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)

EEG registered hippocampal status epilepticus (HSE) was provoked in 41 adult albino rats by intraseptal injection of ouabain, and the hippocampus was studied from 1 1/2 to 24 hr with the enzyme histochemical tests for succinic dehydrogenase (SDH), lactic dehydrogenase (LDH), thiaminopyrophosphatase (TPPase), acid phosphatase (AcPase), Mg2+ adenosine triphosphatase (Mg2++ ATPase), and with general and neurohistological stains. In a first group of animals (1 1/2 to 10 hr of HSE), a stage of general increase in enzymatic activity was detected in the pyramidal neurons (SDH, LDH, AcPase, and TPPase). Mg2+ ATPase showed a marked increase in astrocytes. In a second group (more than 10 hr of HSE), SDH was found decreased in the dendritic fields. LDH activity persisted in neuronal bodies, and AcPase and TPPase showed diffuse activity in the cytoplasm of some pyramidal neurons. In a third group (more than 18 hr of HSE), SDH activity was low. No AcPase granules were observed in some pyramidal neurons and TPPase was negative in some areas of pyramidal layer. Mg2+ ATPase reaction showed scare and retracted astroglial processes. These changes were coincident with "cellular ghosts" observed with hematoxylin-eosin techniques of the same samples in the pyramidal field and were interpreted as cellular death, attributed to relative anoxia following neuronal discharge.
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PMID:Enzyme histochemistry of the rat hippocampus during experimental status epilepticus. 15 26

Considerable evidence indicates that ATP, acting intracellularly of as a neurotransmitter, can influence nerve cell physiology in a variety of ways. Defects in the functioning of ATP-metabolizing enzymes could therefore lead to disturbances in neurotransmission and creation of sustained neuronal discharges characteristic of status epilepticus. In this study we investigated synaptosomal ATPase changes in rat brains during lithium/pilocarpine-induced status epilepticus. After 2 h of continuous electroencephalographic spiking, both Mg(2+)- and Ca(2+)-dependent ecto-ATPases were significantly decreased in freshly prepared synaptosomal preparations from the status rats. The intracellularly acting Ca2+Mg(2+)-ATPase (Ca-pump) was also decreased, but no changes occurred in synaptosomal Na+K(+)-ATPase activity. The difference between ecto-ATPase activities of the control and status rat brains was not affected by repeated freezing-thawing and lengthy storage. Possible involvement of reduced synaptosomal divalent cation-dependent ATPases in the pathophysiology of status epilepticus is discussed.
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PMID:Reduced cortical ecto-ATPase activity in rat brains during prolonged status epilepticus induced by sequential administration of lithium and pilocarpine. 937 20

Results from experiments performed with permanent non-neuronal cell lines suggest that endoplasmic reticulum (ER) calcium homeostasis plays a key role in the control of protein synthesis (PS). It has been concluded that disturbances in ER calcium homeostasis may contribute to the suppression of PS triggered by a severe metabolic stress (W. Paschen, Med. Hypoth., 47 (1996) 283-288). To elucidate how an emptying of ER calcium stores of these cells would effect PS and ribosomal aggregation of non-transformed fully differentiated cells, experiments were run on primary neuronal cell cultures. ER calcium stores were depleted by treating cells with thapsigargin (TG, a selective, irreversible inhibitor of ER Ca(2+)-ATPase), cyclopiazonic acid (CPA, a reversible inhibitor of ER Ca(2+)-ATPase), or caffeine (an agonist of ER ryanodine receptor). Changes in intracellular calcium activity were evaluated by fluorescence microscopy using fura-2-loaded cells. Protein synthesis was determined by measuring the incorporation of [3H]leucine into proteins. The degree of aggregation of ribosomes was evaluated by electron microscopy. TG induced a permanent inhibition of PS to about 10% of control which was only partially reversed within 2 h of recovery. CPA caused about 70% inhibition of PS, and PS recovered completely 60 min after treatment. Caffeine produced an inhibition of PS to about 50% of control. Loading cells with the calcium chelator BAPTA-AM (33.3 microM) alone suppressed PS without reversing TG- or caffeine-induced inhibition of PS, indicating that the suppression of PS was caused by a depletion of ER calcium stores and not by an increase in cytosolic calcium activity. TG-treatment of cells induced a complete disaggregation of polysomes which was not reversed within the 4 h recovery period following TG-treatment. After caffeine treatment of cells, we observed a heterogenous pattern of ribosomal aggregation: in some neurons ribosomes were almost completely aggregated while in other cells a significant portion of polyribosomes were disaggregated. The results indicate that a depletion of neuronal ER calcium stores disturbs protein synthesis in a similar way to the effects of transient forms of metabolic stress (ischemia, hypoglycemia or status epilepticus), thus implying that a disturbance in ER calcium homeostasis may contribute to the pathological process of stress-induced cell injury.
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PMID:Relation of neuronal endoplasmic reticulum calcium homeostasis to ribosomal aggregation and protein synthesis: implications for stress-induced suppression of protein synthesis. 943 27

