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 effects of intraseptal application of atropine on c-fos proto-oncogene expression related to soman treatment were studied by immunohistochemistry for c-Fos-like proteins. In control rats, 2 h after the onset of convulsion, c-Fos-like immunoreactivity was intense in the piriform and entorhinal cortices, but also in the cingulate, frontoparietal and retrosplenial cortices. In addition, the staining was moderate in the hypothalamus, amygdala and fascia dentata. The intraseptal application of atropine, which prevented soman-induced convulsions, reduced or even blocked c-Fos-like protein production related to soman treatment. This inhibition of Fos induction was significant in most of the limbic structures but also in non-limbic areas. The data in this study strongly suggest that the cholinergic cells of the medial septal area play a key role in soman-induced seizures, and confirm that c-Fos-like protein induction is closely related to neuronal hyperactivity.
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PMID:Influence of medial septal cholinoceptive cells on c-Fos-like proteins induced by soman. 145 Sep 6

In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls. Increased expression of c-fos mRNA was observed in animals demonstrating cocaine-induced seizures acutely or following pharmacological kindling. Rats that experienced acute seizures after cocaine (65 mg/kg) showed pronounced increase in expression of c-fos mRNA in the dentate gyrus of the hippocampus and olfactory bulb. Increases were also observed in several other limbic cortical regions, as well as the striatum and ventromedial hypothalamic nucleus (VMH). In rats that were injected daily with an initially subconvulsive dose of cocaine-HCl (40 mg/kg), the cocaine-kindled seizures induced elevations in c-fos mRNA in the same brain regions as with an acute cocaine-induced seizure with the single exception of the VMH. These findings not only suggest the involvement of limbic, cortical and striatal structures in the cocaine-induced seizure, but also raise the possibility that alterations in the proto-oncogene c-fos and its subsequent impact on gene expression could play a role in the changes in neural excitability associated with cocaine-induced kindling.
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PMID:Expression of c-fos mRNA in acute and kindled cocaine seizures in rats. 149 73

In rats made susceptible to audiogenic seizures by exposing them to an intense noise at a critical time during development, subsequent noise exposure elicited seizures and induced the proto-oncogene c-fos in auditory regions of the brain. Cells showing Fos-like immunoreactivity were especially dense in dorsal and external cortices of the inferior colliculus, and were nearly absent after pretreatment with the N-methyl-D-aspartate (NMDA) antagonist MK-801. Noise exposure alone (i.e. no seizure) produced a localized zone of c-fos induction within the inferior colliculus, but only when presented during the time period when susceptibility to audiogenic seizures can be most effectively induced.
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PMID:Audiogenic seizures induce c-fos in a model of developmental epilepsy. 154 26

Induction of the proto-oncogene c-fos is often considered to be a marker of increased neuronal activity. We have used in situ hybridization to study the pattern of c-fos expression in limbic structures following kainic acid-induced seizures during the postnatal period in the rat. Prior to postnatal day 13 (P13), seizure activity did not result in c-fos induction in any limbic structure. Between P13 and P25, a gradual increase in c-fos expression was observed in hippocampus and cortical structures. These results were corroborated by nuclear run-off transcription assay. Thus, alterations in c-fos transcription that may facilitate stimulus-transcription coupling occur during postnatal development. The possible relationship between the postnatal maturation of c-fos expression and the increase in susceptibility of specific neuronal populations to seizure-induced cell damage is discussed.
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PMID:Absence of c-fos induction in neonatal rat brain after seizures. 163 64

c-fos is a proto-oncogene that encodes for a nuclear phosphoprotein with DNA binding properties and is presumed to have an important role in the long-term regulation of neuronal function. It is thought to act as a 'third messenger' molecule in signal transduction systems and its expression has been shown to be induced by a variety of exogenous and endogenous stimuli. This study examines the differential expression of the Fos protein in various brain regions after a single electroconvulsive shock (ECS) in 6-, 13-, and 28-month-old B6C3 mice. The animals received an acute electroconvulsive shock (90 V for 0.3 s), without prior anesthesia, through earclip electrodes and exhibited generalized tonic-clonic seizures lasting 20-36 s. Animals were anesthetized and perfused intracardially with 2.5% acrolein, 4% paraformaldehyde at 0.5, 1.0, 2.0 and 4.0 h postshock. The brains were Vibratome-sectioned (30 microns) and examined using a Fos antibody, directed against a conserved region of both mouse and human Fos by standard immunocytochemical methods. Systematic sampling of the total number of Fos immunostained neurons in amygdala, hippocampus and the cerebral cortex showed peak values at the 1-h time point followed by a steady decline thereafter in all age groups. In a second experiment, Fos-like immunoreactivity was compared 1 h after ECS in the hippocampus, amygdala and the cortex in all 3 age groups. There was increased expression of Fos-like immunoreactivity after ECS- compared to non-ECS-treated controls in all age groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Attenuation of Fos-like immunoreactivity induced by a single electroconvulsive shock in brains of aging mice. 168 5

Expression of the proto-oncogene c-fos is known to increase in rat brain following various types of seizures. Measuring c-fos mRNA or protein levels was shown to be a good cellular marker for neurons activated during central nervous system (CNS) excitation. In this study, we used in situ hybridization analysis of c-fos mRNA to determine brain regions activated by a peptide that has been closely linked to stress responsivity and kindling-like seizure activity. Corticotropin-releasing hormone (CRH) was injected into the left lateral ventricle of rats and produced the late onset of seizures between 1.5-5 h after its administration. Rats were sacrificed at various time points after the administration of CRH or sterile water, and c-fos mRNA levels were determined. In the preseizure state, CRH increased c-fos unilaterally in several cerebral cortical structures (most prominently in the dorsal endopiriform nucleus and in the piriform and insular cortices). CRH-induced seizures increased c-fos bilaterally in the same cortical regions, and in addition, in the hippocampus and olfactory bulb. The data are congruous with the hypothesis that intracerebroventricularly (i.c.v.) administered CRH elicits a rapid kindling-like response.
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PMID:Expression of c-fos mRNA in rat brain after intracerebroventricular administration of corticotropin-releasing hormone. 178 25

