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

To assess long-term metabolic consequences of recurrent ictal events arising during development, seizures were repeatedly generated in rats at different stages of cerebral maturation. Seizures were induced by i.p. injections of bicuculline for three consecutive days, starting from postnatal day 5 (P5), when the brain is very immature, or from P15, a period at which the brain is more structurally organized. Local cerebral metabolic rates for glucose were measured in 74 structures at P15, P25 and in adults (P60), by the autoradiographic method using 2-D-[14C]deoxyglucose. Repeated seizures in P5 to P7 pups led to a reduction (16-34%) of glucose consumption at P15, mainly significant in sensory, motor and functionally non-specific areas as well as in cerebellar nuclei. Selective decreases in metabolic activity were still recorded in adults, mostly in auditory system (20%) and cerebellar nuclei (27%). Seizures generated from P15 to P17 led to an overall mortality rate of 62% (versus 22% at P5 to P7). Surviving animals exhibited reduced metabolic rates for glucose (by 7-27%) at P25, significant in 23 structures, and depicting pronounced changes in limbic, hypothalamic, sensory and white matter areas, whereas brain functional activity finally returned to basal values at P60. Therefore, while younger rats seemed to better tolerate repeated bicuculline-induced seizures than older animals, the reverse was true for long-term metabolic effects, and the more immature the brain when seizures arise, the more persistent the functional consequences.
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PMID:Medium- and long-term effects of repeated bicuculline-induced seizures in developing rats on local cerebral energy metabolism. 968 3

Whether febrile seizures lead to hippocampal necrosis is a question of paramount clinical importance. This study attempted to simulate a complex febrile seizure, compared with hyperthermia (HYP) alone and prolonged seizure alone (produced by continuous hippocampal stimulation (CHS)). Four groups of rats were studied at each of two ages, immature (postnatal day, P20) and adult (P60). Group 1 was subjected to 45 min of HYP (body temperature 40 degrees C) plus CHS, Group 2 received 45 min of HYP alone, Group 3 got 45 min of CHS alone, and Group 4 was sham-handled control rats. Baseline and post-session EEGs were recorded in all groups. Subsequently, brains were examined histologically for evidence of hippocampal damage. Both CHS-treated groups (with and without HYP) exhibited behavioral and EEG seizures while the group undergoing HYP alone did not have seizures. There were no gross histological lesions in any group. Cell counts in regions CA1, CA3, dentate gyrus and dentate hilus did not differ in rats under any condition of hyperthermia and CHS, in either P20 or P60 rats compared to age-matched controls. These results indicate that both immature and mature rodents are resistant to hyperthermic brain damage and raises the question of whether febrile seizures play a role in the genesis of mesial temporal sclerosis.
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PMID:Effects of hyperthermia and continuous hippocampal stimulation on the immature and adult brain. 1041 19

In order to assess long-lasting consequences of recurrent seizures during development, the effects of repeated seizures in developing rats were investigated on brain adenosine A1 and A2A receptors. The characteristics of A1 and A2A receptors were analyzed by measuring the binding of the selective agonists [3H]CHA (N6-cyclohexyladenosine) and [3H]CGS 21680 (2-[p-(2-carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamido adenosine), respectively, on cerebral membrane preparations, whereas receptor coupling to G-proteins was examined by using a GTP analogue (Gpp(NH)p; guanylyl-5'-imidodiphosphate). Seizures were induced by bicuculline once a day at two different developmental stages: either from postnatal day 5 to postnatal day 7 (P5-P7) or from P15 to P17. Adenosine receptors were then studied at P15, P25 and P60. P5-P7 seizures led to an increase in A1 receptor density at P60 and to a decrease in their coupling to G-proteins at P15, but they did not affect A2A receptors. P15-P17 seizures decreased the coupling of A1 receptors to G-proteins at P25 and P60, reduced the density of A2A receptors at P25 and increased their affinity at P60. These results depict a persistent sensitivity of both A1 and A2A brain adenosine receptors to repeated seizures, with selective receptor alterations according to the cerebral maturational stage when seizures occur. In respect to the neuromodulatory and anticonvulsant properties of adenosine, such changes might be implicated in long-term functional brain reorganization after early seizures and future susceptibility to convulsive disorders.
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PMID:Medium- and long-term alterations of brain A1 and A2A adenosine receptor characteristics following repeated seizures in developing rats. 1041 17

