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At least 199 records · Page 11Linked to original sources
PubMed1992

Quantification of rat cerebral cortex Na+,K(+)-ATPase: effect of age and potassium depletion.

Na+,K(+)-ATPase concentration in rat cerebral cortex was studied by vanadate-facilitated [3H]ouabain binding to intact samples and by K(+)-dependent 3-O-methylfluorescein phosphatase activity determinations in crude homogenates. Methodological errors of both methods were evaluated. [3H]Ouabain binding to cerebral cortex obtained from 12-week-old rats measured incubating samples in buffer containing [3H]ouabain, and ouabain at a final concentration of 1 x 10(-6) mol/L gave a value of 11,351 +/- 177 (n = 5) pmol/g wet weight (mean +/- SEM) without any significant variation between the lobes. Evaluation of affinity for ouabain was in agreement with a heterogeneous population of [3H]ouabain binding sites. K(+)-dependent 3-O-methylfluorescein phosphatase activity in crude cerebral homogenates of age-matched rats was 7.24 +/- 0.14 (n = 5) mumol/min/g wet weight, corresponding to a Na+,K(+)-ATPase concentration of 12,209 +/- 236 pmol/g wet weight. It was concluded that the present methods were suitable for quantitative studies of cerebral cortex Na+,K(+)-ATPase. The concentration of rat cerebral cortex Na+,K(+)-ATPase showed approximately 10-fold increase within the first 4 weeks of life to reach a plateau of approximately 11,000-12,000 pmol/g wet weight, indicating a larger synthesis of Na+,K+ pumps than tissue mass in rat cerebral cortex during the first 4 weeks of development. K+ depletion induced by K(+)-deficient fodder for 2 weeks resulted in a slight tendency toward a reduction in K+ content (6%, p > 0.5) and Na+,K(+)-ATPase concentration (3%, p > 0.4) in cerebral cortex, whereas soleus muscle K+ content and Na+,K(+)-ATPase concentration were decreased by 30 (p < 0.02) and 32% (p < 0.001), respectively. Hence, during K+ depletion, cerebral cortex can maintain almost normal K+ homeostasis, whereas K+ as well as Na+,K+ pumps are lost from skeletal muscles.

Aging↗
PubMed2003

Aberrant lamination in the cerebral cortex of mouse embryos lacking DNA topoisomerase IIbeta.

We have examined corticogenesis in mouse embryos lacking DNA topoisomerase IIbeta (IIbeta) in the brain or in all tissues. The absence of IIbeta, a type II DNA topoisomerase normally expressed in postmitotic cells in the developing cortex, severely affects cerebral stratification: no subplate is discernible, and neurons born at later stages of corticogenesis fail to migrate to the superficial layers. This abnormal pattern of neuron positioning in the cerebral cortex is reminiscent of that observed in mouse mutants defective in the reelin-signaling pathway. Significantly, the level of reelin in the neocortex is much reduced when IIbeta is absent. These results implicate a role of IIbeta in brain development. The enzyme may be required in implementing particular genetic programs in postmitotic cells, such as reelin expression in Cajal-Retzius cells, perhaps through its action on nucleoprotein structure of particular chromosomal regions.

Animals↗
PubMed2004

Uncoupling of flow and metabolism induced by sodium nitroprusside in rat cerebral cortex.

The effects of sodium nitroprusside (SNP) on cerebral blood flow and glucose metabolism were investigated by the microinfusion of SNP into rat cerebral cortex. A significant enhancement in glucose metabolism, as measured using [14C]deoxyglucose (DG), was observed throughout widespread areas of the cerebral cortex within 1 h of microinjection of 50 nmol/microl SNP. Using a kinetic analysis, the increase in glucose metabolism was found to be due to an increase in the phosphorylation of [14C]DG in the brain. On the other hand, regional cerebral blood flow, as measured using [14C]iodoantypirine, was not significantly altered by the SNP infusion. No significant cell death was detected by 2,3,5-triphenyltetrazolium chloride (TTC) staining 1 h after the SNP infusion. The uncoupling of flow and metabolism was almost completely prevented by pretreatment with an NMDA antagonist, MK-801. However, pretreatment with MK-801 did not prevent the SNP-induced neural cell death detected 6 h after the SNP infusion. These results suggest that the SNP-induced uncoupling of flow and metabolism was not directly related to neural cell death in the cerebral cortex.

