Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute and chronic effects of seizures induced by intraperitoneal (i.p.) injection of kainic acid (KA) were studied in developing rats (postnatal days (P) 5, 10, 20, 30, and adult 60). For 3 months following KA-induced status epilepticus, spontaneous recurrent seizure (SRS) occurrence was quantified using intermittent video monitoring. Latency to generalized seizures was then tested using flurothyl, and brains were histologically analyzed for CA3 lesions. In P5-10 rats, KA caused generalized tonic-clonic ('swimming') seizures. SRS did not develop, and there was no significant difference between control and KA-treated rats in latency to flurothyl-induced seizures. In contrast, rats P20 and older exhibited limbic automatisms followed by limbic motor seizures which secondarily generalized. Incidence and frequency of SRS increased with age. P20-30 rats with SRS had shorter latencies to flurothyl seizures than did KA-treated P20-30 rats without SRS or controls. KA-treated P60 rats (with or without SRS) had shorter latencies than controls to flurothyl seizure onset. SRS in P60 rats occurred sooner after KA than in P20-30 rats. CA3 lesions were seen in P20-60 rats with and without SRS, but not in P5-10 rats. These data suggest that there are developmental differences in both acute and chronic responses to KA, with immature animals relatively protected from the long-term deleterious effects of this convulsant.
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PMID:Kainic acid seizures in the developing brain: status epilepticus and spontaneous recurrent seizures. 157 66

The present study was devoted to the long-term effects of seizures induced by pentylenetetrazol in immature rats on cerebral metabolic rates in young adult animals. Seizures were induced by repetitive intraperitoneal injections of subconvulsive doses of pentylenetetrazol either in 10- (P10) or in 21- (P21) day-old rats. The long-term metabolic effects of the seizures were studied at P60 in 54 cerebral structures by means of the [14C]deoxyglucose method. At P60, metabolic activity was decreased in 10 brain regions of rats exposed to pentylenetetrazol at P10 and in 29 structures in rats exposed to seizures at P21. Among the structures whose metabolic activity was reduced at P60 by seizures occurring either at P10 or at P21 were mainly sensory, cortical and hippocampal regions plus mammillary body, i.e. all the structures metabolically characterized as most vulnerable to pentylenetetrazol-induced status epilepticus in our previous study [Pereira de Vasconcelos A. et al. (1992) Devl Brain Res. 69, 243-259]. In the animals exposed to seizures at P21, metabolic activity was also reduced at P60 in additional sensory and cortical regions, as well as in limbic, thalamic and hypothalamic nuclei, also considered as highly sensitive to short-term pentylenetetrazol-induced seizures [Pereira de Vasconcelos A. et. al. (1992)]. Rates of glucose utilization were also reduced in a few additional areas such as the monoaminergic cell groupings. In conclusion, there are some parallels between the structures metabolically most sensitive during pentylenetetrazol-induced status epilepticus in immature rats and the long-term regional metabolic decreases recorded at P60. Our data also confirm the well-known higher sensitivity to seizures during the third postnatal week in rodents.
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PMID:Long-term metabolic effects of pentylenetetrazol-induced status epilepticus in the immature rat. 767 78

The long-term behavioral and cognitive effects of seizures at different ages were studied using the kainic acid (KA) seizure model. Rats of postnatal (P) ages (in days) 5, 10, 20, 30, and 60 were administered KA intraperitoneally (i.p.), which induced status epilepticus for several hours, or an equivalent volume of saline. Occurrence of spontaneous recurrent seizures (SRS) was then monitored for 3 months by a closed-circuit videotaping system. Rats began behavioral testing on P80; a separate group of rats that received KA on P60 began testing on P120. Behavioral tests included the Morris water maze (visuospatial learning and memory), the open field test (response to a novel environment), and the handling test (emotionality). When tested on P80, KA-treated P5 and P10 rats had no demonstrable deficits on any test as compared with controls. KA-Treated P20 rats differed from controls only on the water maze spatial bias test. KA-Treated P30 rats had deficits in spatial bias, were more active in the open field, and were more aggressive when handled. KA-Treated P60 rats, whether tested on P80 or P120, had deficits in learning platform position and spatial bias in the water maze, were more active in the open field, and were more aggressive when handled. P60 rats with SRS performed poorer in water maze place learning and spatial bias testing, although the number of SRS did not correlate with overall task acquisition. Our findings suggest age-related behavioral and cognitive deficits after KA-induced seizures. Pubescents and adults had alterations in learning, memory, exploratory behavior, and response to handling, whereas younger animals had no obvious behavioral or cognitive deficits.
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PMID:Age-dependent cognitive and behavioral deficits after kainic acid seizures. 850 77

