Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.1 (RNase)
 16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the effects of convulsive seizures on in vitro RNA synthesis by cerebral cortex nuclei in El mice. The rate of incorporation of [3H]uridine-5'-triphosphate by intact nuclei during seizures was decreased to 47.4% compared with the rate during the interictal period, but gradually recovered. During the 30-min period after onset of seizures, the rate of RNA synthesis was significantly lower in El mice than in identically stimulated ddY mice. Seizures in El mice had no effect on liver RNA synthesis, suggesting that the alteration of RNA polymerase activity is specific to the brain. Analysis of gel electrophoresis of polyadenylated RNA synthesized in the presence of ammonium sulphate revealed a marked decrease in high-molecular weight RNA species 15 min after seizures in El mice compared with the pattern in nonstimulated ddY mice. This shift from high- to low-molecular weight RNA species was not attributable to RNase activity, but it appeared to be related RNA polymerase.
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PMID:Alteration of RNA synthesis in vitro in intact cerebral cortex nuclei induced by convulsions in seizure-susceptible El mice. 243 22

Animals from the El (susceptible to seizures) and ddy (nonsusceptible) mouse strains were subjected to vestibular stimulation by tossing. After convulsions in the El mice, both the stimulated El mice and ddY mice were intracranially injected with [14C]- and [3H]adenosine, respectively. In the control experiment, nonstimulated El and ddY mice received radioactive adenosines in the same manner. The rate of incorporation of adenosine into brain nuclear RNA, expressed as a percentage of the 3H; 14C ratio, was reduced to an average of 68% at 15 min after convulsions, then increased and reached a control value at 5 h. This reduction in nuclear RNA synthesis was not due to alteration of the adenosine triphosphate pool. Gel electrophoresis of RNA revealed no obvious differences in the labeling distribution between El and ddY mice, but the synthesis of RNA species larger than 35S in heterogeneous nuclear RNA (HnRNA) was impaired in convulsed El mice. Nuclear resistant segments of HnRNA with both T1 RNase and RNase A, were chromatographed with poly(U)-Sepharose followed by urea-polyacrylamide gel electrophoresis. The ologo(A) and poly(A) segments consisted of 29, 19, and 11, and 203, 135, and 69 nucleotides, respectively. The convulsions of El mice reduced the incorporation of radioactive adenosines into oligo(A) and poly(A) segments, suggesting that they inhibited transcription as well as polyadenylation within HnRNA.
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PMID:Effect of convulsions of the synthesis of heterogeneous nuclear RNA associated with polyadenylate and oligoadenylate sequences from El mouse brain as a convulsive strain. 669 Mar 28

Mouse adenovirus type 1 (MAV-1) produces a lethal disease in newborn or suckling mice characterized by infectious virus and viral lesions in multiple organs. Previous reports of MAV-1 infection of adult mice generally described serologic evidence of infection without morbidity or mortality. However, our current results demonstrate that MAV-1 causes a fatal illness in adult C57BL/6(B6) mice (50% lethal dose, [LD50], 10(3.0) PFU) but not in adult BALB/c mice at all of the doses tested (LD50, > or = 10(5.0) PFU). Adult (BALB/c x B6)F1 mice were intermediately susceptible (LD50, 10(4.5) PFU). Clinically, the sensitive B6 mice showed symptoms of acute central nervous system (CNS) disease, including tremors, seizures, ataxia, and paralysis. Light microscopic examination of CNS tissue from the B6 animals revealed petechial hemorrhages, edema, neovascularization, and mild inflammation in the brain and spinal cord. Analysis by electron microscopy showed evidence of inflammation, such as activated microglia, as well as swollen astrocytic endfeet and perivascular lipid deposition indicative of blood-brain barrier dysfunction. Outside of the CNS, the only significant pathological findings were foci of cytolysis in the splenic white pulp. Assessment of viral replication from multiple tissues was performed by using RNase protection assays with an antisense MAV-1 early region 1a probe. The greatest amounts of viral mRNA in MAV-1-infected B6 animals were located in the brain and spinal cord. Less viral message was detected in the spleen, lungs, and heart. No viral mRNA was detected in BALB/c mouse tissue, with the exception of low levels in the heart. Viral titers of organ tissues were also determined and were concordant with RNase protection findings on the brain and spinal cord but failed to demonstrate significant infectious virus in additional organs. Our experiments demonstrate that MAV-1 has a striking tropism for the CNS that is strain dependent, and this provides an informative in vivo model for the study of adenoviral pathogenesis.
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PMID:Mouse adenovirus type 1 causes a fatal hemorrhagic encephalomyelitis in adult C57BL/6 but not BALB/c mice. 749 76

