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At least 19 recordsLinked to original sources
PubMed1992

Presenile dementia with progressive supranuclear palsy tangles and Pick bodies: an unusual degenerative disorder involving the cerebral cortex, cerebral nuclei, and brain stem nuclei.

Degeneration of heterogeneous systems in the central nervous system, with widespread distribution of argyrophilic neuronal fibrillary inclusions, was found in a patient with presenile dementia. Atrophy was circumscribed in the frontal and temporal lobes. Neuronal loss was severe in the basal ganglia, subthalamic nucleus, and substantia nigra. Immunocytochemical study using anti-phosphorylated tau and anti-ubiquitin antibodies in conjunction with ultrastructural observations revealed two types of inclusions: neurofibrillary tangles (NFTs) of progressive supranuclear palsy (PSP) in the Edinger-Westphal nucleus, locus coeruleus, cerebellar dentate nucleus, inferior olivary nucleus, and posterior horn of the spinal cord; and Pick bodies (PBs) in the atrophied cerebral cortex and red nucleus. PSP-type NFTs and PBs have been demonstrated in a single case for the first time. Despite their pathognomonic significance in certain disorders, we suggest that these inclusions may reflect a form of cytoskeletal disorganization, which is not entirely restricted to a single disease entity.

Adult↗
PubMed1991

Evidence that two stereochemically different alpha-2 adrenoceptors modulate norepinephrine release in rat cerebral cortex.

Cerebral cortex slices from the rat were loaded with [3H]norepinephrine ([3H]NE) and superfused in order to measure the release of radioactivity at rest and in response to electrical stimulation. The (-)-isomer and the (+)-isomer of CH-38083 ([7,8-(methylenedioxy)-14- alpha-hydroxyalloberbane HCl), a selective alpha-2-adrenoceptor antagonist with an alloberbane skeleton, increased the electrically induced release of [3H]NE in a concentration-dependent manner, and a similar effect was observed with racemic CH-38083 and idazoxan. The stereoisomers of CH-38083 applied in a concentration range of 10(-8) to 10(-6) mol/l were equipotent in facilitating stimulation-evoked [3H]NE release: concentrations needed to enhance tritium outflow by 50% were 1.3 X 10(-7) mol/l for (-)-CH-38083 and 1.4 X 10(-7) mol/l for (+)-CH-38083. Exogenous NE decreased the electrically stimulated release of [3H]NE, and the stereoisomers of CH-38083 antagonized this inhibition with different potencies: the dissociation constant (KB) values for (-)-isomer and for (+)-isomer of CH-38083 were 14.29 and 97.18 nmol/l. These data indicate that presynaptic alpha-2 adrenoceptors that are available for NE released from axon terminals do not show stereospecificity toward enantiomers of CH-38083, whereas those that are occupied by exogenous NE are much more sensitive toward (-)-CH-38083. The alpha-1 adrenoceptor antagonist prazosin also differentiated between the alpha-2 adrenoceptor subtypes: prazosin (10(-6) mol/l) did not alter the increase of electrically induced [3H]NE release evoked by (-)- and (+)-CH-38083; however, in its presence, the stereoisomers of CH-38083 failed to antagonize the inhibitory effect of exogenous NE on its own release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1990

Phospholipid and ganglioside composition in rat cerebral cortex and cerebral white matter after chronic diazepam treatment.

Male Wistar rats with an initial weight of 170 g were maintained on a nutritionally adequate diet, and diazepam was administered in a dose of 10 mg/kg/d. Control animals were pair-fed on adequate diet. The feeding was continued for 180 days, and the effects on cerebral cortex and white matter lipid contents were studied. A generalized increase in the lipid phosphorus and lipid-N-acetylneuraminic acid (NeuAc) level was found. The increase was statistically significant for phosphatidylethanolamine and phosphatidylserine, ganglioside GM1, GD1a and GDIb in the cerebral cortex, as well as for phosphatidylinositol and phosphatidic acid in the cerebral white matter. There were no significant differences in the content and patterns of gangliosides in the cerebral white matter after the chronic diazepam treatment.

