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 adenosine receptor antagonist, caffeine, transiently induced proto-oncogene c-fos mRNA in mouse brain in a dose-dependent fashion. In situ hybridization revealed that caffeine-induced c-fos expression was high in caudate-putamen and olfactory tubercle at both subconvulsive and convulsive doses. The pattern of c-fos mRNA distribution following caffeine administration differs from that reported after seizures induced by electroconvulsive shock (ECS) or other chemical convulsants, and closely parallels the distribution of adenosine A2 receptors. Furthermore, the potent adenosine A2 receptor agonist, 5'-N-ethylcarboxamide adenosine (NECA) blocked caffeine-induced c-fos expression whereas the adenosine A1 receptor ligand, N6-cyclohexyladenosine (CHA), had no effect. This study suggests that the caffeine-induced expression of c-fos mRNA may be mediated by the adenosine A2 receptor in mouse brain.
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PMID:Adenosinergic modulation of caffeine-induced c-fos mRNA expression in mouse brain. 251 Sep 4

Fos and Jun form a heterodimeric complex that associates with the nucleotide sequence motif known as the AP-1 binding site. Although this complex has been proposed to function as a transcriptional regulator in neurons, no specific target gene has yet been identified. Proenkephalin mRNA increased in the hippocampus during seizure just after an increase in c-fos and c-jun expression was detected. Fos-Jun complexes bound specifically to a regulatory sequence in the 5' control region of the proenkephalin gene. Furthermore, c-fos and c-jun stimulated transcription from this control region synergistically in transactivation assays. These data suggest that the proenkephalin gene may be a physiological target for Fos and Jun in the hippocampus and indicate that these proto-oncogene transcription factors may play a role in neuronal responses to stimulation.
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PMID:Regulation of proenkephalin by Fos and Jun. 251 42

The regional distribution of c-fos mRNA in the mouse brain has been investigated by in situ hybridization autoradiography after seizures induced by an acute electroconvulsive shock (ECS). ECS led to a widespread induction of the proto-oncogene c-fos in the brain, with highest concentrations in discrete areas within the limbic system and also in the hypothalamus and cerebellum. The mild stress of sham treatment in earclipped animals induced a weaker and qualitatively different pattern of c-fos mRNA expression involving the cortex, hippocampus, and cerebellum. These data suggest the usefulness of c-fos in situ hybridization as a marker of neuronal stimulation and in mapping a range of effects from a mild stress to the robust changes of an electroconvulsive seizure.
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PMID:Mouse brain c-fos mRNA distribution following a single electroconvulsive shock. 272 51

Alterations in neuronal gene expression have been proposed to account for permanent changes in brain function such as learning and memory. In particular, it has been suggested that protooncogenes such as c-fos may be rapidly induced in conditions that lead to neuronal plasticity and evoke permanent changes in the expression of effector genes. Concentrations of the c-fos proto-oncogene increase rapidly following depolarization-induced calcium influx in non-dividing neuronally differentiated PC 12 cells. Recently, the presence and induction of c-fos in the adult brain and spinal cord has been observed. Here we report that electrically-induced seizure activity, which leads to a permanent increase in the response of the brain to future seizures (kindling), rapidly and transiently increases c-fos protein-like immunoreactivity in the nuclei of granule cells in the rat dentate gyrus. These results suggest that c-fos protein is present within the nuclei of adult mammalian neurons, and could be involved in plastic changes in the nervous system associated with seizure activity.
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PMID:Kindling stimulation induces c-fos protein(s) in granule cells of the rat dentate gyrus. 311 33

Increased but transient expression of the proto-oncogene c-fos has been recently reported in metrazol and kindling-induced seizures. Here we tested whether kainic acid-induced status epilepticus may result in a long-term increase of this oncogene. A specific pattern of immunoreactive c-fos material was observed with the development of the seizures. Intense labeling first appeared in the dentate gyrus of the hippocampus and the entorhinal cortex. Pyramidal cell layer CA3, CA4 and CA1 as well as other limbic structures were then positively stained during status epilepticus. In addition, the duration of c-fos expression was different according to the anatomical sites. In the dentate gyrus labeling did not exceed 4-5 h whereas the pyramidal cell layer CA1 exhibited increased c-fos expression for as long as 24 h. Here we propose that c-fos which has been related to growth and differentiation in previous studies, could be involved in processes inducing long-term plastic alterations in the limbic system.
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PMID:Long-lasting and sequential increase of c-fos oncoprotein expression in kainic acid-induced status epilepticus. 313 54

