[Phase manifestations of the cerebral cortex; physiopathology of the cerebral cortex following electric shock, aphasia, apraxia and agnosia].
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Agnosia↗
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Results for “cerebral cortex”
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[Comparative proteomic analysis of cerebral cortex between middle cerebral artery occlusion rats and normal controls].
In order to provide a complete picture of pathogenesis in cerebral ischemia, cerebral cortex in MCAO rats were analysed for alteration in their proteomes. Comparative proteome analysis was used to compare signal corresponding to individual cerebral cortex proteins on a two-dimensional gel between MCAO rats and the normal control (NC) group. After sample preparation, two-dimensional electroghoresis separated proteins were stained with Commassie Brilliant Blue. The image data were analyzed on a Dell computer using Image Master v 3.01 software. In cerebral cortex, 30 proteins were differentially expressed in MCAO rats compared with NC. There were 11 spots significantly increased, 15 spots significantly decreased and Adenylate kinase isoenzyme 1 was detected only in NC group, biliverdin reductase B, small inducible cytokine A4 [Precursor] only in MCAO group. Peroxiredoxin 2 divided into two points in MCAO6h group. In the end, this approach may lay a foundation for the further investigation of pathogenic mechanisms in cerebral ischmic injury.
Animals↗
Electron microscopic investigation of the cerebral cortex after cerebral ischemia and reperfusion in the gerbil.
Prompt dendritic damage has been observed in the hippocampus of the gerbil brain after transient cerebral ischemia. In the present study, we studied the frontoparietal cortex of the gerbil brain electron microscopically after brief bilateral carotid occlusion to assess the vulnerability of dendritic processes. After ischemia for 5 min, there was swelling of the periphery of dendrites accompanied by swelling of mitochondria, cytoplasmic vacuolation and disintegration of microtubules in layer I, which spread to layer III after ischemia for 20 min. After reperfusion for 3-24 h following ischemia for 20 min, swelling in the periphery of dendrites and of mitochondria inside receded but vacuole formation and disintegration of microtubules propagated proximally. In neuronal perikarya, polyribosomal disaggregation was observed after ischemia for 20 min and persisted thereafter, while fragmentation of rough endoplasmic reticulum (ER) and microvacuolation occurred after reperfusion for 3 h. Electron-dense clumping of neuronal perikarya was observed after reperfusion for 6 h particularly in layers III and Vb, which increased in number for up to 72 h. The observed progressive damage in dendrites may be common to neurons vulnerable to cerebral ischemia and may significantly contribute to development of delayed neuronal death.
Animals↗
[Structural changes in the intracochlear fibers of the acoustic nerve and in the auditory region of the cerebral cortex in cerebral circulatory disturbances].
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Auditory Cortex↗
Pyridine nucleotide redox state and blood flow of the cerebral cortex following middle cerebral artery occlusion in the cat.
Acute changes in the redox state of NADH in the cerebral cortex of cats were investigated following occlusion of the middle cerebral cortex (MCA) and were correlated with alterations of regional cerebral blood flow in the ischemic cortex determined autoradiographically. Arterial occlusion was accomplished via the transorbital approach. Cortical fluorescence and reflected light signals were recorded from the central MCA territory by means of a beam-splitting fluorometer, and a fluorescence signal corrected for alterations in intravascular hemoglobin was derived. Following arterial occlusion, there was a rapid increase in cortical NADH fluorescence, peaking within 30 to 70 seconds at 20% to 40% of full scale. This was followed by a slow linear decline in fluorescence over the next several minutes. The behavior of cortical NADH fluorescence was unaffected by replacement of the ambient air over the cortical surface with nitrogen. Mean regional blood flow values in the most ischemic gyri two to 15 minutes following arterial occlusion were 21% to 23% of the corresponding values in the opposite, nonischemic hemisphere. In individual animals, peak NADH fluorescence values following arterial occlusion correlated with the extent of blood flow reduction in the affected ischemic gyri (P less than 0.05).