Glutamate NMDA receptor has been implicated in brain developmental processes as well as in excitotoxicity and seizure mediation. A previous study has shown that an acute episode of seizures for 30 min in rats altered NMDA receptor characteristics, mainly in the very immature animal. In order to assess whether receptor modifications may also account for long-lasting cerebral disabilities, medium- and long-term consequences of repeated seizures in developing rats on brain NMDA receptor properties were investigated. Seizures were induced once a day for 3 consecutive days, either from post-natal day 5 (P5) to P7 or from P15 to P17. NMDA receptors were then analysed at P15, P25 and P60 (adulthood) by measuring specific binding of [3H]MK-801 on brain membrane preparations. In addition, allosteric modulation of NMDA receptors by exogenous glutamate and glycine was investigated. Seizures from P5 to P7 led to a 22% increase in the density of [3H]MK-801 binding sites measured at P15, but did not affect NMDA receptor density or affinity at P25 or P60. P15-P17 seizures led to a 21% decrease in the density of binding sites and to a 33% decrease in receptor dissociation constant at P25, while they were without effect at P60. Moreover, P5-P7 and P15-P17 seizures were both associated with a suppression of the glutamate/glycine-induced receptor activation at P60. These modifications might account for long-term alterations in cerebral excitability or plasticity after early convulsive disorders, with regards to altered cognitive capacities, epileptogenesis and brain susceptibility to recurrent seizures.
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PMID:Repeated seizure-associated long-lasting changes of N-methyl-D-aspartate receptor properties in the developing rat brain. 1047 71

Strong evidences link status epilepticus (SE) in childhood with the later development of epilepsy. Pilocarpine-induced SE in developing rats leads to late appearance of spontaneous epileptic seizures only when SE is induced after the 18th day of life. We examined the possibility that 3 consecutive episodes of pilocarpine-induced SE on postnatal days 7, 8 and 9 could induce behavioral, electrographic and histological epileptic changes in adult life. The animals also underwent behavioral tests (inhibitory step-down avoidance, skinner box, rota-rod, open field and elevated plus-maze). EEG recordings made at the age of 30, 60 and 90 days showed the occurrence of several episodes of spikes and/or polyspikes appearing simultaneously in hippocampus and cortex. Only three isolated spontaneous seizures were observed during the whole period of observation (120 days). The long-term effects of three consecutive episodes of SE include increased spontaneous exploratory activity, learning impairment, and reduced anxiety when tested on P60. Our findings provide evidence for EEG changes and cognitive deficits in adult life following recurrent SE on postnatal days 7-9.
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PMID:Epileptogenesis in immature rats following recurrent status epilepticus. 1075 77

Seizure incidence varies significantly with age, with seizure susceptibility particularly high during the first few years of life. Of significant concern is what effects do brief, repetitive seizures have on the developing brain. We approached this issue by examining the change in seizure threshold, and related markers of neuronal activity and metabolic activity (c-fos mRNA and 2-deoxyglucose [2DG]), as a function of repetitive seizure episodes in immature and mature rats. Starting on postnatal day 15 (P15) (immature) or P60 (adult) rats were given two flurothyl seizures a day for 5 days (nine or ten seizures). The seizure latency profile, our measure of threshold, in immature versus adult rats across the 5-day testing period was different. In immature rats, threshold for the second seizure on each day was significantly lower than for the first seizure, suggesting that there was little refractoriness after the first seizure of the day. In contrast, the mature animal had a significantly longer threshold latency to the second seizure for the first 3 days of testing. The immature animal was also more likely than the adult to exhibit tonic extension as a feature of the first seizure of the day. Following repetitive seizures, more regions of the CNS showed c-fos mRNA expression in the immature animal than adults, suggesting that repetitive seizures in the immature animal activated a greater percentage of the brain. Compared with the effects of a single seizure, repetitive seizures resulted in less 2DG labeling in most regions of the brain (except the hippocampus); in the immature brain this difference was more distinct than in adults. The consequences of repetitive seizures in the immature animal results in distinctly different seizure behavior and neuronal activity pattern (c-fos expression) than that observed in the mature animal.
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PMID:Behavioral and metabolic features of repetitive seizures in immature and mature rats. 1151 22