Animals↗
PubMed1975

An ultrastructural study of methionine sulphoximine-induced glycogen accumulation in astrocytes of the mouse cerebral cortex.

Glycogen distribution in the mouse cerebral cortex was examined with electron microscopy following treatment with the experimental convulsant, methionine sulphoximine (M.S.O.). Both at 24 and 48 h followed administration of M.S.O., accumulation of particulate glycogen was prominent in astrocytes throughout the cerebral cortex. In astrocyte cell bodies and in subpial, pericapillary and perineuronal astrocyte processes the glycogen often completely filled the cytoplasm, crowding the remaining organelles and inclusions. The present findings correlate well with biochemical studies of M.S.O. effects of glutamine synthetase activity and energy metabolism. It is suggested that the glycogen may be derived from glutamate which under normal conditions would be converted to glutamine.

Animals↗
PubMed1989

Comparative distributions of dopamine D-1 and D-2 receptors in the cerebral cortex of rats, cats, and monkeys.

The distributions and laminar densities of cerebral cortical dopamine D-1 and D-2 receptors were studied in rats, cats, and monkeys. Distributions were determined by using alternate, adjacent tissue sections processed for D-1 and D-2 receptor subtypes and compared to an adjacent, nearly adjacent, or similar sections stained for Nissl substance. [3H]-SCH 23390 and [3H]-spiroperidol (in the presence of 100 nM mianserin) were used to label the D-1 and D-2 receptors, respectively. The regional distribution and laminar density of dopamine receptors were determined by in vitro quantitative autoradiography and video densitometry of selected isocortical and peri-allocortical regions. Granular (prefrontal, primary somatosensory, and primary visual), agranular (primary motor and anterior cingulate), and limbic (entorhinal and perirhinal) cortices were examined. Where possible, homologous areas among the species were compared. The D-1 receptor was present in all regions and laminae of the cerebral cortex of rats, cats, and monkeys. The regional densities for the D-1 receptor were higher in the cat and monkey than in the rat. The rat D-1 receptor displayed a relatively homogeneous laminar pattern in most regions except that the deeper laminae (V and VI) contained more receptors than the superficial layers. The cats and monkeys, however, had distinctly heterogeneous laminar patterns in all regions of cortex that varied from one region to another and were quite different from that seen in the rat. The cats and monkeys had highest densities of the D-1 receptor in layers I and II and lowest densities in layers III and IV, whereas layers V and VI were intermediate. The density of D-1 receptors was greater than the density of D-2 receptors in all regions and laminae of cerebral cortex of the cat and monkey and greater in most regions and laminae of the rat cerebral cortex. The D-2 receptor was also distributed in all regions of the cerebral cortex of rats, cats, and monkeys. The D-2 receptor was very homogeneous in its regional distribution and laminar pattern compared to the D-1 receptor in all 3 species. The D-2 receptor was denser in the superficial layers (I and II) of the cortex than in the deeper layers in the rats, but more homogeneous in the different laminae of the cat and monkey cerebral cortex. The rat cortical D-2 receptor exceeded the D-1 receptor in restricted laminae of selective regions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1978

Size and detergent binding of adenylate cyclase from bovine cerebral cortex.

Adenylate cyclase from the bovine cerebral cortex has been solubilized with the nonionic detergent Triton X-100. The physical properties of the enzyme have been determined. These are: sedimentation coefficient, 8.1 S; Stokes radius, 70 A; partial specific volume, 0.79 ml/g; mass, 305,000 daltons; f/f0 1.5. The high partial specific volume measured in the presence of detergent indicates that the enzyme binds a large quantity of detergent (0.28mg of Triton X-100/mg of protein). The mass of the enzyme protein alone is 220,000 daltons. The size and detergent-binding properties of adenylate cyclase from bovine cerebral cortex are different from those previously reported for adenylate cyclase from the rat renal medulla (Neer, E. J. (1974) J. Biol. Chem. 249, 6527-6531). The renal enzyme is smaller by 60,000 daltons than the cerebral enzyme and does not bind measurable amounts of detergent. The amount of detergent bound by cerebral adenylate cyclase is characteristic of intrinsic membrane proteins. It suggests that there is a hydrophobic region on the surface of the molecule by which it is held in the plasma membrane.

Adenylyl Cyclases↗
PubMed2001

Effects of changes in power setting of an ultrasonic aspirator on amount of damage to the cerebral cortex of healthy dogs.

