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

Homozygous and heterozygous Brattleboro rats and Long--Evans control rats were subjected to repeated electrical stimulation of the amygdala or pyriform cortex in a kindling paradigm. The homozygous Brattleboro group stimulated in the amygdala was retarded in its kindling rate relative to heterozygous Brattleboros and Long--Evans controls. The retarded kindling rate of the homozygous Brattleboros stimulated in the amygdala is attributed to a delay in seizure development at stages 1 and 2 which suggests that vasopressin may be necessary for normal kindling from the amygdala to take place.
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PMID:Amygdala and pyriform cortex kindling in vasopressin deficient rats (Brattleboro strain). 661 85

Interrelationship between the breakdown of the blood-brain barrier (BBB) to Evans blue and elevations in the regional cerebral blood flow (rCBF) was studied in rabbits subjected to adrenaline- or metaraminol-induced systemic hypertension and also in bicuculline-induced seizures. The rCBF was assessed in small samples from various regions of the brain with the use of [3H]nicotine, and the permeability of the BBB was evaluated with an Evans blue tracer. In acute hypertension, Evans blue extravasations were observed in the occipital cortex and sometimes in the superior colliculus, i.e., the regions which also showed the highest elevations in rCBF. The breakdown of the BBB in acute hypertension was clearly related to the rate of mean arterial blood pressure rise, being much less pronounced in the metaraminol group, which showed a much slower blood pressure elevation rate. In bicuculline-induced seizures, there was no evident correlation between the amplitude of rCBF elevations and Evans blue extravasations. Preservation of BBB integrity was observed in areas showing high elevations in the rCBF.
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PMID:Regional changes in cerebral blood flow and blood-brain barrier permeability during epileptiform seizures and in acute hypertension in rabbits. 669 17

Male Long-Evans rats were stereotaxically implanted with a bipolar electrode in the central amygdala and with a stainless-steel cannula in the lateral cerebral ventricle. Rats were then kindled once daily until 3 consecutive Stage 5 kindled seizures were elicited. Adenosine analogues were injected into the lateral cerebral ventricle to examine their effects on behavioral seizures and afterdischarge duration following a kindling stimulus. 5'-N-ethylcarboxamidoadenosine (NECA) and (-)-N-(1-methyl-2-phenylethyl)-adenosine(L-phenylisopropyladenosine) (L-PIA) produced dose-related reductions of amygdaloid-kindled seizures with NECA exhibiting slightly more potent anticonvulsant activity than L-PIA. Parenteral injections of caffeine, at a dose which had no effect on seizure parameters, antagonized the anticonvulsant effects of NECA. These results are consistent with the notion that adenosine is a modulator of synaptic activity in the CNS and methylxanthines exert a specific antagonism of central adenosine receptors.
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PMID:Anticonvulsant effects of adenosine analogues on amygdaloid-kindled seizures in rats. 673 23

Rats were treated with kainic acid (KA) i.v. to produce increasingly severe limbic seizures that were monitored with a behavioral rating scale. At various times after the induction of seizures, the animals; blood-brain barriers (B-BB) were studied with alpha-[14C]aminoisobutyric acid ([14C]AIBA) autoradiography. Using optical density ratios, a coefficient was devised to assess the functional integrity of the B-BB in discrete anatomic regions and to quantitatively compare these measurements among different groups of experimental animals. In animals that exhibited only mild seizures, the B-BB was not different from controls. Animals with severe limbic seizures, however, showed alterations. For as long as 2 h after delivery of KA, the B-BB appeared normal; from 2 to 24 h, the permeability to [14C]AIBA was markedly increased throughout the brain, especially in limbic regions; from 24 h to 7 days the B-BB returned to normal except for a small residual change in limbic structures. These findings were confirmed with Evans blue dye studies of the B-BB. A correlation between focal accentuation of B-BB alterations and neuropathologic changes was found. These experiments indicted that recurrent limbic seizures may lead to a breakdown in the B-BB independent of systemic metabolic derangements. Marked focal metabolic and electrical changes, however, occurred in several limbic structures several hours before the blood-brain barrier was altered.
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PMID:Blood-brain barrier changes with kainic acid-induced limbic seizures. 682 73