Status epilepticus is associated with sustained and elevated levels of cytosolic Ca(2+). To elucidate the mechanisms associated with changes of cytosolic Ca(2+) after status epilepticus, this study was initiated to evaluate the effect of pilocarpine-induced status epilepticus on Mg(2+)/Ca(2+) ATPase-mediated Ca(2+) uptake in microsomes isolated from rat cortex, because the Ca(2+) uptake mechanism plays a major role in regulating intracellular Ca(2+) levels. The data demonstrated that the initial rate and overall Ca(2+) uptake in microsomes from pilocarpine treated animals were significantly inhibited compared with those in microsomes from saline-treated control animals. It was also shown that the inhibition of Ca(2+) uptake caused by status epilepticus was not an artifact of increased Ca(2+) release from microsomes, selective isolation of damaged microsomes from the homogenate, or decreased Mg(2+)/Ca(2+) ATPase protein in the microsomes. Pretreatment with the NMDA antagonist dizocilpine maleate blocked status epilepticus-induced inhibition of the initial rate and overall Ca(2+) uptake. The data suggest that inhibition of microsomal Mg(2+)/Ca(2+) ATPase Ca(2+) uptake is involved in NMDA-dependent deregulation of cytosolic Ca(2+) homeostasis associated with status epilepticus.
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PMID:Pilocarpine-induced status epilepticus causes N-methyl-D-aspartate receptor-dependent inhibition of microsomal Mg(2+)/Ca(2+) ATPase-mediated Ca(2+) uptake. 1093 4

The aim of the present study was to obtain information about the effects of pentylenetetrazol-induced status epilepticus (SE) and streptozotocin-induced diabetes on brain cortex Ca(2+)ATPase activity. Treatment with pentylenetetrazol (PTZ) and streptozotocin (STZ) to rats resulted in significant decrease in brain cortex Ca(2+)ATPase activity as compared with controls. However, PTZ-treated diabetic rats had a slight but non-significant decrease in enzyme activity. Treatment with PTZ caused a more pronounced effect in inhibiting enzyme activity than that of treatment with STZ. Our results concluded that reduced brain cortex Ca(2+)ATPase activity following PTZ and STZ treatments to rats, may be an initial biochemical lesion which triggers a sequence of events which may culminate in cell death.
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PMID:Effects of streptozotocin-induced diabetes and pentylenetetrazol-induced seizure on brain cortex (Ca2+)ATPase activity in rats. 1093 61

In the rat pilocarpine model, 1 h of status epilepticus caused significant inhibition of Mg(2+)/Ca(2+) ATPase-mediated Ca(2+) uptake in cortex endoplasmic reticulum (microsomes) isolated immediately after the status episode. The rat pilocarpine model is also an established model of acquired epilepsy. Several weeks after the initial status epilepticus episode, the rats develop spontaneous recurrent seizures, or epilepsy. To determine whether inhibition of Ca(2+) uptake persists after the establishment of epilepsy, Ca(2+) uptake was studied in cortical microsomes isolated from rats displaying spontaneous recurrent seizures for 1 year. The initial rate and total Ca(2+) uptake in microsomes from epileptic animals remained significantly inhibited 1 year after the expression of epilepsy compared to age-matched controls. The inhibition of Ca(2+) uptake was not due to individual seizures nor an artifact of increased Ca(2+) release from epileptic microsomes. In addition, the decreased Ca(2+) uptake was not due to either selective isolation of damaged epileptic microsomes from the homogenate or decreased Mg(2+)/Ca(2+) ATPase protein in the epileptic microsomes. The data demonstrate that inhibition of microsomal Mg(2+)/Ca(2+) ATPase-mediated Ca(2+) uptake in the pilocarpine model may underlie some of the long-term plasticity changes associated with epileptogenesis.
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PMID:Chronic inhibition of cortex microsomal Mg(2+)/Ca(2+) ATPase-mediated Ca(2+) uptake in the rat pilocarpine model following epileptogenesis. 1167 60

An increase in intra-neuronal Ca(2+) concentration has been associated to status epilepticus (SE). Ca(2+) is stored in the endoplasmic reticulum, mediated by the Ca(2+)-ATPases (SERCAs). Here we studied the Ca(2+)-ATPase activity and the SERCA2b distribution in the hippocampus of rats submitted to 5h of SE. The Ca(2+)-uptake was measured using [45Ca]CaCl(2) and the hippocampal distribution of SERCA2b was analyzed by immunohistochemistry. A reduction in the amount of cells expressing SERCA2b in CA1, CA3 and dentate gyrus was observed. However, the surviving cells of these regions increased the SERCA2b immunoreactivity, when compared with control tissues. The Ca(2+)-ATPase activity measured in all hippocampal formation was not modified by SE. These results suggest that SE promotes a redistribution of SERCA2b in the hippocampus as a compensatory Ca(2+)-transport mechanism.
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PMID:Status epilepticus induced by pilocarpine and Ca2+ transport by microsome in the hippocampus of rats. 1528 37