Previous work by others has demonstrated that neocortical injury results in the induction of c-fos protooncogene both at and distal to the site of injury. However, secondary effects of focal brain injury, such as spreading depression and seizure activity, also have been shown to induce the expression of c-fos. Thus, it is unclear whether the stimulus inducing c-fos expression after generalized brain trauma is direct neuronal injury or associated, secondary effects of injury. In this study, we tested the hypothesis that a specific axonal disconnection would induce the expression of c-fos proto-oncogene in the injured neurons. The injury paradigm that was used was peripheral axotomy of rodent facial motoneurons. The right facial nerve was severed distal to the stylomastoid foramen, with the left side serving as an internal control. As positive controls, in a separate group of animals, seizures were invoked using bicuculline administered intraperitoneally. At the end of postoperative survival times ranging from 30 min to 24 hr, the animals were sacrificed. For northern blot analysis using a c-fos cDNA probe, total RNA was isolated from the dissected facial nuclear groups in the injury experiments, or whole brain and neocortex in the seizure experiments. For immunocytochemical analysis using a battery of c-fos antibodies, the animals were perfused with paraformaldehyde and processed for routine light microscope immunocytochemistry. In the bicuculline-injected animals, c-fos mRNA was massively induced in whole brain in a manner proportional to the overall level of gross seizure activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential neuronal expression of c-fos proto-oncogene following peripheral nerve injury or chemically-induced seizure. 190 55

Recently the nuclear proto-oncogene c-fos has been shown to be rapidly and transiently expressed following seizures in many types of epilepsies. Until now, immunohistochemical as well as in situ hybridization studies have reported that the dentate gyrus of the hippocampus and most of the cortical areas were invariably heavily labeled. In order to see whether this distribution was reproduced or not in a model of epilepsy which has been proved to not involve these structures, a study was performed on genetically epilepsy-prone DBA/2 mice. Here we show that following audiogenic seizures, c-fos oncoprotein is not expressed in cortical and limbic structures but rather mapped the subcortical auditory nuclei.
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PMID:Audiogenic seizures evoked in DBA/2 mice induce c-fos oncogene expression into subcortical auditory nuclei. 211 90

Induction of messenger RNA encoding the 70-kDa heat shock or stress protein, hsp70, and the product of the proto-oncogene c-fos was evaluated in gerbil hippocampus by in situ hybridization at various recirculation intervals after 5 minutes of ischemia. Striking increases in c-fos RNA were observed in dentate granule cells within 15 minutes of recirculation and remained evident through 1 hour, returning to undetectable control levels by 3 hours. Modest c-fos hybridization was seen in CA1 and CA3 neurons during the same time course. These results are consistent with the rapid and transient stimulation-induced c-fos expression observed in many experimental systems. Hsp70 expression showed a longer time course, being strongly induced in all major hippocampal neuron populations within 3 hours and persisting for approximately 12 hours in dentate granule cells and through 24 hours in CA3 pyramidal neurons. Notably, the most prolonged expression of hsp70 RNA was observed in vulnerable CA1 neurons that minimally accumulate the immunoreactive protein, with hybridization detected essentially until the death of this cell population at 3-4 days. These studies demonstrate an overlapping distribution of hsp70 and c-fos expression in gerbil hippocampus after ischemia, although there are differences in time course and in the relative induction observed in different neuron populations. The transient increase in c-fos hybridization in dentate granule cells is identical to that seen in various seizure paradigms and provides further support for activation of hippocampal circuitry after ischemia. The prolonged time course of hsp70 messenger RNA expression in vulnerable CA1 neurons may provide a molecular correlate of proposed excitotoxic mechanisms mediating delayed neuronal death.
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PMID:70-kDa heat shock protein and c-fos gene expression after transient ischemia. 212 54

Extracellular adenosine acts through specific cell surface receptors to modulate numerous physiological processes in both the CNS and peripheral tissues (e.g. neurotransmitter release and blood flow). Activation of A1 or A2 adenosine receptors leads to decreased or increased intracellular cAMP levels, respectively. Fos and Jun are nuclear proto-oncogene products, which, like cAMP, appear to act as intermediates in a number of signal transduction pathways. Since increases in both adenosine release and Fos and Jun expression occur in the brain following seizures, we wanted to determine whether Fos and Jun induction might occur as a result of adenosine receptor activation. 3T3 fibroblasts and NG108-15 neuroblastoma-glioma hybrid cells were chosen for study, since they were known to respond to adenosine agonists with changes in cAMP levels. The membranes of NG108-15 cells were shown to have A2-like binding activity in a competitive binding assay. Cultures of each cell line were treated with the adenosine agonists, CHA (A1-selective) and NECA (non-selective adenosine agonist). Both lines responded with a concentration-dependent transient increase in c-fos, but not c-jun, mRNA content after treatment with either agonist. The kinetics of the response were much more rapid for 3T3 cells (peak between 15 and 30 min) than for NG cells (peak between 60 and 90 min). The slower, more prolonged response in the NG108-15 cells is more similar to the time interval between adenosine release and the peak of c-fos mRNA induction in brains of animals following the administration of seizure-promoting drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of adenosine receptors induces c-fos, but not c-jun, expression in neuron-glia hybrids and fibroblasts. 217 6


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