C-fos Protein In Cortex Research Articles

택지개발 현장 내 비위생매립지의 매립쓰레기 처리방안 연구

China is one of countries with the highest mercury production in the world. The Guizhou Province in Southwestern China is currently one of the world's most important mercury production areas. In order to study the neurotoxicity of rice from Qingzhen Chemical Plant area and probe into the signal transduction molecular mechanism of injury in rat brain stimulation by mercury contaminated rice. The rats were exposed to mercury contaminated rice for 20 d. Both of the measurements of NO and NOS were processed according to the protocol of the kit. The effect of Hg contaminated rice on the expression of c-fos mRNA in rat brain and the expression of c-FOS protein in cortex, hippocampus were observed using reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemical methods. The results showed the neural transmitter NO and NOS in brain were significantly change between exposure groups and control group; the mercury polluted rice induced significantly the expression of c-fos mRNA; the c-FOS positive cells in hippocampus and cortex of exposure groups were significant different from control group (p < 0.01). It could be concluded that nitric oxide was involved in mercury contaminated rice induced immediate early gene c-fos expressions in the rat brain. Through food chain, local ecosystem and health of local people iave been deteriorated seriously by mercury. This serious situation will last a long period. In order to alleviate mercury pollution, more work needs to do.

Unilateral induction of c-fos protein in cortex following cortical devascularization

The proto-oncogene c-fos is rapidly induced by a variety of stimuli including wounding of the cortex. In an attempt to define the conditions necessary for c-fos activation, we have studied the effects of cerebral devascularization (CD; unilateral pial disruption), a procedure which results in ischaemia without producing direct physical damage to the tissues. Cerebral devascularization produces c-fos activation throughout the ipsilateral cortex; this effect lasts for about 4 h and is not confined to the area subjacent to pial disruption. The activation of c-fos is not 3revented by even high doses of benzodiazepines but is effectively reduced by the N- methyl- d - aspartate (glutamate) receptor antagonist ketamine.

Potassium outflux from rabbit cortex during spreading depression.

ArticlesPOTASSIUM OUTFLUX FROM RABBIT CORTEX DURING SPREADING DEPRESSIONF. J. Brinley JR., E. R. Kandel, and Wade H. MarshallF. J. Brinley JR., E. R. Kandel, and Wade H. MarshallPublished Online:01 May 1960https://doi.org/10.1152/jn.1960.23.3.246MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByControl of Spreading Depression with Electrical Fields8 June 2018 | Scientific Reports, Vol. 8, No. 1Inadequate brain glycogen or sleep increases spreading depression susceptibility24 January 2018 | Annals of Neurology, Vol. 83, No. 1The CGRP receptor antagonist BIBN4096 inhibits prolonged meningeal afferent activation evoked by brief local K+ stimulation but not cortical spreading depression-induced afferent sensitizationPAIN ReportsSpreading Depression, Spreading Depolarizations, and the Cerebral VasculatureCenk Ayata and Martin Lauritzen1 July 2015 | Physiological Reviews, Vol. 95, No. 3Mechanisms of Spreading Depression and Hypoxic Spreading Depression-Like DepolarizationGeorge G. Somjen1 July 2001 | Physiological Reviews, Vol. 81, No. 3Unilateral induction of c-fos protein in cortex following cortical devascularizationBrain Research, Vol. 503, No. 2Extracellular K+ accumulation in the central nervous systemProgress in Biophysics and Molecular Biology, Vol. 42Functional interactions between neurons and astrocytes. II. Potassium homeostasis at the cellular levelProgress in Neurobiology, Vol. 20, No. 1-2Functional interactions between neurons and astrocytes I. Turnover and metabolism of putative amino acid transmittersProgress in Neurobiology, Vol. 13, No. 3Extracellular ionic variations during spreading depressionNeuroscience, Vol. 3, No. 11Potassium activity in rabbit cortexBrain Research, Vol. 75, No. 1Reactivity of penicillin-induced epileptogenic foci to selective blockade of membrane sodium-potassium ATPase via ouabainExperimental Neurology, Vol. 42, No. 3A comparative study of membrane potential changes in neurons and neuroglial cells during spreading depression in the rabbitBrain Research, Vol. 65, No. 3Measurement of extracellular potassium activity in cat cortexBrain Research, Vol. 50, No. 2Potassium-selective microelectrodes used for measuring the extracellular brain potassium during spreading depression and anoxic depolarization in ratsBrain Research, Vol. 39, No. 1Potassium accumulation in interstitial space during epileptiform seizuresExperimental Neurology, Vol. 26, No. 3Spreading depression in the striatum and optic lobes of the chickenBrain Research, Vol. 13, No. 1Hippocampal epileptic activity induced by localized ventricular perfusion with high-potassium cerebrospinal fluidExperimental Neurology, Vol. 20, No. 1Blockade of thalamocortical and pyramidal pathways by striatal spreading depression in ratsExperimental Neurology, Vol. 18, No. 4Spreading depression in subcortical structures in rabbitBrain Research, Vol. 2, No. 1Intracellular potentials from “idle” cells in cerebral cortex of catElectroencephalography and Clinical Neurophysiology, Vol. 20, No. 6Thalamic spreading depression in the ratElectroencephalography and Clinical Neurophysiology, Vol. 20, No. 1Reversible deafferentation of cerebral cortex by thalamic spreading depressionExperimental Neurology, Vol. 12, No. 1Specific impedance of cerebral cortex during spreading depression, and an analysis of neuronal, neuroglial, and interstitial contributionsExperimental Neurology, Vol. 9, No. 1Influence of transcortical d-c currents on cortical neuronal activityExperimental Neurology, Vol. 5, No. 6Inhibitory action of carbon dioxide and acetazoleamide in seizure activityElectroencephalography and Clinical Neurophysiology, Vol. 13, No. 5 More from this issue > Volume 23Issue 3May 1960Pages 246-256 https://doi.org/10.1152/jn.1960.23.3.246PubMed13804482History Published online 1 May 1960 Published in print 1 May 1960 Metrics