Animals↗
Action of protoveratrine on the metabolism of cerebral cortex. 2. Electrically stimulated cerebral-cortex tissue.
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Cerebral Cortex↗
Elevation of mRNA levels of tissue-type plasminogen activator and urokinase-type plasminogen activator in hippocampus and cerebral cortex following middle cerebral artery occlusion in rats.
Tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) have been used for thrombolitic therapy. In contrast, it is suggested that these compounds might be involved in neuronal cell damage. The activation and the function of tPA and uPA are less understood in ischemic brain tissue. Therefore, changes in tPA and uPA mRNA in rat brain tissue after MCA occlusion and in the neuronal cell line, PC12 cells, during the hypoxic stimulation were examined. Permanent middle cerebral artery (MCA) occlusion was induced by advancing a filament into the internal carotid artery in 36 adult male Sprague-Dawley rats. The ischemic cerebral cortex and contralateral cortex of MCA area, and bilateral hippocampus were collected at 0 (controls), 1, 3, 6, 12 and 24 h after occlusion. Hypoxia was induced in PC12 cells with a multigas incubator (set to 1% O2). The quantitative reverse transcription-polymerase chain reaction acted as a measurement of alteration in mRNA levels. The mRNA levels of tPA and uPA were significantly increased after MCA occlusion in the ischemic cerebral cortex. The magnitude of the increase in tPA and uPA mRNA in 24 h after occlusion was twice the value in sham-operated rat (0 h). The increases of tPA mRNA were time-dependent in insult and contralateral hippocampus. The increase of uPA mRNA was also seen in the hippocampus bilaterally, although the increase was more significant on the ipsilateral side. In PC12 cells, necrotic (approximately 35%) and apoptotic cells (approximately 65%) could be distinguished by hypoxic stimulus for 24 h, and the mRNA for tPA was significantly increased for 6 h-12 h, while the mRNA for uPA was not detected at any point in the study. Our results suggest that focal ischemia might result in the activation of these proteases not only in the insult but also in the contralateral brain tissue.
Animals↗
Changes of amino acid by the deprivation of energy sources in the cerebral cortex.
After cerebral cortex slices from adult or infant rats had been incubated in medium containing glucose or beta-hydroxybutyrate as an energy source, the concentrations of ATP and amino acids in the tissue and incubation medium were examined. In the adult cerebral cortex, on the substitution of beta-hydroxybutyrate for glucose, the levels of ATP and amino acids were not maintained. The concentrations of glutamate, glutamine and gamma-aminobutyrate decreased, and that of aspartate increased together with the decrease in ATP in the tissue. Similar changes were observed when iodoacetate (10 microM) was added to the incubation medium. Moreover, the depletion of an energy source led to more drastic changes. On the other hand, in the infant cerebral cortex, the substitution of beta-hydroxybutyrate did not affect the levels of ATP and glutamate, glutamine and gamma-aminobutyrate. There are good correlations between the concentrations of ATP and glutamate and related amino acids in the cerebral cortex.
3-Hydroxybutyric Acid↗
Effects of a peptide mixture with a high Fischer's ratio on serum and cerebral cortex amino acid levels and on cerebral cortex monoamine levels, compared with an amino acid mixture with a high Fischer's ratio.
Peptide mixtures with high and low Fischer's ratios (i.e., the ratio of branched-chain amino acids to aromatic amino acids), obtained from an enzymatic hydrolysate of casein, and the corresponding amino acid mixtures were intragastrically force-fed to rats. Cerebral cortex monoamines were more influenced by the ingestion of the peptide than that of the amino acid mixture.
Amino Acids↗
Compensatory adjustment in blood flow of the rabbit cerebral cortex during graded cerebral ischemia.
