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)

A 45-year-old male patient developed focal seizures in his right arm. Neuroimaging demonstrated a tumor of the left frontal lobe. Tumor classification was undecided after stereotactic biopsy. Neuropathological examination of the open biopsy specimen revealed overlapping morphological features of an oligodendroglioma and a central neurocytoma. Groups of tumor cell featured the typical "fried egg" appearance seen in oligodendroglioma; microcalcifications and a network of branching non-proliferating vessels were present. Neurocytoma-like features included small nucleus-free areas of neuropil and perivascular pseudorosettes. Neuron specific enolase was strongly expressed cytoplasmically in the tumor cells and the "neuropil islands" were found to express synaptophysin. The final diagnosis of an oligodendroglioma with neurocytic differentiation was based on tumor location, clinicopathological findings and diagnostic genotyping. Combined loss of heterozygosity (LOH) on the short arm of chromosome 1 (1p) and the long arm of chromosome 19 (19q), the "molecular signature" of oligodendrogliomas, was revealed. Besides supporting the diagnosis of an oligodendroglioma, the molecular data allow for additional therapeutic options. These tumors may point to the presence of yet another potential tumor precursor cell similar to the recently discovered "N-O"-cells in the cerebral cortex of rats, capable of differentiation into neurons and oligodendrocytes.
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PMID:45-year-old male with symptomatic mass in the frontal lobe. 1661 88

We report a rare skull base neurocytoma. A 44-year-old female with a history of focal seizure and progressive right-sided weakness sought treatment at an outside institution, where she underwent total resection of a "left medial sphenoid wing paraganglioma" in 1984. In 1995 after experiencing intense left-sided headaches for 3 weeks, the patient presented to our institution. Magnetic resonance imaging revealed a large local recurrence. She had deficits dating to her initial surgery, including moderate right-sided hemiparesis, complete left ophthalmoplegia, and left facial numbness.The patient underwent a craniotomy with extensive removal of the involved sphenoid bone and a subtotal resection of the tumor. Neurocytoma was diagnosed based on strong immunohistochemical staining for synaptophysin and no reactivity for glial fibrillary acidic protein. Postoperatively, her headaches resolved completely and her neurologic status remained at baseline. The residual tumor was treated with radiation therapy. After 5 years, she remains clinically and radiographically stable.Although typically located adjacent to the foramen of Monro, neurocytomas have now been reported in almost every subcompartment of the craniospinal axis. Finding neurocytomas in extraventricular locations may require revisiting the current theory that subependymal progenitor cells are the cells of origin for these tumors.
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PMID:Skull base neurocytoma: case report and review of the literature of extraventricular neurocytomas. 1716 46

A 12-year-old, male black and white colobus monkey (Colobus guereza kikuyuensis) from a small community zoo presented with a 6-month history of mild, slowly progressive ataxia and paresis culminating in an acute episode of recumbency, depression, and seizures. The animal was humanely euthanatized. Gross post-mortem examination revealed significant abnormalities including diffuse pallor of the carcass and a firm, pale, 8-cm diameter mass, adherent to the serosa of the proximal duodenum and colon, and embedded within the pancreas and mesenteric root. Histologically, the mass had characteristics of a neuroendocrine or endocrine tumor. Immunohistochemical stains for chromogranin, synaptophysin, insulin, and glucagon were positive, confirming the diagnosis of a mixed pancreatic islet cell tumor. These tumors are rare in all species except ferrets and unreported previously in colobus monkeys.
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PMID:Spontaneous pancreatic islet cell tumor in a black and white colobus monkey (Colobus guereza kikuyuensis). 1826 22

The epileptic brain is characterized by increased susceptibility to neuronal hyperexcitability. The rat lithium-pilocarpine model, which mimics many features of temporal lobe epilepsy, has been used to study processes leading to the development of recurrent seizures. After a prolonged seizure episode, termed status epilepticus (SE), neural changes occur during a period known as epileptogenesis and include neuronal cell death, reactive gliosis, axonal sprouting, and synaptogenesis. Extracellular matrix adhesion molecules are important regulators of synaptogenesis and axonal sprouting resulting from SE. SC1, also known as hevin, is an antiadhesive extracellular matrix molecule that localizes to synapses in the mammalian brain. In this study, the distribution of SC1 protein in neurons following SE was examined using the lithium-pilocarpine model. SC1 protein levels in neuronal cell bodies showed a transient decrease at 1 day post-SE, which coincided with an increase of SC1 in the synapse-rich neuropil that was identified with the synaptic marker synaptophysin. Immunoelectron microscopy confirmed the decrease of SC1 signal in neurons at 1 day post-SE and showed that SC1 remained localized to postsynaptic elements throughout the seizure time course. Increased colocalization of SC1 was detected with the excitatory synaptic markers vesicular glutamate transporter 1 (VGLUT1), AMPA receptor subunit GluR1, and N-methyl-D-aspartate receptor subunit NR1, but not with the inhibitory synaptic markers vesicular gamma-aminobutyric acid (GABA) transporter (VGAT) and GABA(A) receptor subunit beta2 (GABA(A) beta2), which could reflect enhanced association of SC1 with excitatory synapses. These findings suggest that SC1 may be involved in synaptic modifications underlying epileptogenesis.
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PMID:The extracellular matrix protein SC1/hevin localizes to excitatory synapses following status epilepticus in the rat lithium-pilocarpine seizure model. 1848 94