Both RNase protection assay and in situ hybridization were used to investigate the effect of intraperitoneal injection of kainate on the messenger RNA levels for basic fibroblast growth factor in the rat central nervous system. Limbic motor seizures were produced by kainate injection and this event was followed by a significant elevation of basic fibroblast growth factor gene expression in rat hippocampus and striatum 6 h after the convulsant injection. The increase in hippocampus was maximal at 24 h and it was delayed with respect to nerve growth factor induction, which peaked 3 h after kainate injection. Animals that suffered prolonged seizure activity also showed a significant elevation of basic fibroblast growth factor gene expression four and 14 days after kainate, when no changes in nerve growth factor gene expression were observed. We show that, within the hippocampus, the increase of basic fibroblast growth factor messenger RNA was localized in dentate gyrus and the CA1 layer 6 and 24 h after kainate injection. Long-term effects on its gene expression were measurable only in the CA1 hippocampal subfield, where major cell damage and astrocytosis have been reported to occur following kainate-induced seizure activity [Ben-Ari Y. et al. (1981) Neuroscience 7, 1361-1391; Lothman E. W. and Collins R. C. (1981) Brain Res. 218, 299-318; Schwob J. E. et al. (1980) Neuroscience 5, 991-1014]. Indeed, the animals which displayed elevated messenger RNA levels for basic fibroblast growth factor four and 14 days after kainate injection showed a marked induction of messenger RNA expression for the astroglial marker glial fibrillary acidic protein. These results indicate that the glutamate analogue kainate produces short- and long-term increases of basic fibroblast growth factor messenger RNA expression with a specific anatomical pattern. Therefore, the gene expression for this neurotrophic factor is probably regulated by neuronal activity at early points in time, whereas the induction observed at later time points is related to adaptive mechanisms taking place following kainate-induced neuronal degeneration.
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PMID:Short- and long-term induction of basic fibroblast growth factor gene expression in rat central nervous system following kainate injection. 819 Feb 72

The mas proto-oncogene encodes a seven membrane-spanning G-protein-coupled receptor which is activated by angiotensins. In the postnatal and adult rat, mas mRNA is specifically expressed at high levels in hippocampal neurons. We report here using in situ hybridization and RNase protection that brief seizure episodes lead to a significant and transient increase in mas mRNA in the hippocampus. Increased levels of mas transcripts were detected 2, 4, and 6 h following seizure. By 24 h post seizure, baseline levels were detected. The presumed subsequent increase of the mas receptor protein may contribute to anatomical and physiological plasticity that is associated with intense activation of hippocampal pathways.
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PMID:Expression of the mas proto-oncogene in the rat hippocampal formation is regulated by neuronal activity. 823 33

The present study examines the influence of electroconvulsive seizure (ECS), as well as antidepressant drugs, on levels of serotonin2 (5-HT2) receptor mRNA in rat frontal cortex. Using a sensitive RNase protective assay, preliminary studies demonstrated the predicted regional distribution for the 5-HT2 receptor mRNA: levels of 5-HT2 mRNA were highest in frontal cortex (2.58 amol/micrograms of total RNA), intermediate in neostriatum, thalamus, and midbrain, and lowest in hippocampus, cerebellum, and choroid plexus. Chronic (10 or 14 days), but not acute (1 or 3 days), ECS treatment significantly increased levels of 5-HT2 receptor mRNA. ECS treatment resulted in a similar time-dependent up-regulation of 5-HT2 receptor ligand binding; chronic, but not acute, ECS treatment significantly increased levels of [3H]ketanserin ligand binding, confirming previous reports. Northern blot analysis demonstrated that 5-HT2 receptor mRNA occurs as two bands (approximately 5 and 6 kb in size), both of which were increased by chronic ECS treatment. The influence of antidepressant drug treatments on 5-HT2 receptor mRNA was also examined. Chronic fluoxetine treatment increased levels of 5-HT2 receptor mRNA, although levels of [3H]ketanserin ligand binding were not altered. In contrast, chronic administration of imipramine, mianserin, and tranylcypromine, treatments that decreased ligand binding, did not decrease levels of 5-HT2 receptor mRNA. In fact, mianserin treatment caused a small, but significant, increase in levels of receptor mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic electroconvulsive seizures increase the expression of serotonin2 receptor mRNA in rat frontal cortex. 837 84

The number of beta 1-adrenergic receptor (beta 1AR) binding sites is decreased by chronic antidepressant treatments, including electroconvulsive seizure (ECS) and imipramine, whereas administration of agents that deplete norepinephrine (NE) increases the number of beta 1AR binding sites in cerebral cortex. The present study was carried out to examine the influence of these treatments on levels of beta 1AR mRNA in frontal cortex to study the molecular mechanisms that underlie the regulation of beta 1ARs in brain. Levels of beta 1AR mRNA were measured by RNase protection analysis using a riboprobe derived from rat beta 1AR cDNA, and the levels of beta AR binding were measured using the nonselective ligand [3H]CGP-12177. Studies to verify the specificity of the RNase protection assay revealed that the distribution of beta 1AR mRNA was in agreement with the reported distribution of beta 1AR ligand binding: Levels of beta 1AR mRNA were highest in cerebral cortex or frontal cortex, intermediate in neostriatum, hippocampus, lung, and heart, and lowest in cerebellum, kidney, and liver. Chronic ECS treatment (once daily for 10 days) significantly decreased levels of beta AR ligand binding and resulted in a corresponding, time-dependent down-regulation of beta 1AR mRNA levels in frontal cortex. However, imipramine administration regulated levels of beta 1AR mRNA in a biphasic manner, with treatments for 7-14 days increasing and treatments for 18-21 days decreasing levels of beta 1AR mRNA in frontal cortex. In contrast, levels of [3H]CGP-12177 ligand binding were decreased at all time points examined (3-21 days).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of beta 1-adrenergic receptor mRNA and ligand binding by antidepressant treatments and norepinephrine depletion in rat frontal cortex. 838 47