OBJECTIVE: To determine the minimal ultrasonic aspirator pressure necessary to damage the cerebral cortex of healthy dogs. ANIMALS: 9 mixed-breed dogs. PROCEDURE: The study comprised 2 parts. In part A, 6 dogs were euthanatized immediately prior to the experiment. In part B, 3 dogs were anesthetized for recording of physiologic variables. In both parts, craniectomy and durotomy were performed to bilaterally expose the lateral aspect of the cerebral cortex. An ultrasonic aspirator was placed in contact with various areas of the cerebral cortex, and aspirator power was altered (10, 20, 30, and 40%). Duration of contact at each power was 5 and 10 seconds. Subsequently, gross morphologic and histologic damage was assessed in the cortex. RESULTS: Gross observations for all dogs were similar. At 10% power, visible or histologic damage was not evident in the cortex. At 20% power, the cortex was slightly indented from contact with the hand piece; however, cortical disruption was not evident. Cortical disruption was initially detectable at 30% power in some dogs and was consistently evident at 40% power in both sets of dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Ultrasonic aspirator power of < 20% created minimal acute morphologic damage to the cortex. Power settings between 20 and 30% may superficially damage the cerebral cortex in healthy dogs, whereas 40% power consistently damages the cerebral cortex. Knowledge of the degree of damage to cerebral cortex caused by various amounts of power for ultrasonic aspirators will allow surgeons to avoid damaging normal brain tissues during surgery.

Animals↗
PubMed2005

Fezl regulates the differentiation and axon targeting of layer 5 subcortical projection neurons in cerebral cortex.

During the development of the cerebral cortex, progenitor cells produce neurons that migrate to laminar positions appropriate for their birth dates, adopt specific neuronal identities, and form appropriate local and long-distance axonal connections. Here, we report that forebrain embryonic zinc-finger-like protein (Fezl), a putative zinc-finger transcriptional repressor, is required for the differentiation of projection neurons in cortical layer 5. In Fezl-deficient mice, these neurons display molecular, morphological, and axonal targeting defects. The corticospinal tract was absent in Fezl(-/-) mice, corticotectal and pontine projections were severely reduced, and Fezl-expressing neurons formed aberrant axonal projections. The expression of many molecular markers for deep-layer neurons was reduced or absent in the Fezl(-/-) cerebral cortex. Most strikingly, Ctip2, a transcription factor required for the formation of the corticospinal tract, was not expressed in the Fezl-deficient cortex. These results suggest that Fezl regulates the differentiation of layer 5 subcortical projection neurons.

Animals↗
PubMed1978

Effect of dihydroergotoxine on cyclic-AMP-generating systems in rat cerebral cortex slices.

In slices of rat cerebral cortex, cyclic-AMP formation is stimulated in response to added noradrenaline (NA), isoproterenol (ISP) or adenosine. The effect of ISP could be antagonized only by the selective beta-adrenoceptor-blocking agent pindolol, whereas the stimulating effect of NA could be antagonized by both alpha- and beta-adrenoceptor-blocking agents. Dihydroergotoxine (DHET) at low concentrations (10(-8)M) antagonized the stimulating effect of NA but not of ISP or adenosine, suggesting that this substance has a high affinity for central alpha-adrenoceptors. We could also show that DHET is accumulated in rat cerebral cortex after repeated oral application. In slices of cortex obtained from rats after treatment with DHET for 3 and 6 weeks, but not after 1 week, NA had a significant lower effect on cyclic-AMP formation than in slices from corresponding controls.

Adenosine↗
PubMed2003

Constitutive and inducible levels of CYP1A1 and CYP1A2 in rat cerebral cortex and cerebellum.

We examined the constitutive and inducible levels of microsomal cytochromes P450 1A1 and 1A2 (CYP1A) in rat cerebral cortex and cerebellum at the level of proteins by western blot analysis, and by catalytic activities via ethoxyresorufin O-deethylase (EROD) and methoxyresorufin O-demethylase (MROD). In the cerebral cortex, cytochrome P450 1A1 (CYP1A1) protein was more abundant than cytochrome P450 1A2 (CYP1A2) protein. Treatment with beta-naphthoflavone (beta-NF) caused a slight decrease in the level of the former but induced the latter 5.8-fold. In the cerebellum, in contrast to the cerebral cortex, CYP1A1 protein was less abundant than CYP1A2 protein in untreated rats, and while beta-NF treatment caused a 3.3-fold induction of CYP1A1 protein, it resulted in a 10-fold decrease in CYP1A2 protein. The CYP1A-preferential activity EROD was 2.3-fold higher in the cerebellum than in the cerebral cortex, and was induced 1.5-fold and 1.9-fold in the cerebellum and cerebral cortex, respectively, by beta-NF treatment. The CYP1A2-preferential activity MROD was 3-fold higher in the cerebellum than in the cerebral cortex, and was repressed 2.2-fold in the cerebellum but induced 3.7-fold in the cerebral cortex following beta-NF treatment. The results show that CYP1A1 and CYP1A2 proteins and catalytic activities are constitutively expressed in brain but are differentially inducible in the rat cerebral cortex and cerebellum.

