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)

When the nervous system is subjected to stressful stimuli, reactive gliosis often ensues. This phenomenon consists of the hypertrophy of astrocyte processes as well as the proliferation of these cells. In this study, the lithium-pilocarpine model of temporal lobe epilepsy was employed to study the effects of status epilepticus (SE) on the localization of SC1 protein in reactive astrocytes. SC1 is an anti-adhesive extracellular matrix protein strongly expressed in the mammalian brain. At 1 day following SE, SC1 transiently localized to hypertrophied astrocyte processes that were closely associated with neurons and blood vessels. SC1 was also detected at 7 days post-SE in proliferating astrocytes labeled with the cell division marker PCNA. These findings indicate that the anti-adhesive protein SC1 is ideally localized to create an environment conducive to process extension and cellular proliferation in reactive astrocytes.
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PMID:Analysis of the extracellular matrix protein SC1 during reactive gliosis in the rat lithium-pilocarpine seizure model. 1762 11

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

Pilocarpine-induced status epilepticus (SE) mimics many features of temporal lobe epilepsy and is a useful model to study neural changes that result from prolonged seizure activity. In this study, distribution of the anti-adhesive extracellular matrix protein SC1 was examined in the rat hippocampus following SE. Western blotting showed decreased levels of SC1 protein in the week following SE. Immunohistochemistry demonstrated that the decrease in overall SC1 protein levels was reflected by a reduction of SC1 signal in granule cells of the dentate gyrus. Interestingly, levels of SC1 protein in neurons of the seizure-resistant CA2 sector of the hippocampus did not change throughout the seizure time course. However, at 1 day post-SE, a subset of neurons of the hippocampal CA1, CA3, and hilar regions, which are noted for extensive neuronal degeneration after SE, exhibited a transient increase in SC1 signal. Neurons exhibiting enhanced SC1 signal were not detected at 7 days post-SE. The cellular stress response was also examined. A prominent induction of heat-shock protein (Hsp70) and Hsp27 was detected following SE, while levels of constitutively expressed Hsp40, Hsp90, Hsp110, and Hsc70 showed little change at the time points examined. The subset of neurons that demonstrated a transient increase in SC1 colocalized with the cellular stress marker Hsp70, the degeneration marker Fluoro-Jade B, and the neuron activity marker activity-regulated cytoskeleton-associated protein (Arc). Taken together, these findings suggest that SC1 may be a component of the 'matrix response' involved in remodeling events associated with neuronal degeneration following neural injury.
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PMID:Extracellular matrix protein SC1/hevin in the hippocampus following pilocarpine-induced status epilepticus. 1880 51

SC1 is an extracellular matrix molecule prominent in the mammalian brain. In the cerebellum, SC1 localizes to Bergmann glial cells and perisynaptic glial processes that envelop synapses in the molecular layer. In the present study, confocal microscopy revealed a punctate distribution of SC1 along Bergmann glial fibers that colocalized with the intermediate filament GFAP when fibers were viewed in cross-section. Immunoelectron microscopy showed that the punctate SC1 pattern corresponded to the localization of SC1 in multivesicular bodies situated within Bergmann glial fibers. The pattern of SC1 localization was not disrupted following hyperthermia or pilocarpine-induced status epilepticus. The present study suggests that SC1 protein may reach its destination in perisynaptic glial processes and glial endfeet by transport along Bergmann glial fibers in multivesicular bodies and that this process is preserved following stress.
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PMID:The extracellular matrix protein SC1/Hevin localizes to multivesicular bodies in Bergmann glial fibers in the adult rat cerebellum. 1975 34