The effects of repetitive pilocarpine-induced status epilepticus (SE) in the hippocampal Na(+)/K(+)ATPase activity were studied in developing rat. Na(+)/K(+)ATPase is a membrane-bound enzyme responsible for the active transport of sodium and potassium ions through the membrane. It is necessary to maintain neuronal excitability. The malfunction of this enzyme has been associated with neuronal hyperexcitability. The pilocarpine-induced status epilepticus in developing rats leads to neuronal hyperexcitability and brain damage. We examined the activity of the Na(+)/K(+)ATPase enzyme in hippocampus of rats submitted to 1 episode of status epilepticus on postnatal day 9 and to 3 episodes of pilocarpine-induced status epilepticus on postnatal days 7, 8 and 9. Our findings showed that one status epilepticus episode does not modify the Na(+)/K(+)ATPase activity in hippocampus of rats studied 7 or 30 days later (at P16 or P39). However, an increase in the Na(+)/K(+)ATPase activity was detected in hippocampus of rats submitted to three consecutive status epilepticus during the development studied 7 (+142%) and 30 (+400%) days following the injections. In addition, a significant reduction in the Na(+)/K(+)ATPase activity was observed in control rats at P39 compared to P16. Our data suggest that multiple pilocarpine-induced status epilepticus in developing rats induce long-lasting increase in the Na(+)/K(+)ATPase activity in the hippocampus, reflecting hyperexcitability.
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PMID:The Na+/K+ATPase activity is increased in the hippocampus after multiple status epilepticus induced by pilocarpine in developing rats. 1727 Jan 50

Status epilepticus-induced hippocampal neuronal loss is mainly associated with excitotoxicity induced by increased levels of extracellular glutamate which is normally neutralized by high-affinity uptake mechanism. The energy source for the glutamate uptake is the electrochemical Na(+) gradient maintained by Na(+)/K(+) ATPase pump. In this study, we investigated the effect of early-life-induced status epilepticus on hippocampal Na(+)/K(+) ATPase activity and glutamate uptake. Rat pups 15 days old were injected i.p. with LiCl (3 mEq/kg) 12-18 h prior to s.c. pilocarpine administration (60 mg/kg). Hippocampal Na(+)/K(+) ATPase activity and glutamate uptake were evaluated 1.5, 12 and 24 h after SE induction. LiCl-pilocarpine-induced SE decreased Na(+)/K(+) ATPase activity and glutamate uptake by 42 and 38%, respectively, 1.5 h after SE induction. However, 12 and 24 h after SE induction the pump activity and glutamate uptake returned to control levels. SE early in life increased hippocampal number of degenerating neurons in the CA1 subfield and dentate gyrus 24 h after SE induction. In conclusion, SE induced early in life causes short-term disruption in hippocampal Na(+)/K(+) ATPase activity and glutamate uptake, which may be related to neuronal death found in CA1 subfield.
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PMID:Early life LiCl-pilocarpine-induced status epilepticus reduces acutely hippocampal glutamate uptake and Na+/K+ ATPase activity. 2097 96

In this study, we investigated the effects of 2,2'-dithienyl diselenide (DTDS), an organoselenium compound, against seizures induced by kainic acid (KA) in rats. Rats were pretreated with DTDS (50 or 100 mg/kg) by oral route 1 h before KA injection (10 mg/kg, intraperitoneal). Our results showed that DTDS (100 mg/kg) was effective in increasing latency for the onset of the first clonic seizure episode induced by KA, as well as in decreasing the appearance of seizures and the Racine's score. DTDS also caused a decrease in the excitatory electroencephalographic (EEG) changes, resulting from KA exposure in hippocampus and cerebral cortex of rats. Besides, elevated reactive species (RS) and carbonyl protein levels and Na(+), K(+)-ATPase activity in hippocampus of rats treated with KA were ameliorated by DTDS (50 and 100 mg/kg). Lastly, as evidenced by Cresyl-Violet stain, DTDS (100 mg/kg) elicited a protective effect against KA-induced neurodegeneration in rat hippocampus 7 days after KA injection. In conclusion, the present study showed that DTDS attenuated KA-induced status epilepticus in rats and the subsequent hippocampal damage.
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PMID:Protective effect of 2,2'-dithienyl diselenide on kainic acid-induced neurotoxicity in rat hippocampus. 2182 Apr 94


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