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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have demonstrated that several transcription factor genes are rapidly activated by neuronal stimulation. For example, we have found that prolonged and repeated seizure activity produced by administration of chemical convulsants induces a rapid and transient increase in mRNA levels of four immediate early genes in rat brain. These genes, zif/268, c-fos, c-jun, and jun-B, encode sequence specific DNA binding proteins thought to act as transcription regulatory factors. To ascertain whether a brief electrically induced seizure discharge of the type utilized in clinical electroconvulsive treatment is sufficient to induce a similar genomic response, we have examined the response of these mRNAs in rat brain following single and repeated electroshock-induced seizures. After electroshock, mRNA levels of each of these genes increase within 15 min, and all except c-jun return to near baseline levels within 4 h. Although this response is most prominent in granule cell neurons of the hippocampus, increases are also apparent in neocortex and pyriform cortex. The rapid mRNA response persists in animals receiving a chronic electroshock protocol similar to that used in clinical electroconvulsive therapy. Intrahippocampal infusion of the sodium channel antagonist tetrodotoxin blocks hippocampal mRNA responses without blocking seizures, indicating a role for electrical excitation in the electroshock-induced mRNA response. By contrast, pretreatment with anticonvulsants or selective NMDA antagonists, which reduce seizure intensity and block hindlimb extension, fails to alter mRNA responses, suggesting that seizure induction, rather than spread, is linked to these mRNA responses. Because electroshock induces robust, highly reproducible mRNA responses, it may be useful to study the neuronal genomic response to stimulation.
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PMID:Rapid rise in transcription factor mRNAs in rat brain after electroshock-induced seizures. 223 Aug 1

We have recently detected low basal levels of c-fos protein-like immunoreactivity in adult mammalian neurons. Here we report that generalized tonic-clonic seizures in mice are associated with a massive increase in c-fos protein-like immunoreactivity in the cingulate and piriform cortices and the dentate gyrus 1 h after injection of pentylenetetrazol. Midazolam, which prevented the pentylenetetrazol seizures also prevented the increase in c-fos protein-like immunoreactivity. These results suggest that seizure activity induces the formation of c-fos proteins in selective brain regions, and raise the possibility that c-fos proteins play as yet undetermined physiological and/or pathological roles in the mature brain.
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PMID:Generalized seizures induce c-fos protein(s) in mammalian neurons. 244 34

A single electroconvulsive shock (ECS) induced a rapid and transient expression of c-fos mRNA in mouse brain. In earclipped sham controls, low but significant expression of c-fos mRNA was also observed. These data suggest that c-fos mRNA may be transiently induced by seizure activity as well as much more subtle and qualitative different stimuli, such as the acute nociceptive stress associated with earclipping.
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PMID:C-fos mRNA expression following electrical-induced seizure and acute nociceptive stress in mouse brain. 250 11

The use of c-fos protein (Fos) immunocytochemistry as a metabolic marker for tracing neuroanatomical connections, seizure pathways and sites of action of neuroactive drugs is discussed in this report. Fos immunocytochemistry will be very useful for these purposes providing that a number of potential problems are recognized and controlled. These include the observations that Fos exists basally in neurons and can be non-specifically elevated after behavioural stress; neuronal bursting is required to elevate Fos in neurons in anaesthetized animals; drugs such as ketamine can block Fos elevation in neurons; the time-course of Fos induction and decay varies with different inducing stimuli and the brain region sampled; and some brain regions do not express Fos after any treatments tried so far. To overcome these potential problems we list a number of steps that should be followed when using Fos immunocytochemistry as a metabolic marker of brain activity.
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PMID:The use of c-fos as a metabolic marker in neuronal pathway tracing. 250 30

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

Recent studies in invertebrates indicate that a rapid genomic response to neuronal stimulation has a critical role in long-term changes in synaptic efficacy. Because several of the genes (immediately early genes; IEGs) that respond rapidly to growth factor stimulation of vertebrate cells in vitro are also activated by neuronal stimulation in vivo, attention has focused on the possibility that they play a part in synaptic plasticity in vertebrate nervous systems. Four IEGs thought to encode transcription factors, zif/268 (also termed Egr-1, NGFI-A, Krox 24), c-fos, c-jun, and jun-B are rapidly induced in the brain by seizure activity, and we have now studied the induction of these genes in a well-characterized model of synaptic plasticity in the vertebrate brain--long-term potentiation (LTP) of the perforant pathgranule cell (pp-gc) synapse in vivo. We found that high-frequency (but not low-frequency) stimulation of the pp-gc synapse markedly increases zif/268 messenger RNA (mRNA) levels in the ipsilateral granule cell neurons; mRNA of c-fos, c-jun and jun-B is less consistently increased. The stimulus frequency and intensity required to increase zif/268 mRNA levels are similar to those required to induce LTP, which is also seen only ipsilaterally, and both responses are blocked by NMDA-receptor antagonists as well as by convergent synaptic inhibitory inputs already known to block LTP. Accordingly, zif/268 mRNA levels and LTP seem to be regulated by similar synaptic mechanisms.
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PMID:Rapid increase of an immediate early gene messenger RNA in hippocampal neurons by synaptic NMDA receptor activation. 254 65

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

c-Fos mRNA expression was studied in mouse brain after vitamin B6 antagonist-induced seizure. The vitamin B6 antagonists used were hydrazine, thiosemicarbazide, penicillamine and deoxypyridoxine. Only deoxypyridoxine was effective in increasing c-fos mRNA and c-fos protein expression in nerve cells. The other 3 antagonists had levels of c-fos mRNA below or equal to basal level. The seizure activity induced by several vitamin B6 antagonists resulted in different effects on c-fos gene expression.
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PMID:c-Fos mRNA induction under vitamin B6 antagonist-induced seizure. 272 47

A dramatic and specific induction of c-fos was observed in identifiable neuronal populations in vivo after administration of the convulsant Metrazole. This effect was time- and dose-dependent and was abolished by prior treatment with the anticonvulsant drugs diazepam or pentobarbital. About 60 minutes after administration of Metrazole, c-fos messenger RNA reached a maximum and declined to basal levels after 180 minutes. A further decrease below that in normal brain was observed before a return to basal levels after 16 hours. While Metrazole still elicited seizures during this period, reinduction of c-fos was largely refractory. At 90 minutes, c-fos protein was observed in the nuclei of neurons in the dentate gyrus, and in the pyriform and cingulate cortices. Subsequently, c-fos protein appeared throughout the cortex, hippocampus, and limbic system. Thus, seizure activity results in increased c-fos gene expression in particular subsets of neurons.
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PMID:Mapping patterns of c-fos expression in the central nervous system after seizure. 303 2


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