Male Long-Evans rats were stereotaxically implanted bilaterally with bipolar electrodes in the central amygdala. Rats were then kindled once daily for 1 sec until 3 consecutive Stage V [25] kindled seizures were elicited. On the following day, animals were injected (IP) with either saline, naloxone (10 mg/kg), naltrexone (10mg/kg) or morphine sulfate (10 mg/kg) and again stimulated at the kindling stimulation parameters. Saline injected animals continued to show long bilateral AD's and behaviors (i.e., forelimb clonus, rearing, falling) typical of Stage V kindled animals. In contrast, rats injected with naloxone or naltrexone showed reduced behavioral seizures. Potentiation of post-ictal spiking by morphine in amygdaloid-kindled rats was also observed supporting previous reports [7,21]. In a second experiment, the reduction of kindled seizure serverity by naloxone was systematically replicated. It is concluded that opiates can significantly modify amygdaloid-kindled seizures, and that brain endorphins may play a role in the development or maintenance of an amygdaloid-kindled seizure focus.
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PMID:Opiate modification of amygdaloid-kindled seizures in rats. 708 32

Motor impairments and seizures are frequent neurologic sequelae of excess lead exposure in children. To evaluate the relative significance of such symptoms in an animal model, Long-Evans rats were lead-exposed from parturition to weaning by adulteration of the dams' drinking water with 0.02% or 0.2% lead acetate. Ontogeny of swimming ability from 6 through 24 days of age was not altered by postnatal lead exposure. Rotorod performance was tested on 21, 30, 60, 90, 150 and 440 days of age and was maximal in rats 30 through 150 days of age, with the poorest performance by 440-day-old rats. Rotorod performance was decreased by both levels of lead exposure and this effect was most evident at 60 and 150 days of age. Both levels of lead exposure increased kidney weights of dams at weaning and the 0.2% lead acetate exposure decreased hematocrit of dams. Kidney weights of lead-exposed pups were not increased at 10 days of age, but pups in the 0.2% lead acetate group had increased kidney weights at 20, 90 and 150 days of age. Hematocrit values of pups in the 0.2%, but not in the 0.02%, lead acetate exposure group were decreased at 20 days of age. No effects of lead exposure on hematocrits were found at 10, 90 or 150 days of age. Wet weight of brain, cerebellum, adrenals, spleen and thymus were not altered at any age by postnatal lead treatment. In a second study, Sprague-Dawley rats exposed to lead via dams drinking 0.2% lead acetate throughout gestation and lactation. Pre- and postnatal lead exposure did not alter the ontogeny of electro-shock seizure thresholds in rats tested on 8 through 20 days of age. The results suggest that the lead exposure levels used were at or near a no-effect level for several common neurobehavioral tasks and that kidney weight may be a more discriminative index of excess lead exposure than some simple neurobehavioral indices.
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PMID:Motor development, tissue weights and seizure susceptibility in perinatally lead-exposed rats. 720 May 84

Trimethyltin (TMT) chloride, administered to adult male Long-Evans hooded rats, produced a unique and distinctive behavioral syndrome consisting of spontaneous seizures, tail mutilation, vocalization and hyperreactivity. The LD50 for TMT was weight dependent; in large rats (e.g., 450 g), 7 mg/kg TMT produced significant weight loss and lethality, whereas in small rats (e.g., 250 g), 7 mg/kg produced neither weight loss nor lethality. TMT produced mild hypothermia and tremors. Results are discussed in comparison with kainic acid-induced morphological alterations and septal lesion-induced behavioral alterations. Histopathological evaluations of hippocampal tissue revealed cell loss that was largely confined to regio inferior pyramidal cells. TMT offers potential as a tool for investigations of limbic system structure and function.
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PMID:The trimethyltin syndrome in rats. 720 Oct 84