The article describes a case of a 15-year old boy after a head contusion with a five-month history of headaches and two seizure episodes. MR imaging revealed a partly solid and partly cystic cortical-subcortical tumour within the precentral gyrus with post-contrast enhancement. The patient underwent gross total resection of the lesion. Histologically the neoplasm was composed of pseudopapillary gliovascular structures surrounded by solid glioneuronal tumour areas. The expression of GFAP and nestin characterized the central parts of the tumour. Moreover the immunolabelling for synaptophysin, neurofilaments, Olig2 and NCAM was present in the peripheral part of the lesion. The neoplasm was consistent with a papillary glioneuronal tumour - one of the new entities in the last WHO CNS tumour classification.
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PMID:Papillary glioneuronal tumour of the precentral gyrus. 1858 11

We report a papillary glioneuronal tumor occurring in the right frontal lobe of a 26-yr-old woman and we review the pertinent literature. Papillary glioneuronal tumor (PGNT) is a rare cerebral neoplasm, identified in approximately 37 cases to date. In 2007, the World Health Organization (WHO) classified the PGNT as a grade I neuronal-glial tumor because of its biphasic neurocytic and glial components and indolent clinical course. Patients commonly present with headaches or seizures, but may be asymptomatic with the mass discovered incidentally upon neuroimaging. Histology demonstrates a pseudopapillary architecture with a single or a pseudostratified layer of glial cells overlying hyalinized vasculature with interpapillary regions of neurocytic or ganglion cells. Peripheral eosinophilic granular bodies, Rosenthal fibers, hemosiderin, and areas of calcification are often noted. The PGNT displays moderate cellularity and is typically devoid of necrosis, microvascular proliferation, and mitoses. Its immunohistochemical profile includes glial fibrillary acidic protein (GFAP)-positive glial cells, synaptophysin-positive interpapillary neurocytes, and MIB-1 labeling in the range of 1-2%.
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PMID:Papillary glioneuronal tumor: a case report and review of the literature. 1871 60

Extracellular signal-regulated protein kinase, ERK1/2 is activated by phosphorylation (p-ERK1/2) during environmental stress such as epileptiform discharge. We investigated the role of ERK1/2 in abnormal axon growth and synapse reorganization in cultured neurons displaying epileptiform activity. The cultured neurons displaying epileptiform activity were treated with magnesium-free extracellular fluid for 3h and monitored epileptiform discharges using whole-cell patch clamp. Two study groups, neurons displaying epileptiform activity and the same neurons treated with ERK1/2 inhibitor U0126, were studied at six time points, 0 min, 30 min, 2h, 6h, 12h, and 24h following discharge. The expressions of p-ERK1/2, C-fos, growth-associated protein 43 (GAP-43) and synaptophysin (SYP), as markers of axon growth and synapse reorganization, were investigated by double-label immunofluorescence and western blotting. In the neurons displaying epileptiform activity, p-ERK1/2 was detected immediately following discharge, and expression peaked at 30 min. The expression of C-fos, GAP-43 and SYP followed the same pattern as p-ERK1/2. In the treated group, p-ERK1/2 was inhibited completely, and C-fos, GAP-43 and SYP were reduced. These findings indicate that epileptiform discharge activates ERK1/2 which regulates C-fos in cultured neurons displaying epileptiform activity, and this cascade may upregulate GAP-43 and SYP to contribute to axon growth and synapse reorganization to potentiate epileptic activities.
Seizure 2009 Dec
PMID:Epileptiform discharge upregulates p-ERK1/2, growth-associated protein 43 and synaptophysin in cultured rat hippocampal neurons. 1981 36