The expression of limbic seizures following kainic acid (KA) administration starts at approximately postnatal day (P) 19 in rats. In this study we investigated whether the expression of Fos-like immunoreactivity (Fos-IR) in limbic regions occurs concomitantly with the behavioural expression of limbic seizures. Immunohistochemistry for c-Fos protein was examined 1, 2, 4, 12 and 24 h following seizure onset (KA-treated rats) or saline injections (controls) in immature and adult rats at P7, P13, P20 and P60. The expression of Fos-IR in limbic structures following KA-induced seizures is age-dependent. There is a strong and selective induction of Fos-IR in the CA3 region of the hippocampus following KA-induced seizures in rats at P7. However, the expression of Fos-IR in KA-treated rats at P13, P20 and P60 involved other hippocampal structures in addition to CA3. Abundant induction of Fos-IR was found in the CA1, CA3 and dentate gyrus (DG) in KA-treated rats at P13, P20 and P60. While immature rats at P7 and P13 showed very few or no Fos-IR neurons in most amygdala nuclei, rat pups at P20 showed strong induction of Fos-IR in the amygdala. Our results demonstrated that the induction of Fos-IR in most amygdala nuclei and the full expression of behavioural limbic seizures occur at the same developmental age, which is consistent with the idea that the amygdala may play a role in the modulation of limbic seizures.
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PMID:The expression of Fos following kainic acid-induced seizures is age-dependent. 1184 99

Recurrent neonatal seizures are associated with a high risk of neurological sequelae. The major concern is whether recurrent neonatal seizures induce adverse effects on long-term cognition and/or motor performance. Rats were treated with intraperitoneal (ip) bicuculline for 3 consecutive days, starting from Postnatal Day 5 (P5). Kainic acid (KA, 4 mg/kg ip) was injected at P53 to investigate the susceptibility to a second insult, and then cognitive function was tested using the Morris water maze, and motor performance using the Rotarod test, in adulthood (P60). Finally, histological assessments of brains were performed. The rats treated with bicuculline had no deficits in cognition function and pathology findings, but had worse motor performance and increased susceptibility to later KA challenge. Our findings indicate that recurrent bicuculline-induced seizures in the developing brain result in long-term motor deficits and increase the risk of subsequent cognitive damage in response to a second insult.
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PMID:Recurrent Bicuculline-Induced Seizures in Rat Pups Cause Long-Term Motor Deficits and Increase Vulnerability to a Subsequent Insult. 1260 54

Nitric oxide (NO) is a short-lived radical, which modulates synaptic plasticity, neuronal oscillations and cerebral blood flow. NOS-containing neurones can be detected anatomically by nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry or by NOS immunohistochemistry. Neuropeptide Y(NPY) is the most abundant peptide in the brain. NPY is connected with several vital functions, such as a feeding behaviour, sexual maturation, regulation of circadian rhythms, body temperature, blood pressure and neuroendocrine secretions. Neuropeptide Y also modulates anxiety-related disorders, limbic epileptic seizures as well as learning and memory processes. The study was performed on 45 Wistar rats of various ages (PO, P4, P7, P10, P14, P21, P30, P60, and P120; P--postnatal day). The free-floating sections were stained with standard immunohistochemistry methods. Thereafter the histological sections were studied using the confocal laser microscope equipped. For 3D reconstruction the image analysis program LaserSharp 2000v. 2.0 (Bio-Rad, UK) was used. We found that in the newborn rat both NOS- and NPY-immunoreactivity was weak. It had been increasing gradually until the 7th day of postnatal life, after that until P14 it was maintained on the similar level, and then the number of immunolabelled cells deceased. The developmental changes concerned cell morphology as well--until the 10th day of life the immunoreactive cells were immature, with round or oval bodies and had only a few fibres. From P14 the cells' morphology became similar to that in adult.
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PMID:Distribution of nitric oxide synthase and neuropeptide Y neurones during the development of the hippocampal formation in the rat. 1272 88

Status epilepticus (SE) can cause spatial learning, memory, and behavioral deficits; however, little information is available, especially regarding the effects of such seizures on emotional memory and learning functions. We investigated the effects of SE on emotional memory, learning, and behavior in mature rats over short and long periods. SE was induced in 50- to 60-day-old rats (P50-P60) using intraperitoneal injections of pentylenetetrazole (PTZ, n = 20); control rats received saline (n = 10). All animals were tested with elevated T-maze and open-field tests on the 1st, 7th, 14th, and 180th days after SE to evaluate emotional memory, learning, and behavior. The number of fecal boli increased, and one-way escape latency was long in a short period after SE. PTZ-induced SE causes transient memory deficits, which is related to unconditioned fear, but it did not cause any persistent abnormalities of behavior, emotional memory, and learning in mature rats.
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PMID:The effects of pentylenetetrazole-induced status epilepticus on behavior, emotional memory, and learning in rats. 1514 9


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