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)

Despite ready induction of severe limbic status epilepticus by systemic kainic acid (KA) in infant rats, excitotoxic neuronal injury has not been observed. The mechanisms of this resistance of the immature hippocampus to excitotoxicity are unknown. Acid fuchsin stain has been used as a marker of irreversibly injured neurons in the adult brain. We speculated that the dye might map reversibly injured neurons in the infant. Subsequent to KA-induced status epilepticus in 11-day-old rats, acid fuchsin stain was evident in the hippocampal CA3, CA1, dentate gyrus and hilus by 24 h, peaked at 48 h and disappeared by 6 days, without evidence for neuronal loss. Acid fuchsin may be a useful tool for delineating the distribution of reversibly injured immature neurons in experimental seizure paradigms.
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PMID:Status epilepticus results in reversible neuronal injury in infant rat hippocampus: novel use of a marker. 751 May 87

In order to follow the spatial and temporal evolution of neuronal damage, cellular activation and stress responses subsequent to lithium-pilocarpine seizures of various durations in the adult rat, we analyzed the expression of Fos protein and local cerebral glucose utilization as markers of cellular activation, HSP72 immunoreactivity and acid fuchsin staining as indicators of cellular stress and injury, and Cresyl violet staining for the assessment of neuronal damage. The expression of Fos appeared very early, 2-30 min after the onset of polyspikes and intensified during the following 4 h. Fos immunoreactivity was especially high in the hippocampus, cerebral cortex, amygdala and anterior olfactory nuclei. Local cerebral glucose utilization measured during the second hour of seizures was largely increased (350-580%) over control levels in cortical areas, amygdala, dentate gyrus, caudate nucleus and mediodorsal thalamus. HSP72 immunoreactivity never appeared earlier than 40-50 min after the onset of polyspikes, and was most prominent in hippocampal CA3 area, cerebral cortex (except the piriform cortex) and anterior olfactory nuclei. Acid fuchsin staining was maximal in the piriform cortex and the polymorphic layer of the dentate gyrus. Staining was moderate in the sensorimotor cortex and the amygdala. Neuronal damage was extensive in the piriform and entorhinal cortices, the hippocampal CA3 area and the polymorphic layer of the dentate gyrus, basal amygdala, mediodorsal thalamus and anterior olfactory nuclei. In conclusion, the present study shows that brain regions with the highest expression of Fos and the largest metabolic activation were also highly stained with acid fuchsin and most heavily damaged. Conversely, there is no clear relationship between HSP72 expression, cellular activation and neuronal damage.
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PMID:Spatial and temporal evolution of neuronal activation, stress and injury in lithium-pilocarpine seizures in adult rats. 963 May 18

To investigate whether long-term functional consequences of status epilepticus (SE) induced by pentylenetetrazol in 10-day-old rats correlated with cell injury and/or death, acid fuchsin and TUNEL staining were performed between 4 to 144 h after SE. Acid fuchsin stained hippocampus, amygdala and cerebral cortex at 24 h but not at 72 and 144 h. No DNA fragmentation was apparent at any time. Thus, immature neurons subjected to sustained seizures suffer transiently but survive probably by activating repair processes.
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PMID:Pentylenetetrazol seizures induce cell suffering but not death in the immature rat brain. 997 68

Rats treated with the neuroepileptic drug, kainic acid, exhibit a specific regional pattern of neurodegeneration 24 h following onset of acute limbic status epilepticus. At 24 h post-seizure, the areas undergoing neurodegeneration also exhibit substantial amounts of the neuropeptide corticotropin-releasing factor (CRF) which is not present under normal conditions. In experimental brains, CRF is localized immunocytochemically to cells and densely labeled fibers in areas with neurodegeneration. Networks of CRF fibers closely surround moribund neurons staining intensely for acid fuchsin. Acid fuchsin, an acidophilic dye, is used routinely as a marker for irreversible neuronal injury, and acid fuchsin-positive neurons are identified in specific areas affected by kainic neurotoxicity. Evidence exists in the literature that CRF functions in brain as a excitatory neurotransmitter/neuromodulator. Under certain pathological conditions (i.e., seizures, brain trauma, ischemia), it has been postulated that CRF could act as an neurotoxic agent. This study provides anatomical evidence that CRF may function following seizures as an neurotoxin because of the close proximity of CRF-labeled fibers to degenerating neurons.
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PMID:Corticotropin-releasing factor--immunolabeled fibers in brain regions with localized kainate neurotoxicity. 1060 38