The role of the bilateral internal carotid and vertebral arteries in supplying cerebral cortex tissue blood flow (CTF) and the compensatory adjustment in CTF during graded cerebral ischemia were studied to determine the relationship to the increase in systemic arterial pressure (SAP) in anesthetized rabbits. CTF was recorded continuously by using Peltier stacks placed on both sides of the surface of the cerebral parietal cortex. Occlusion of the bilateral internal carotid arteries caused a decrease in CTF to 81.9% of the control value for the right hemisphere, and 83.5% of that for the left. Occlusion of the bilateral vertebral arteries produced no appreciable change in CTF. Compensatory adjustment in CTF was incomplete, i.e., CTF was reduced to a lower level, in the range of internal carotid flow (ICF) from 2 to 6 ml/min, and was severely reduced at 1 and 0 ml/min. The relationships between ICF and SAP, and ICF and CTF formed rectangular hyperbolic curves. No significant difference was observed between the decreases in CTF obtained before and after bilateral sectioning of the cervical sympathetic trunks. The relationship between SAP and CTF was described by a linear regression equation. These results indicate that the internal carotid arteries play a much more important role in supplying CTF than the vertebral arteries, that SAP rises in inverse proportion to the decrease in CTF, and that the cervical sympathetic trunks do not influence the compensatory adjustment in CTF caused by cerebral ischemia.
Animals↗
[Electrical activity of cerebral cortex and diencephalon during stimulation of cerebral cortex, rhinencephalon and diencephalon].
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Cerebral Cortex↗
Golgi electron microscopic study of the cerebral cortex after transient cerebral ischemia and reperfusion in the gerbil.
Fine structures of defined neurons and their dendritic processes were studied in the cerebral cortex of gerbil brains by using Golgi electron microscopy during progressive cerebral ischemia for 10 and 20 min and after reperfusion for up to 72 h following transient ischemia for 20 min. The periphery of ascending dendrites of the vulnerable neurons in layers III and Vb became distended immediately after ischemia with swollen mitochondria and disintegrated microtubules, but the proximal portion of the same dendrites remained unchanged. After reperfusion for 6 h, distension of the dendroplasm of the impregnated dendrites in layer I receded, but the proximal portion of the same dendrites showed indentation caused by swollen astrocytic processes and derangement of microtubules inside. Polyribosomes in most neuronal perikarya were disaggregated, but severe neuronal damage was rarely found among those neuronal cell bodies impregnated by the Golgi method. Recovery with reaggregation of polyribosomes and realignment of microtubules was more clearly observed after reperfusion for 24 h and thereafter in impregnated neurons. These results indicated that impregnation during progressive ischemia occurred in many neurons with progressive structural damage but that impregnation during reperfusion occurred in a limited number of neurons with limited damage, allowing us to observe the recovery process, and that neuronal derangement in the dendrosomatic direction initially occurred both in the irreversibly damaged neurons and in the reversibly damaged ones. It is possible that disintegration of microtubules and the resulting disruption of dendritic transport may contribute to subsequent development of delayed neuronal death, if the recovery process does not take place promptly. Golgi electron microscopy is useful for ultrastructural investigation of defined neurons and their dendrites together and may be applicable for investigation of selected neuropathologic conditions.
Animals↗
Differential expression patterns of gangliosides in the ischemic cerebral cortex produced by middle cerebral artery occlusion.
Neuronal damage subsequent to transient cerebral ischemia is a multifactorial process involving several overlapping mechanisms. Gangliosides, sialic acid-conjugated glycosphingolipids, reduce the severity of acute brain damage in vitro. However their in vivo effects on the cerebral cortex damaged by ischemic infarct are unknown. To assess the possible protective role of gangliosides we examined their expression in the cerebral cortex damaged by ischemic infarct in the rat. Ischemia was induced by middle cerebral artery (MCA) occlusion, and the resulting damage was observed by staining with 2, 3, 5-triphenylterazolium chloride (TTC). High-performance thin-layer chromatography (HPTLC) showed that gangliosides GM3 and GM1 increased in the damaged cerebral cortex, and immunofluorescence microscopy also revealed a significant change in expression of GM1. In addition, in situ hybridization demonstrated an increase in the mRNA for ganglioside GM3 synthase. These results suggest that gangliosides GM1 and GM3 may be synthesized in vivo to protect the cerebral cortex from ischemic damage.
