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At least 685 records · Page 38Linked to original sources
PubMed2000

Transient induction of neuronal nitric oxide synthase in neurons of rat cerebral cortex after status epilepticus.

The change in neuronal nitric oxide synthase (nNOS) expression after status epilepticus induced by kainate was examined in the rat cerebral cortex. Expressional change was assessed using nNOS immunohistochemistry and reverse transcription-polymerase chain reaction for nNOS mRNA. Constitutive nNOS-positive neurons was observed in the cerebral cortex of the control group. At 1 and 3 days after status epilepticus, nNOS-positive neurons were present in a deep layer of various cortical regions such as primary motor cortex, secondary motor cortex, primary somatosensory cortex, secondary somatosensory cortex, parietal association cortex, insular cortex, ectorhinal cortex, temporal association cortex, auditory cortex and visual cortex. The level of nNOS mRNA increased at 1, 3, 6 and 12 days after status epilepticus compared to controls. This report provides the first morphological evidence that nNOS are induced in neurons of the cerebral cortex following seizure.

Animals↗
PubMedDate not supplied

Inhibition of calcium transport by mercury salts in rat cerebellum and cerebral cortex in vitro.

The present investigation was initiated to study the differential effects of mercury salts on calcium pump activity of rat cerebellum and cerebral cortex in vitro. The calcium pump activity was studied by assaying calcium-adenosine triphosphatase (Ca(2+)-ATPase) in synaptic plasma membranes (SPMs) and microsomes of cerebellum and cerebral cortex in the presence of different micromolar concentrations of mercury and methylmercury. The 45Ca uptake in microsomes of cerebellum and cerebral cortex was also determined in the presence of both the salts of mercury. The SPMs and microsomes were prepared by differential centrifugation using a sucrose gradient (0.8/1.2 M). The Ca(2+)-ATPase activity was determined by estimating the inorganic phosphate. The 45Ca uptake was measured in microsomes by using 45CaCl2. Calcium-ATPase in SPMs was significantly inhibited by these two mercury salts in a concentration-dependent manner. In cerebellum and cortex, the IC50 values for mercuric chloride were 0.065 and 0.081 microM, respectively, whereas they were 0.354 and 0.384 microM for methylmercury chloride, indicating that mercuric chloride was more potent in inhibiting the plasma membrane Ca2+ extrusion process when compared to methylmercury chloride. As seen in SPMs, Ca(2+)-ATPase and 45Ca uptake in microsomes were also significantly inhibited in both cerebellum and cortex by mercury salts in a concentration-dependent manner, the effect being greater with mercuric chloride. These results indicate that both mercury and methylmercury inhibited the Ca2+ pumps located in SPMs and microsomes differentially, and to some extent the effects were also region specific.

Animals↗
PubMed1980

An application of numerical taxonomy to the study of the cerebral cortex of Natrix maura (L).

The separate cellular regions of the reptilian cerebral cortex were studied using Numerical Taxonomy. Three parameters were employed: a) The area occupied by each region at the several levels studied. b) The total area of the cell nuclei present in each level. c) The average are of these nuclei. Numerical Taxonomy resolves the problem by means of a dendrogram which represents the normalised distances, which indicate levels of similarity on absciassas. The elements studies are on the ordinate axis. The dendrogram shows the different levels of similarity existing between each one of the chosen populations. Depending upon the degree of similarity one may deduce the similarities or differences existing between these populations, and also the characteristics of each cellular population throughout the length of its presence in the cerebral cortex and the variations between the regions. These results, in the first place, relate to the four cortical regions: medialis cortex, dorsomedialis cortex, dorsalis cortex, and lateralis cortex, and in the second place, to each one of the regions within the entire telencephalic cortex.

Animals↗
PubMed1984

Perfusion of the cerebral cortex by use of abdominal counterpulsation during cardiopulmonary resuscitation.