An experimental and clinical study was undertaken to determine whether Zenker's solution without glacial acetic acid (modified Zenker's solution) applied to the external surface of the dura mater can penetrate to injure the underlying cortex. Adult cats and dogs, the dura of which had an average thickness of 0.2 and 0.25 mm, respectively, were given intravenous Evans blue dye as an indicator of blood-brain barrier breakdown. This was followed by the application of modified Zenker's solution to the dura in a manner identical to the clinical practice. When the animals were killed 1 or 2 hours later, the cortex beneath the dura painted with modified Zenker's solution was stained massively. The thickness of human dura was measured; it varied from 0.22 to 0.28 mm in infants of 3 months or less, 0.27 to 0.42mm in infants 4 months to 12 months of age, and 0.32 to 0.45 mm in children to 1 to 18 years of age. Modified Zenker's solution applied to fresh dura for 3 minutes at autopsy gave visual evidence 1 hour later of penetration to the cortex beneath. In operative procedures for craniosynostosis, 69 patients were treated with modified Zenker's solution; of these, 7 developed seizures in the immediate postoperative period. No seizures occurred among the 39 patients on whom modified Zenker's solution was not used. It is concluded that modified Zenker's solution applied to the dura can damage the cortex beneath.
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PMID:Cortical damage from Zenker's solution applied to the dura mater. 720 76

Zenker's solution is a tissue fixative containing mercuric chloride, potassium bichromate, sodium sulfate, and glacial acetic acid. In 1956, Anderson and Johnson reported its use in clinical neurosurgery. They applied the solution to the exposed dura after craniectomy. Delayed bone formation was thought to be due to the suppression of the osteoblastic activity of the outer layer of the dura. The fixative has since become a well-accepted adjuvant to the treatment of craniosynostosis. In 1972, Pawl and Sugar reported postoperative seizures in 6 of 34 patients treated with this solution. They assumed that the fixative penetrated the dura and irritated or damaged the cortex. To clarify the effect of Zenker's solution on the underlying brain, we performed bilateral parasagittal craniectomies in a group of kittens and adult cats. Zenker's solution was applied to one side and the other side served as a control. The animals were killed after periods varying from 24 hours to 2 months. We then examined the cortex under the craniectomies. There was immediate breakdown of the blood-brain barrier, as evidenced by the penetration of intravenous Evans blue. In the postoperative period investigated, an inflammatory response in the underlying brain with thickening of the arachnoid occurred. The results and implications of these experiments are presented. (Neurosurgery, 6: 45--48, 1980)
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PMID:Effect of the dural application of Zenker's solution on the feline brain. 735

The effect of increased brain GABA levels on fully kindled amygdala seizures was investigated in Long-Evans rats. The newly synthesized GABA-transaminase inhibitor, gamma-acetylenic GABA (GAG) administered on four consecutive days (100 mg/kg, followed by 50 mg/kg, i.p.) was found to either significantly reduce, or eliminate entirely, the behavioral seizures normally produced by amygdala stimulation. The effect is seen after the first injection of GAG although its magnitude was greater on subsequent days. Behavioral seizures reappeared 2 to 3 days after termination of GAG treatment. The duration of electrographic seizures (self-sustained amygdala after discharge) was either unchanged or greater on the first day of GAG treatment, but was briefer on subsequent days. The duration of afterdischarges returned to normal levels 1 to 2 days earlier than the behavioral seizures after the termination of GAG. Picrotoxin (1.5-2 mg/kg, i.p.) did not antagonize either electrographic or behavioral effects of inhibition produced with GAG. Electrical stimulation of amygdala delivered during the initial sedation stage induced by picrotoxin resulted in further regression of kindled seizures in the majority of animals. Although in doses employed, GAG alleviates amygdaloid-kindled seizures its use requires caution in view of its ability to reduce arousal level.
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PMID:Amygdaloid kindling and the GABA system. 735 42


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