Seizures early in life cause long-term behavioral modifications, namely long-term memory deficits in experimental animals. Since caffeine and adenosine A(2A) receptor (A(2A)R) antagonists prevent memory deficits in adult animals, we now investigated if they also prevented the long-term memory deficits caused by a convulsive period early in life. Administration of kainate (KA, 2 mg/kg) to 7-days-old (P7) rats caused a single period of self-extinguishable convulsions which lead to a poorer memory performance in the Y-maze only when rats were older than 90 days, without modification of locomotion or anxiety-like behavior in the elevated-plus maze. In accordance with the relationship between synaptotoxicity and memory dysfunction, the hippocampus of these adult rats treated with kainate at P7 displayed a lower density of synaptic proteins such as SNAP-25 and syntaxin (but not synaptophysin), as well as vesicular glutamate transporters type 1 (but not vesicular GABA transporters), with no changes in PSD-95, NMDA receptor subunits (NR1, NR2A, NR2B) or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor subunits (GluR1, GluR2) compared with controls. Caffeine (1 g/L) or the A(2A)R antagonist, KW6002 (3 mg/kg) applied in the drinking water from P21 onwards, prevented these memory deficits in P90 rats treated with KA at P7, as well as the accompanying synaptotoxicity. These results show that a single convulsive episode in early life causes a delayed memory deficit in adulthood accompanied by a glutamatergic synaptotoxicity that was prevented by caffeine or adenosine A(2A)R antagonists.
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PMID:Caffeine and an adenosine A(2A) receptor antagonist prevent memory impairment and synaptotoxicity in adult rats triggered by a convulsive episode in early life. 1987 34

Alterations in N-methyl-d-aspartate receptor (NMDAR) protein levels or subcellular localization in brain after chronic ethanol exposure may contribute to withdrawal-associated seizures and neurotoxicity. We have investigated synaptic localization of NMDARs in cultured hippocampal pyramidal neurons after prolonged (7 days) exposure to, and acute withdrawal from, 80 mM ethanol using fluorescence immunocytochemistry techniques. After chronic ethanol exposure, there was a significant increase in the clustering of NR1 and NR2B subunits and their colocalization with the synaptic proteins synaptophysin and postsynaptic density protein 95, respectively. There was also increased expression of NR1 variants containing the C2' cassette after chronic ethanol exposure. The ethanol-induced synaptic clustering and colocalization were rapidly reversed within 4 h after ethanol withdrawal. Surface labeling of NR2B subunits suggested that this rapid reversal involved lateral receptor movement to extrasynaptic sites rather than internalization of receptors. Receptor removal from the synapse during ethanol withdrawal was associated with changes in the phosphorylation state of NR2B Ser1480, controlled by the protein kinase CK2. The redistribution of NMDAR to synapses produced by long-term ethanol exposure, as well as the rapid removal during withdrawal, may not only affect neuronal withdrawal hyperexcitability but also may sensitize the system to subsequent synaptic plasticity.
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PMID:Phosphorylation regulates removal of synaptic N-methyl-D-aspartate receptors after withdrawal from chronic ethanol exposure. 2000 87

Repeated seizures induce permanent alterations of the brain in experimental models and patients with intractable temporal lobe epilepsy (TLE), which is a common form of epilepsy in humans. Together with cell loss and gliosis in many brain regions, synaptic reorganization is observed principally in the hippocampus. However, in the amygdala this synaptic reorganization has been not studied. The changes in Zn density, synaptophysin and MAP(2) as markers of reactive synaptogenesis in medial extended amygdala induced by kainic acid (KA) as a model of TLE was studied. Adult male rats (n=6) were perfused at 10 days, 1, 2, 3 and 4 months after KA i.p. injection (9 mg/kg). Controls were injected with saline. The brains were processed by the Timm's method to reveal synaptic Zn and analyzed by densitometry. Immunohistochemistry was used to reveal synaptophysin and MAP(2) expression. A two-way ANOVA was used for statistics, with a P<0.05 as a significance limit. Normal dark staining was seen in all medial extended amygdala subdivisions of control animals. At 10 days post KA injection a dramatic loss of staining was observed. A slow but steady recovery of Zn density can be followed in the 4 month period studied. Parallel, from 10 days to 2 months stronger synaptophysin expression could be observed, whereas MAP(2) expression increased from 1 month with peak levels at 3-4 months. The results suggest that a process of sprouting exists in surviving neurons of medial extended amygdala after status epilepticus and that these neurons might be an evidence of a reactive synaptogenesis process.
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PMID:Timed changes of synaptic zinc, synaptophysin and MAP2 in medial extended amygdala of epileptic animals are suggestive of reactive neuroplasticity. 2014 92


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