Perfusion of the cerebral cortex (rCCBF) during resuscitation from cardiac arrest was studied using 24 large dogs and three different resuscitation models. Conventional cardiopulmonary resuscitation (CPR) was compared with interposed abdominal compression CPR (IAC-CPR) and with IAC-CPR together with infusion of epinephrine. Conventional CPR produced a mean rCCBF of only 11% (0.057 +/- 0.07 ml/min/g) normal perfusion (0.54 +/- 0.14 ml/min/g). Even without epinephrine, IAC-CPR produced mean rCCBF equal to 51% (0.27 +/- 0.17 ml/min/g) of normal. With epinephrine, IAC-CPR produced rCCBF (0.93 +/- 0.49 ml/min/g) statistically indistinguishable from normal. Both models of IAC-CPR were significantly superior to conventional CPR in perfusion of the cerebral cortex.

Animals↗
PubMed2005

Delayed maturation of neuronal architecture and synaptogenesis in cerebral cortex of Mecp2-deficient mice.

We detected morphologic abnormalities in the cerebral cortex of Mecp2-hemizygous (Mecp2(-/y)) mice. The cortical thickness of both somatosensory and motor cortices in mutants did not increase after 4 weeks of age, as compared with that in wild-type male mice. The density of neurons in those areas was significantly higher in layers II/III and V of Mecp2(-/y) mice than in wild-type mice, particularly in layers II/ III after 4 weeks of age. In layer II/III of the somatosensory cortex of Mecp2(-/y) mice, the diameter of the apical dendrite was thin and the number of dendritic spines was small. Electron microscopy revealed that two-week-old mutants already had numerous premature postsynaptic densities. These results indicate that Mecp2(-/y) mice suffered delayed neuronal maturation of the cerebral cortex and that the initial neuronal changes were caused by premature synaptogenesis. Rett syndrome patients with a heterozygous mutation of Mecp2 display developmental disorders including cortical malfunctions such as mental retardation, autism, and epilepsy. Our results provide evidence of the similarity with Rett syndrome brains in some respects and suggest that MeCP2/Mecp2 plays some role in synaptogenesis.

Age Factors↗
PubMed1997

Ultrastructural characteristics of blood vessels in the infant and adult human cerebral cortex.

Blood vessels in frontal and temporal cerebral cortex of adults and two infants aged 5 months and 5 years were studied by electron microscopy. The cells outside the endothelium were classified on their ultrastructural characteristics. Fibroblasts had prominent rough endoplasmic reticulum and few mitochondria in the cytoplasm. They were different from pericytes, which contained a prominent Golgi apparatus but only a few, isolated profiles of rough endoplasmic reticulum. Smooth muscle cells were distinguished from fibroblasts and pericytes by the presence of filaments and caveolae. Perivascular cells were characterised by the presence of lysosomes and granules of different sizes and electron densities, and were present at all ages studied. Plasma cells had abundant rough endoplasmic reticulum in the cytoplasm, and were present only in the 5-month-old infant cortex. Cortical vessel diameter increased with age.

Adult↗
PubMed1989

High affinity serotonin binding sites in human brain: a comparison of cerebral cortex and basal ganglia.

The high-affinity binding of 3H-serotonin and 3H-DPAT was studied in membrane preparations and tissue sections of cerebral cortex and basal ganglia of human brain. In tissue sections, 3H-serotonin bound to sites present at high density in the cerebral cortex, hippocampus and basal ganglia. 3H-DPAT bound predominantly to the outer layers of the cerebral cortex and the hippocampus, no significant binding was observed in the basal ganglia. In cortical membranes 3H-serotonin bound to a heterogeneous population of sites, one of which was similar to a binding site labelled by 3H-DPAT (the putative 5HT-1A receptor). 3H-serotonin binding to membranes prepared from the putamen displayed low affinity for DPAT, mesulergine and spiperone, RU24969 was considerably less potent than serotonin itself. This 3H-serotonin binding site does not have the properties of those sites described in rodent brain (5HT-1A, 5HT-1B, and 5HT-1C), and may represent a novel serotoninergic binding site.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1997

Ethanol-induced changes in prostaglandin E concentration in the intact cerebral cortex of preterm and near-term fetal sheep.