Animals↗
PubMedDate not supplied

Alpha- and beta-adrenergic receptors of the rat cerebral cortex and cerebral microvessels in aging, and their response to denervation.

We studied the effects of aging and norepinephrine depletion 2 weeks after unilateral locus ceruleus lesion on alpha 1-, alpha 2- and beta-adrenergic receptors by ligand binding methods in the ipsilateral and contralateral cerebral cortex of Fischer-344 rats. We also studied the effects of aging and noradrenergic denervation on beta-adrenergic receptors in isolated cerebral microvessels. We found that specific [125I]HEAT binding to alpha 1-adrenergic receptors was not affected by aging or by norepinephrine depletion. Although aging also had no effect on the density or affinity of [3H]UK-14,304 and [125I]pindolol binding to alpha 2- and beta-adrenergic receptors, the density of receptors increased significantly in all age groups after noradrenergic denervation. beta-Adrenergic receptors of cerebral microvessels also were unaffected by aging, but increased their density after noradrenergic denervation at all ages. In all instances, there were no significant effects on the affinity of ligand binding. We conclude that aging does not affect the density or the affinity of adrenergic receptors in the cerebral cortex of Fischer-344 rats, nor does it affect the response of these receptors to norepinephrine depletion.

Aging↗
PubMed1989

Pyruvate dehydrogenase activity in the rat cerebral cortex following cerebral ischemia.

The effect of cerebral ischemia on the activity of pyruvate dehydrogenase (PDH) enzyme complex (PDHC) was investigated in homogenates of frozen rat cerebral cortex following 15 min of bilateral common carotid occlusion ischemia and following 15 min, 60 min, and 6 h of recirculation after 15 min of ischemia. In frozen cortical tissue from the same animals, the levels of labile phosphate compounds, glucose, glycogen, lactate, and pyruvate was determined. In cortex from control animals, the rate of [1(-14)C]pyruvate decarboxylation was 9.6 +/- 0.5 nmol CO2/(min-mg protein) or 40% of the total PDHC activity. This fraction increased to 89% at the end of 15 min of ischemia. At 15 min of recirculation following 15 min of ischemia, the PDHC activity decreased to 50% of control levels and was depressed for up to 6 h post ischemia. This decrease in activity was not due to a decrease in total PDHC activity. Apart from a reduction in ATP levels, the acute changes in the levels of energy metabolites were essentially normalized at 6 h of recovery. Dichloroacetate (DCA), an inhibitor of PDH kinase, given to rats at 250 mg/kg i.p. four times over 2 h, significantly decreased blood glucose levels from 7.4 +/- 0.6 to 5.1 +/- 0.3 mmol/L and fully activated PDHC. In animals in which the plasma glucose level was maintained at control levels of 8.3 +/- 0.5 mumol/g by intravenous infusion of glucose, the active portion of PDHC increased to 95 +/- 4%. In contrast, the depressed PDHC activity at 15 min following ischemia was not affected by the DCA treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

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↗
PubMedDate not supplied

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↗
PubMed1989

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↗
PubMed1990

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↗
PubMed1985

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↗
PubMed1992

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↗
PubMed1975

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↗
PubMed1988

Effects of nifedipine and felodipine on adenosine and inosine release from the hypoxemic rat cerebral cortex.

The cerebral cortical cup technique has been used to study the effects of nifedipine and felodipine on adenosine and inosine release from the rat brain. After basal and hypoxia (8% 02)-evoked control levels of purine release had been established, these 1,4-dihydropyridine calcium antagonists were administered intraperitoneally (1 mg/kg). Both agents depressed basal levels of purine efflux and suppressed the hypoxia-evoked release of adenosine and inosine. An inhibition of the transporter that mediates purine efflux from brain cells is likely to account for the suppression of release from the cerebral cortex. A reduced release of adenosine into the interstitial space also explains the ability of both agents to block the increase in CBF evoked by hypoxic challenges.

Adenosine↗