Animals↗
Actions of somatostatin on lipid metabolism in mouse cerebral cortex slices.
Cerebral cortex slices from mice were used to investigate the variations of lipid metabolism by somatostatin. Somatostatin decreased [14C]acetate incorporation into all lipid fractions significantly. Likewise, the peptide evoked a decrease of triglyceride lipase activity. The incorporation of [32P]orthophosphate into phospholipids was diminished by somatostatin. These results add more information about the effects of somatostatin in cerebral cortex.
Acetates↗
Widespread dispersion of neuronal clones across functional regions of the cerebral cortex.
The cerebral cortex of the mammalian brain has expanded rapidly during the course of evolution and acquired structurally distinguishable areas devoted to separate functions. In some brain regions, topographic restrictions to cell intermixing occur during embryonic development. As a means of examining experimentally whether such restrictions occur during formation of functional subdivisions in the rat neocortex, clonally related neocortical cells were marked by retroviral-mediated transfer of a histochemical marker gene. Clonal boundaries were determined by infection of the developing brain with a library of genetically distinct viruses and amplification of single viral genomes by the polymerase chain reaction. Many clonally related neurons in the cerebral cortex became widely dispersed across functional areas of the cortex. Specification of cortical areas therefore occurs after neurogenesis.
Animals↗
Functional characterization of types of plasma membranes in cerebral cortex.
The cerebral cortex of normal oxygenated and of asphyxiated mice has been studied by freeze-fracturing technique with a twofold purpose. First, to investigate changes, if any, in the molecular organization of the plasma membrane of any specific cell type(s) that could be correlated with permeability changes thought to take place as a consequence of asphyxiation. Secondly, to attempt characterization of plasma membranes on the basis of the organization of their fractured faces. The decrease in the extracellular material in asphyxiated cerebral cortex seen in electron micrographs of thin sections could not be correlated with change(s), if any, in the molecular organization of the plasma membrane of any particular cell type. Plasma membranes of various types could be characterized on the basis of the arrangement of particles on the fractured faces. Some of these types correspond to identifiable cell processes, while others have not yet been identified with certainty. Fusion of synaptic vesicles with the presynaptic membrane is mediated through clustering of 100-150 A membrane-associated particles.
Animals↗
The transcription factor, Pax6, is required for cell proliferation and differentiation in the developing cerebral cortex.
The cerebral cortex develops from the dorsal telencephalon, at the anterior end of the neural tube. Neurons are generated by cell division at the inner surface of the telencephalic wall (in the ventricular zone) and migrate towards its outer surface, where they complete their differentiation. Recent studies have suggested that the transcription factor Pax6 is important for regulation of cell proliferation, migration and differentiation at various sites in the CNS. This gene is widely expressed from neural plate stage in the developing CNS, including the embryonic cerebral cortex, where it is required for radial glial cell development and neuronal migration. We report new findings indicating that, in the absence of Pax6, proliferative rates in the early embryonic cortex are increased and the differentiation of many cortical cells is defective. A major question concerns the degree to which cortical defects in the absence of Pax6 are a direct consequence of losing the gene function from defective cells themselves, rather than being secondary to abnormalities in other cells. Cortical defects in the absence of Pax6 become much more pronounced later in cortical development, and we propose that many result from a compounding of abnormalities in proliferation and differentiation that first appear at the onset of corticogenesis.
Animals↗
A comparison of the capacities of isomers of amphetamine, deoxypipradrol and methylphenidate to inhibit the uptake of tritiated catecholamines into rat cerebral cortex slices, synaptosomal preparations of rat cerebral cortex, hypothalamus and striatum and into adrenergic nerves of rabbit aorta.
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Amphetamine↗