In order to assess acute, short and long-term effects of seizures in the immature rat brain, we studied the metabolic, circulatory and histopathological changes induced by pentylenetetrazol (PTZ) given at postnatal day 10 (P10) or 21 (P21). Seizures were induced by repetitive subconvulsive injections of PTZ given as a first dose of 40 mg/kg followed 10 min later by 20 mg/kg. Thereafter, rats received every 10 min additional injections of PTZ 10 mg/kg until the onset of status epilepticus. Local cerebral metabolic rates for glucose (LCMRglc) were measured both during the seizures in P10 and P21 rats and in the young adult animal at P60 by means of the quantitative 2-deoxyglucose technique. Rates of local cerebral blood flow (LCBF) were determined during the seizures by the iodoantipyrine technique. Short-term histological changes were assessed by acid fuchsin and hematoxylin-eosin staining and by HSP72 immunohistochemistry. At P10, LCMRglcs uniformly increased (38-400%) over control values during seizures. At P21, metabolic increases (39-181%) occurred only in 20% of the structures while LCMRglcs decreased in most cortical, hippocampal and sensory areas as well as in mammillary body, discrete thalamic nuclei and white matter areas. At P10, LCBF rose (32-184%) in all brain structures whereas, at P21, LCBF decreased in cortical, hippocampal and sensory regions and increased in most other areas. At P60, in animals having seized at either age, significant long-term decreases in LCMRglcs were recorded in hippocampus, auditory and piriform cortex, medial geniculate body and mammillary body. In P60 animals exposed to PTZ at P10, LCMRglcs were also decreased in 3 other sensory areas. In P60 animals exposed to seizures at P21, LCMRglcs were additionally decreased in sensory regions, cortices, thalamic and hypothalamic regions. Neuronal cells were transiently stained with acid fuchsin, with a peak occurring at 24 h after the seizures. The stain was visible in all regions of cerebral cortex and hippocampus and in some thalamic and hypothalamic nuclei. This transient staining was not accompanied by cell degeneration as assessed by hematoxylin-eosin histology. No HSP72 expression could be detected 24 h after the seizures, neither at P10 nor at P21. The present study shows that the immature rat neurons undergo altered metabolic rates and local circulatory decreases in the acute phase, a change in the affinity of acid fuchsin as a short-term effect and long-term metabolic decreases. All these changes are located in the same regions, i.e., cerebral cortex, hippocampus, sensory regions as well as scattered thalamic and hypothalamic nuclei. Thus, short- and long-term metabolic changes induced by seizures can be used as an index of cell stress in the immature rat brain. Since all these changes occur in the absence of visible neuronal death, they might be related to changes in the final arborization and synaptic organization of the developing brain.
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PMID:The model of pentylenetetrazol-induced status epilepticus in the immature rat: short- and long-term effects. 898 91

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

P35 rats subjected to kainate induced status epilepticus (SE) subsequently underwent four consecutive series of the Morris Water Maze. They demonstrated, compared with controls, an early (P46-49), and subsequent (P60-63) disturbance in acquisition, but not in long term retention, of spatial memory. They eventually achieved performance levels similar to those of controls (P74-77, P91-94). These data support the hypothesis that acquisition, but not long term retention, of spatial material is impaired in this model of temporal lobe epilepsy (TLE), probably due to the hippocampal injury that occurs after SE.
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PMID:Time sequence and types of memory deficits after experimental status epilepticus. 1116 98