Animals↗
PubMed2000

Computational analysis of functional connectivity between areas of primate cerebral cortex.

Recent analyses of association fibre networks in the primate cerebral cortex have revealed a small number of densely intra-connected and hierarchically organized structural systems. Corresponding analyses of data on functional connectivity are required to establish the significance of these structural systems. We therefore built up a relational database by systematically collating published data on the spread of activity after strychnine-induced disinhibition in the macaque cerebral cortex in vivo. After mapping these data to two different parcellation schemes, we used three independent methods of analysis which demonstrate that the cortical network of functional interactions is not homogeneous, but shows a clear segregation into functional assemblies of mutually interacting areas. The assemblies suggest a principal division of the cortex into visual, somatomotor and orbito-temporo-insular systems, while motor and somatosensory areas are inseparably interrelated. These results are largely compatible with corresponding analyses of structural data of mammalian cerebral cortex, and deliver the first functional evidence for 'small-world' architecture of primate cerebral cortex.

Animals↗
PubMed1986

Glycoprotein properties of muscarinic acetylcholine receptors from bovine cerebral cortex.

Muscarinic acetylcholine receptors from bovine cerebral cortex were solubilized in digitonin for the subsequent determination of several biochemical properties. The digitonin-solubilized receptors were representative of the entire membrane-bound population of muscarinic receptors with respect to carbohydrate content, isoelectric point, and molecular weight. The glycoprotein nature of the solubilized receptors was demonstrated by their quantitative binding to wheat germ agglutinin-agarose. The presence of a bound antagonist did not decrease the extent of receptor binding to this lectin. Treatment of receptors with neuraminidase to remove N-acetylneuraminic acid residues reduced binding to wheat germ agglutinin-agarose by 40%; further treatment with endoglycosidases D and H, to remove all N-linked carbohydrate, decreased binding by a total of 67%. Removal of N-acetylneuraminic acid residues had no effect on agonist binding properties of the membrane-bound receptors. The carbohydrate-specific enzymes were further used to assess the contribution of carbohydrate to the isoelectric point and molecular weight of the receptor. Muscarinic receptors solubilized in either digitonin or Triton X-100 focused as one major species with a pI of 4.3. Neuraminidase treatment resulted in an increase of 0.17 units in the pI of the receptor. Muscarinic receptors labeled with the covalent muscarinic antagonist propylbenzilylcholine mustard migrated as a single major polypeptide with a molecular weight of 73,000 on sodium dodecyl sulfate-urea-polyacrylamide gels. The exclusion of urea from these gels severely retarded receptor mobility, indicating a strong tendency for aggregation of receptors in SDS. Removal of N-linked carbohydrate by endoglycosidase treatment reduced the molecular weight of the antagonist binding polypeptide by no more than 5%. These results demonstrate the glycoprotein nature of muscarinic receptors from mammalian cerebral cortex and provide evidence for their heterogeneity with respect to carbohydrate content.

Animals↗
PubMed2001

Real-time measurement of glutamate release from the ischemic penumbra of the rat cerebral cortex using a focal middle cerebral artery occlusion model.

Following permanent middle cerebral artery occlusion, extracellular penumbral glutamate levels, measured by a real-time glutamate electrode, increased in two different patterns. In 7/11 rats, glutamate increased from baseline levels of 19+/-4 (mean+/-SEM) to 208+/-29 microM and then declined towards baseline levels. Blood flow in the penumbral area declined to 30% of pre-ischemic levels with recovery to 60 and 70% of baseline values by 3 and 6 h, respectively. Four of 11 rats in the study also exhibited late peaks of glutamate release (120+/-40 microM ) 2 h after the onset of ischemia. There were no changes in the EEG recordings or cerebral blood flow during these late glutamate peaks.

Animals↗
PubMed1987

Differential effect of temperature on histamine- and carbachol-stimulated inositol phospholipid breakdown in slices of guinea-pig cerebral cortex.

