Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The somatosensory evoked potential (SEP) was recorded in 14 patients undergoing unilateral ECT for the treatment of depression. All patients received right-sided ECT. One patient was studied on a second occasion during leftsided ECT. The index and middle fingers of each hand were electrically stimulated 1/sec throughout anaesthesia, the fit and the 0.5 h period following the fit. During barbiturate anaesthesia the SEP showed the characteristic change of the P49 component and enhancement of P32, while during the seizure induced by right ECT, the SEP was seen more clearly on the left side of the head, despite the high voltage epileptic activity. No significant asymmetries of any of the SEP components were seen post-ictally, the response returning rapidly on both sides. The subjective threshold to electrical stimulation of the fingers of each hand was significantly raised following ECT.
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PMID:Evoked potentials following unilateral ECT. I. The somatosensory evoked potential. 615 56

Accumulated evidence have shown that a series of morphological alternations occur in patients with epilepsy and in different epileptic animal models. Given most of animal model studies have been focused on adulthood stage, the effect of recurrent seizures to immature brain in neonatal period has not been well established. This study was designed to observe the certain morphological changes following recurrent seizures occurred in the neonatal rats. For seizure induction, neonatal Wistar rats were intraperitoneally injected with pilocarpine on postnatal day 1 (P1), P4 and P7. Rat pups were grouped and sacrificed at 1d, 7d, 14d and 42d after the last pilocarpine injection respectively. Bromodeoxyuridine (BrdU) was intraperitoneally administered 36h before the rats were sacrificed. BrdU single and double labeling with neuronal markers were used to analyze cell proliferation and differentiation. Nissl and Timm staining were performed to evaluate cell loss and mossy fiber sprouting. Rats with neonatal seizures had a significant reduction in the number of Bromodeoxyuridine-(BrdU) labeled cells in the dentate gyrus compared with the control groups when the animals were killed either 1 or 7 days after the third seizure (P<0.05) but there was no difference between two groups on P21. On the contrary, BrdU-labeled cells significantly increased in the experimental group compared with control group on P49 (P<0.05). The majority of the BrdU-labeled cells colocalized with neuronal marker-NF200 (Neurofilament-200). Nissl staining showed that there was no obvious neuronal loss after seizure induction over all different time points. Rats with the survival time of 42 days after neonatal seizures developed to increased mossy fiber sprouting in both the CA3 region and supragranular zone of the dentate gyrus compared with the control groups (P<0.05). Taken together, the present findings suggest that synaptic reorganization only occurs at the later time point following recurrent seizures in neonatal rats, and neonatal recurrent seizures can modulate neurogenesis oppositely over different time window with a down-regulation at early time and up-regulation afterwards.
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PMID:Consequences of pilocarpine-induced recurrent seizures in neonatal rats. 1700 43

For the purpose of investigating the role of physical exercise in developmental seizure-induced cognitive deficit, hippocampal mossy fiber sprouting and related gene expression, a seizure was induced by penicillin every other day in Sprague-Dawley rats from postnatal day 24 (P24). The authors assigned ten rats each randomly into the control group (CONT1), the control plus exercise group (CONT2), the seizure group (EXP1) and the seizure plus exercise group (EXP2). Morris water maze test was used respectively during P39-P45 and P61-P66. Treadmill exercise was performed daily by CONT2 and EXP2 rats during P49-P54. On P66, mossy fiber sprouting and gene expression in hippocampus were assessed by Timm staining and real-time RT-PCR. EXP2 rats performed better than EXP1 rats in the second water maze navigation test. In the entire two spatial probe tests, both EXP1 and EXP2 rats performed worse than the two control rats. Physical exercise remarkably reduced the aberrant mossy fiber sprouting in the supragranular region of dentate gyrus and CA3 subfield of hippocampus. Both EXP1 and EXP2 rats had a higher amount of glutamate receptor 1 (GluR1) and lower amount of the ratio of GluR2/GluR1 in hippocampus when compared with CONT rats. In addition, there was long-term enhancement of both gamma-aminobutyric acid receptor A-alpha3 (GABA-Aalpha3) and cholecystokinin (CCK) of EXP2 rats compared with the other three groups. These results showed that physical exercise improved learning capacity by modulating hippocampal regenerative sprouting and related gene expression in a developmental rat model of penicillin-induced recurrent epilepticus.
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PMID:Physical exercise improves learning by modulating hippocampal mossy fiber sprouting and related gene expression in a developmental rat model of penicillin-induced recurrent epilepticus. 1966 89