Rat pups age of 14 postnatal day (P14) were subjected to lithium-pilocarpine (Li-PC) model of status epilepticus (SE). Control rats (n=6) were given an equivalent volume of saline intraperitoneally. Behavioral testing began on P60 including the Morris water maze, the radial arm maze, and the rotarod test. Brain were then analyzed with cresyl violet stain for histological lesions and evaluated for mossy fiber sprouting with the Timm stain. We observed spatial memory deficits both in the Morris water maze and radial arm maze in Li-PC-treated rat. There was no motor impairment in Li-PC-treated rat by the rotarod test. Two of six Li-PC-treated rats showed cell loss in hippocampal CA1 subfield. The Timm staining pattern was similar in both control and Li-PC-treated rats. Result of this study suggests that Li-PC-induced SE in immature rats cause long-term cognitive deficit and permanent cell loss in hippocampal CA1, but spare motor impairment.
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PMID:Lithium-pilocarpine-induced status epilepticus in immature rats result in long-term deficits in spatial learning and hippocampal cell loss. 1159 47

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

Elevated Ca(2+) concentrations have been implicated in cell death mechanisms following seizures, however, the age and brain region of intracellular Ca(2+) accumulations [Ca(2+)](i), may influence whether or not they are toxic. Therefore, we examined regional accumulations of (45)Ca(2+) by autoradiography from rats of several developmental stages (P14, P21, P30 and P60) at 5, 14, and 24h after status epilepticus. To determine whether the uptake was intracellular, Ca(2+) was also assessed in hippocampal slices with the dye indicator, Fura 2AM at P14. Control animals accumulated low homogeneous levels of (45)Ca(2+); however, highly specific and age-dependent patterns of (45)Ca(2+) uptake were observed at 5h. (45)Ca(2+) accumulations were predominant in dorsal hippocampal regions, CA1/CA2/CA3a, in P14 and P21 rats and in CA3a and CA3c neurons of P30 and P60 rats. Selective midline and amygdala nuclei were marked at P14 but not at P21 and limbic accumulations recurred with maturation that were extensive at P30 and even more so at P60. At 14 h, P14 and P21 rats had no persistent accumulations whereas P30 and P60 rats showed persistent uptake patterns within selective amygdala, thalamic and hypothalamic nuclei, and other limbic cortical regions that continued to differ at these ages. For example, piriform cortex accumulation was highest at P60. Fura 2AM imaging at P14 confirmed that Ca(2+) rises were intracellular and occurred in both vulnerable and invulnerable regions of the hippocampus, such as CA2 pyramidal and dentate granule cells. Silver impregnation showed predominant CA1 injury at P20 and P30 but CA3 injury at P60 whereas little or no injury was found in extrahippocampal structures at P14 and P20 but was modest at P30 and maximal at P60. Thus, at young ages there was an apparent dissociation between high (45)Ca(2+) accumulations and neurotoxicity whereas in adults a closer relationship was observed, particularly in the extrahippocampal structures.
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PMID:Age- and region-dependent patterns of Ca2+ accumulations following status epilepticus. 1868 97

The central histaminergic neuron system is an important regulator of activity stages such as arousal and sleep. In several epilepsy models, histamine has been shown to modulate epileptic activity and histamine 1 (H1) receptors seem to play a key role in this process. However, little is known about the H1 receptor-mediated seizure regulation during the early postnatal development, and therefore we examined differences in severity of kainic acid (KA)-induced status epilepticus (SE) and consequent neuronal damage in H1 receptor knock out (KO) and wild type (WT) mice at postnatal days 14, 21, and 60 (P14, P21, and P60). Our results show that in P14 H1 receptor KO mice, SE severity and neuronal damage were comparable to those of WT mice, whereas P21 KO mice had significantly decreased survival, more severe seizures, and enhanced neuronal damage in various brain regions, which were observed only in males. In P60 mice, SE severity did not differ between the genotypes, but in KO group, neuronal damage was significantly increased. Our results suggest that H1 receptors could contribute to regulation of seizures and neuronal damage age-dependently thus making the histaminergic system as a challenging target for novel drug design in epilepsy.
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PMID:Histamine 1 receptor knock out mice show age-dependent susceptibility to status epilepticus and consequent neuronal damage. 2234 91


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