dentate granule cells and the perforant-temporoammonic pathway had decreased visibly by 6 h and had increased markedly by 48 h following KA. A visible decrease in DYN-LI in mossy fiber axons within 6 h was followed by a substantial increase at 48 h. To determine whether the increases in hippocampal ME-LI reflected changes in ME biosynthesis, levels of mRNA coding for preproenkephalin (mRNAenk) and cryptic ME-LI cleaved by enzyme digestion from preproenkephalin were measured. Following the convulsive period (6 h), mRNAenk was 400% of control, and by 24 h, cryptic ME-LI was 300% of control. Increases in native and cryptic ME-LI and in mRNAenk were also noted in entorhinal cortex, but not in hypothalamus or uninjected striatum. Our data suggest that KA-induced seizures cause an increase in ME release, followed by a compensatory increase in ME biosynthesis in the hippocampus and entorhinal cortex. Several lines of evidence from this study have suggested that hippocampal enkephalins are intimately related to KA-elicited WDS. The shaking behavior was attenuated by pretreatment with naloxone or antisera against [Met5]-enkephalin. We also observed that KA-induced WDS can be mimicked by intrahippocampal injection of enkephalin-related peptides. Furthermore, this study demonstrated that intact dentate granule cells are essential for KA- and enkephalin-induced WDS, since a colchicine injection into the ventral hippocampus, which selectively destroys granule cells, abolished this behavior.
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PMID:Kainic acid as a tool to study the regulation and function of opioid peptides in the hippocampus. 289 Feb 24

Kainic acid administration induces status epilepticus seizures in the rat which damage CA1 and CA3 hippocampal neurons. Rats made hypoglycemic prior to seizure had enhanced volumes of damage, when compared to normo- or hyperglycemic rats. The mild hypoglycemia was not in the range which, itself, typically produces hippocampal damage. This suggests that limited energy availability compromised the ability of neurons to survive seizures. Our data also suggest that the CA1 damage seen after status epilepticus is not hypoxic-ischemic in origin, since elevating pre-seizure glucose concentrations to a range which typically exacerbates hypoxic-ischemic CA1 damage did not augment status-epilepticus CA1 damage.
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PMID:Status epilepticus-induced hippocampal damage is modulated by glucose availability. 291

[3H]Kainic acid binding sites with a slow dissociation rate in the rat limbic system were investigated in detail. Extensively washed membranes prepared from the hippocampal formation and from the region comprising the amygdala and the piriform cortex yielded non-linear Scatchard plots. Microdissection showed that the high-affinity component (affinity constant around 1 nM) was present in the hippocampal CA3 region (4.2 fmol/mg wet tissue) and the amygdaloid complex (4.6 fmol/mg wet tissue), whereas the remaining part of the hippocampal formation and the piriform lobe contained the low-affinity component (affinity constant 5-20 nM; 11.6 and 11.3 fmol/mg wet tissue, respectively). In the lateral + medial septum we detected only the low-affinity component. Severe limbic seizures, induced by unilateral injection of 0.7 or 0.8 microgram kainic acid in 0.3 microliter of phosphate-buffered saline into the amygdala, reduced kainic acid binding sites in the ipsilateral amygdala and CA3 region. The decline of kainic acid binding sites in the injected amygdala was followed by a similar effect in the contralateral amygdala ("mirror focus") and later by a moderate loss also in the contralateral CA3 region. Kainic acid receptor autoradiography demonstrated that binding sites were lost from the stratum lucidum in hippocampus. Septal lesion had no effect on kainic acid binding sites in the hippocampus. Comparison with previous results on the histopathological changes after this lesion shows that high-affinity kainic acid binding sites are preferentially located on neurons that undergo selective degenerations after severe kainic acid-induced seizures.
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PMID:Effect of seizures induced by intra-amygdaloid kainic acid on kainic acid binding sites in rat hippocampus and amygdala. 301 84


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