Slices of guinea-pig cerebral cortex were incubated with [3H]-inositol at 37 degrees C before exposure to histamine or carbachol at 37 degrees C or 25 degrees C. Histamine-stimulated accumulation of [3H]-inositol 1-phosphate ([3H]-IP1) at 25 degrees C was only 5-7% of that at 37 degrees C, whereas for carbachol the response at 25 degrees C was 45-49% of that at 37 degrees C. The affinity of benzilylcholine, obtained from inhibition of carbachol-induced accumulation of [3H]-IP1 was similar at 25 degrees C and 37 degrees C, but the EC50 for carbachol was lower at 25 degrees C (20 +/- 2 microM) than at 37 degrees C (42 +/- 2 microM). The IC50 for histamine inhibition of [3H]-mepyramine binding to homogenates of guinea-pig cerebral cortex did not differ significantly at 25 degrees C and 37 degrees C. Histamine-induced accumulations of [3H]-IP2 and [3H]-IP3 at 25 degrees C, expressed as a percentage of the accumulation at 37 degrees C, were also much less than the corresponding value for carbachol. These observations imply that the locus or pathway(s) of agonist-induced formation of [3H]-IP1 are not the same for histamine and carbachol.

Animals↗
PubMed1992

Determination of alpha 1-adrenoceptor subtype selectivity by [3H]-prazosin displacement studies in guinea-pig cerebral cortex and rat spleen membranes.

1. [3H]-prazosin homogeneously labels alpha 1-adrenoceptors in guinea-pig cerebral cortex and rat spleen membranes with dissociation constants of 1.28 and 1.49 x 10(-10) M respectively. 2. Phentolamine and WB 4101 displacement studies show that guinea-pig cerebral cortex contains 30% alpha 1A- and 70% alpha 1B-adrenoceptor subtypes, whereas rat spleen contains a virtually homogeneous alpha 1B-adrenoceptor subtype population. The alpha 1-adrenoceptor population of rat thoracic aorta is predominantly of the alpha 1A-adrenoceptor subtype, and in guinea-pig thoracic aorta it is mainly of the alpha 1B-adrenoceptor subtype. 3. Half of the compounds displacing [3H]-prazosin bound to guinea-pig cerebral cortex membranes display alpha 1A-adrenoceptor selectivity. Among these compounds, WB 4101 and methoxamine are most selective, displaying selectivity ratios of approximately 38 and approximately 26 respectively. 4. The affinity constants of the non-selective compounds for the alpha 1-adrenoceptor in guinea-pig cerebral cortex membranes correlate well with the affinity constants obtained for alpha 1B-adrenoceptors in rat spleen membranes. The affinities of selective compounds for the alpha 1B-adrenoceptor subtype in guinea-pig cerebral cortex correlate very well with their affinity for alpha 1B-adrenoceptor in the rat spleen homogenate. Both regression lines coincide with the line of identity. The affinity constants of selective compounds for the alpha 1A-adrenoceptors in guinea-pig cerebral cortex only apparently correlate with the affinity for either the alpha 1B-adrenoceptors in guinea-pig cerebral cortex or in the rat spleen. Regression analyses indicate a straight line relationship (r2>0.9) between pKEA and Pk1B but the regression lines deviate from the line of identity.

Adrenergic alpha-Agonists↗
PubMed1995

Effect of diet on the fatty acid composition of the major phospholipids of infant cerebral cortex.

The fatty acid compositions of the major cerebral cortex phospholipids, phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine were measured in 16 term and one preterm 'cot death' infants fed exclusively either breast milk or one of two formulas. Docosahexaenoic acid (DHA; C22:6n-3) content in cerebral cortex phosphatidylethanolamine and phosphatidylserine of breast fed infants was greater than in both formula groups with significances varying between p < 0.1 and p < 0.001. Compensation for this deficiency in DHA in the formula fed infants was largely achieved by increased incorporation of docosapentaenoic acid (C22:5n-6) in the cerebral cortex of term infants and Mead (C20:3n-9) and dihomo Mead acids (C22:3n-9) in the preterm infant. As the phospholipids most affected are known to perform an important role in membrane function and are possibly integral to neurotransmission it is recommended that breast milk substitute infant formulas should contain n-3 and n-6 series polyunsaturated fatty acids in proportions similar to those of human milk.

8,11,14-Eicosatrienoic Acid↗