Rapid expression of ICER (inducible cyclic AMP early repressor), an inducible member of the CREM (cyclic AMP response element modulator) family of transcription factors, has been reported in neuroendocrine tissues and cell lines, but not in brain. In the present study, we demonstrate that acute electro-convulsive seizure (ECS) increases the expression of ICER in several rat brain regions. RNase protection analysis demonstrated that 1-2 h after administration of ECS, levels of mRNA for ICER and a splice variant, ICER gamma, were significantly increased in hippocampus, frontal cortex, and cerebellum. It is surprising that ECS also increased levels of mRNA for several CREM isoforms that previous studies have reported were not rapidly inducible. In situ hybridization analysis confirmed these findings and demonstrated that ECS induction of ICER was most obvious in the dentate gyrus granule cell layer of hippocampus and deep layers of cerebral cortex. Induction of ICER and CREM was accompanied by increased expression of two small CRE-binding complexes. Gel supershift analysis with CREM/ICER antisera confirmed that the inducible CRE-binding complexes contain CREM/ICER. Induction of CREM and ICER may contribute to negative feedback regulation of gene transcription that is increased by acute seizure and activation of CREB (cyclic AMP response element-binding protein.
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PMID:Electroconvulsive seizure increases the expression of CREM (cyclic AMP response element modulator) and ICER (inducible cyclic AMP early repressor) in rat brain. 852 85

In this study we have shown, by in situ hybridization and RNase protection assay, a significant trkC mRNA increase confined to the dentate gyrus of hippocampus, both after seizures induced by intracerebroventricular injection of kainic acid and bicuculline. Moreover, after bicuculline treatment we observed an earlier increase of trkC mRNA level, which peaked after 3 h and returned back to normal levels by 12 h. In contrast, the kainic acid treatment produced a delayed increase of trkC mRNA, which initiated after 6 h, peaked at 12 h, and returned to normal levels at 24 h. This increase, which involves also trkC mRNA receptor with tyrosine kinase activity, was mediated by non-NMDA receptors and counteracted by GABA potentiating agent diazepam. Using embryonic neuronal cultures from cerebral hemispheres, including hippocampus, we found that glutamate receptor agonists, including glutamate, kainate, NMDA, and t-ACPD, increase trkC mRNA levels with the following rank order of efficacy: NMDA > t-ACPD > kainic acid > glutamate. In conclusion, our data show that trkC mRNA expression in granule cells of the hippocampus dentate gyrus is increased during seizure activity and that it is mediated by non-NMDA receptors.
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PMID:Seizures increase trkC mRNA expression in the dentate gyrus of rat hippocampus. Role of glutamate receptor activation. 856 16

Chronic ethanol exposure and subsequent withdrawal are known to change NMDA receptor activity. This study examined the effects of chronic ethanol administration and withdrawal on the expression of several NMDA receptor subunit and splice variant mRNAs in the rat cerebral cortex. Ethanol dependence was induced by ethanol vapour exposure. To delineate between seizure-induced changes in expression during withdrawal and those due to withdrawal per se, another group of naive rats was treated with pentylenetetrazol (PTZ) injection (30 mg/kg, i.p.). RNA samples from the cortices of chronically treated and withdrawing animals were compared to those from pair-fed controls. Changes in NMDA receptor mRNA expression were determined using ribonuclease protection assays targetting the NR2A, -2B, -2C and NR1-pan subunits as well as the three alternatively spliced NR1 inserts (NR1-pan describes all the known NR1 splice variants generated from the 5' insert and the two 3' inserts). The ratio of NR1 mRNA incorporating the 5' insert vs. that lacking it was decreased during ethanol exposure and up to 48 h after withdrawal. NR2B mRNA expression was elevated during exposure, but returned to control levels 18 h after withdrawal. Levels of NR2A, NR2C, NR1-pan and both 3' NR1 insert mRNAs from the ethanol-treated groups did not alter compared with the pair-fed control group. No changes in the level of any NMDA receptor subunit mRNA was detected in the PTZ-treated animals. These data support the hypothesis that changes in NMDA receptor subunit composition may underlie a neuronal adaptation to the chronic ethanol-inhibition and may therefore be important in the precipitation of withdrawal hyperactivity.
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PMID:Chronic ethanol exposure and withdrawal influence NMDA receptor subunit and splice variant mRNA expression in the rat cerebral cortex. 1008 58


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