The ketogenic diet (KD) has been shown to be effective as an antiepileptic therapy in adults, but it has not been extensively tested for its efficacy in neonatal seizure-induced brain damage. We have previously shown altered expression of zinc/lipid metabolism-related genes in hippocampus following penicillin-induced developmental model of epilepsy. In this study, we further investigated the effect of KD on the neurobehavioral and cognitive deficits, as well as if KD has any influence in the activity of zinc/lipid transporters such as zinc transporter 3 (ZnT-3), MT-3, ApoE, ApoJ (clusterin), and ACAT-1 activities in neonatal rats submitted to flurothyl-induced recurrent seizures. Postnatal day 9 (P9), 48 Sprague-Dawley rats were randomly assigned to two groups: flurothyl-induced recurrent seizure group (EXP) and control group (CONT). On P28, they were further randomly divided into the seizure group without ketogenic diet (EXP1), seizure plus ketogenic diet (EXP2), the control group without ketogenic diet (CONT1), and the control plus ketogenic diet (CONT2). Neurological behavioral parameters of brain damage (plane righting reflex, cliff avoidance reflex, and open field test) were observed from P35 to P49. Morris water maze test was performed during P51-P57. Then hippocampal mossy fiber sprouting and the protein levels of ZnT3, MT3, ApoE, CLU, and ACAT-1 were detected by Timm staining and Western blot analysis, respectively. Flurothyl-induced neurobehavioral toxicology and aberrant mossy fiber sprouting were blocked by KD. In parallel with these behavioral changes, rats treated with KD (EXP2) showed a significant down-regulated expression of ZnT-3, MT-3, ApoE, clusterin, and ACAT-1 in hippocampus when compared with the non-KD-treated EXP1 group. Our findings provide support for zinc/lipid transporter signals being potential targets for the treatment of neonatal seizure-induced brain damage by KD.
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PMID:Neurobehavioral Deficits in a Rat Model of Recurrent Neonatal Seizures Are Prevented by a Ketogenic Diet and Correlate with Hippocampal Zinc/Lipid Transporter Signals. 2577 34

While a ketogenic diet (KD) is a well-established therapy for medically intractable epilepsy, clinical evidence of relevant adverse events of a KD has also been reported. We asked whether this kind of diet would have deleterious effects on wild-type brain function by evaluating KD-induced biochemical changes in the hippocampus as well as neurobehavioral changes occurring in wild-type rats. Fifty-four Sprague-Dawley rats were randomly assigned to three groups on postnatal day 28 (P28): wild-type rats fed with a KD qd (daily for 4 weeks, KD) or qod (every other day for 4 weeks, KOD), and wild-type rats fed with standard normal laboratory diet (ND). Neurobehavioral changes were observed on P35, P42, and P49. The hippocampal mossy fiber sprouting, the expression levels of zinc transporters (ZnTs) and lipid metabolism related genes were detected by Timm staining, RT-qPCR and western blot analysis, respectively, on P58. The KD-treated KOD and KD groups showed a significant delay of negative geotaxis reflex on P35, but not on P42 or P49. In the open field test, daily KD treatment only led to a reduction in exploratory activity and increased grooming times but induced no significant changes in the scores of vertical activity or delay time. KD qod treated rats (KOD) displayed a slight delay in the place navigation test on P35 compared with the KD group. There were no significant differences in Timm staining among the three groups. In parallel with these changes, KD treatment (both KD and KOD) induced significantly downregulated mRNA levels of Apoa1, Pdk4, and upregulated expression of ApoE, ANXN7, and cPLA2 in the hippocampus when compared with the ND group (except in the case of ApoE in the KOD group). Notably, both the mRNA and protein levels of cPLA2 in the KOD rats were significantly downregulated compared with the KD group but still markedly higher than in the ND group. No significant difference was found in ZnTs among the three groups. Our data suggest that early-life KD can provoke minor neurobehavioral effects in particular a delay in negative geotaxis reflex and an increase in grooming activity. The hippocampal lipid metabolism signaling pathway, especially cPLA2, may be the target of the protective effect of KD on long-term brain injury after developmental seizures.
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PMID:Neuro-Behavioral Status and the Hippocampal Expression of Metabolic Associated Genes in Wild-Type Rat Following a Ketogenic Diet. 3080 81