The amounts of the mRNAs for the neuropeptide precursor proteins preproenkephalin, preprocholecystokinin and preproneuropeptide Y were measured in the entorhinal cortex of normal rats and rats that had experienced recurrent limbic seizures induced by a small contralateral lesion of the dentate gyrus hilus. Additionally, the amount of mRNAs for preproenkephalin as well as for the cellular proto-oncogenes c-myc, c-fos and c-H-ras, which are thought to be mediators of intracellular signal transduction, was determined in hippocampus in these same animals. It was determined that the hilus lesion led to a dramatic (18-fold) increase in the content of preproenkephalin mRNA in the entorhinal cortex whereas only a modest increase in preproneuropeptide Y mRNA content and no change in preprocholecystokinin mRNA was detected in this same brain region. In hippocampus a large and very rapid increase in c-fos mRNA was observed to precede the previously reported increase in preproenkephalin mRNA following hilus lesion-induced seizures. Like the increase in opioid peptide mRNA, the increase in c-fos mRNA began early in the period of seizure activity and could be blunted by maintaining the animals under anesthesia with the anticonvulsant sodium pentobarbital. Messenger RNA for c-H-ras was not altered at any time following the lesion and c-myc mRNA was not reliably detected in either control or hilus lesioned rats. These data demonstrate that neuropeptide genes within the entorhinal cortex and proto-oncogenes within the hippocampus are differentially regulated by seizure activity and suggest that the c-fos proto-oncogene may be involved in events which mediate the physiological regulation of enkephalin gene expression.
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PMID:Differential regulation of neuropeptide and proto-oncogene mRNA content in the hippocampus following recurrent seizures. 342 45

The anticonvulsant activity of calmodulin antagonist W-7, was investigated on convulsions induced in mice by the insecticide lindane and by the calcium channel agonist BayK-8644. We also studied the inhibitory effect of W-7 on on c-fos mRNA expression induced by both convulsants. We observed a good correlation between doses and the acute convulsive effects of lindane and BayK-8644. The incidence rate and time to onset were clearly dose-dependent. W-7 antagonized the convulsive effects of lindane and BayK-8644 in all the parameters studied. A significant decrease in the incidence rate and time to onset were observed when they are compared with the values obtained with the ED100 of lindane- and BayK-8644 induced seizures. Both were able to activate the mRNA expression of the proto-oncogene. The pattern of this expression displayed by in situ hybridization was very similar. A dramatic increase was found in dentate gyrus and high levels of mRNA expression also occurring in hippocampal fields and cortical regions. In accordance with the behavioural results, W-7 antagonized also the c-fos expression induced by lindane and BayK-8644. Our results suggest that lindane as BayK-8644 may activate voltage-dependent calcium channels leading to calmodulin activation.
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PMID:Anticonvulsant activity of calmodulin antagonist W-7 in convulsions induced by lindane and BayK-8644: effects in c-fos expression. 753 29

The induction of the proto-oncogene c-fos has been used extensively to identify spatially distributed neural systems activated by seizures. The substantia nigra pars reticulata (SNpr) has been implicated as a critical structure in neural networks involved in the modulation of seizure expression, yet the SNpr has not been reported to express Fos following seizures induced in a variety of seizure paradigms. In this study we determined whether (1) the temporal characteristics of Fos induction in the SNpr were different than those of other brain areas following kindled seizures, (2) neurons in the SNpr possess the cellular machinery to express Fos, (3) Fos can be induced in SNpr by direct electrical stimulation, and (4) Fos expression is induced in the SNpr following kainate or pilocarpine-induced status epilepticus. Results indicate that Fos is not induced in SNpr at any time point (1-12 h) after kindled seizures, and that serum response factor, a constitutively expressed nuclear protein necessary for Fos expression, is present in SNpr neurons. Results further indicate that Fos expression in the SNpr is induced following either direct electrical stimulation or pilocarpine status, but not status elicited by kainate. We conclude that, in so far as the SNpr represents a critical structure for modulating seizure expression, seizure activity does not represent a sufficient stimulus to induce Fos in SNpr neurons. Further, the neural networks defined by Fos expression following seizure may be incomplete, and should be interpreted conservatively.
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PMID:The substantia nigra pars reticulata, seizures and Fos expression. 771 58

Focal seizures in rats were elicited by electrical stimulation (using parameters necessary for induction of kindling) of the amygdala or two different sites of the piriform cortex, including the previously described 'area tempestas' [26]. Although seizures were behaviorally and electrophysiologically identical, a different pattern of induction of the proto-oncogene c-fos was found. Only the ipsilateral piriform cortex showed strong immunohistochemical labeling of Fos protein, regardless of stimulation site, while the hippocampus was not labeled after focal seizures. It is concluded that the piriform cortex is the epileptogenic focus of limbic seizures, at least during the first stages of electrical kindling.
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PMID:Strong induction of c-fos in the piriform cortex during focal seizures evoked from different limbic brain sites. 774 27

Expression of the proto-oncogene zif/268 was investigated by in situ hybridization in the hippocampus and cerebral cortex of nerve growth factor (NGF)-transgenic mice during pentylenetetrazol (PTZ)-induced seizures. NGF-transgenic mice displayed normal basal levels of zif/268 mRNA in cortex and hippocampal formation except for the dentate gyrus which contained significantly reduced levels. PTZ induced a similar transient increase of zif/268 mRNA in cortex and Ammon's horn of normal and NGF-transgenic mice. On the other hand, increase of zif/268 mRNA in the dentate gyrus was significantly lower in transgenic mice. Reduced PTZ-induced activation of zif268 may reflect a decreased sensitivity of NGF-transgenic animals to epilepsy by direct or indirect interaction of NGF with immediate early genes.
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PMID:Decreased pentylenetetrazol-induced expression of zif/268 in NGF-transgenic mice. 788 Oct 37


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