Ethanol-induced changes in fetal prostaglandin E (PGE) concentration may play a role in the toxic effects of prenatal ethanol exposure. Using the novel technique of in utero microdialysis, the present study tested the hypothesis that acute ethanol exposure changes PGE concentration in the intact cerebral cortex of preterm (93 +/- 1 days of gestation) and near-term (124 +/- 1 days of gestation; term, approximately 147 days) fetal sheep. Fetal sheep were surgically instrumented with a microdialysis probe placed in the parasagittal parietal cortex. Three days later, the effects of maternal infusion of 1 g of ethanol/kg maternal body weight on preterm (n = 6) and near-term (n = 7) fetal cerebral cortical and plasma PGE concentrations were determined. In the preterm fetal cerebral cortex, PGE concentration was increased after ethanol infusion in all six animals studied. The median peak increase was 160% with a 95% confidence interval of 115 to 784%. There was considerable variation in the time of occurrence, magnitude, and duration of this increase. In the near-term fetal cerebral cortex, an increase in PGE concentration was observed after ethanol infusion in 5 of the 7 animals studied, whereas a decrease in PGE concentration was observed in the other two animals. Overall, ethanol did not increase significantly near-term fetal cerebral cortical PGE concentration. For both age groups, ethanol infusion had no effect on fetal plasma PGE concentration. These data indicate that ethanol can affect PGE production in the fetal cerebral cortex and that this effect seems to be gestational-age-dependent.

Animals↗
PubMedDate not supplied

Desensitization of H2-like histamine receptors stimulating cyclic AMP formation in the chick cerebral cortex.

Histamine potently stimulates cyclic AMP formation in slices of the chick cerebral cortex. Pretreatment of the tissue slices with 10 microM histamine for 2-30 min led to a time-dependent attenuation (when compared with values observed in the control tissue) of the cyclic AMP response produced by subsequent re-stimulation with 1, 10 or 100 microM histamine. The observed histamine-induced desensitization appears to be specific and homologous as the increase in cyclic AMP formation evoked by both forskolin or pituitary adenylate cyclase-activating polypeptide (PACAP) in slices pretreated with 10 microM histamine for 15 min was unchanged. It is concluded that in the chick cerebral cortex, H2-like receptors linked to cyclic AMP-generating system undergo rapid homologous desensitization.

Animals↗
PubMed2004

Distribution of N-cadherin in human cerebral cortex during prenatal development.

An important subgroup of adhesion molecules is the superfamily of cadherins, which takes part in cell recognition and differentiation during development. To our knowledge only one study describing N-cadherin expression in developing human brain has been performed so far. Our aim is to identify N-cadherin expression to establish a relationship between its expression and function in human cerebral cortex during prenatal development. In the present study, localization and intensity of N-cadherin was investigated in developing cerebral cortex. Fetuses from spontaneous abortions (n=13) were obtained from first, second, and third trimesters. Western blot analysis revealed three bands and the third trimester samples showed the strongest bands for N-cadherin. Cell processes, axon bundles, and some of the developing neurons revealed immunoreactivity for N-cadherin throughout pregnancy. The immunoreactivity increased in the developing neocortex and expanded from the ventricular layer toward the marginal zone as development progressed. Moreover, the immunoreactivity was strong in vascular endothelium during all three trimesters. We conclude that N-cadherin is dynamically related to the organization of cerebral cortex layers during prenatal development. The dynamic expression pattern implicates N-cadherin as a potential regulator of cell migration, axon extension and fasciculation, the establishment of synaptic contacts, and neurovascular angiogenesis in the developing human cerebral cortex.

Abortion, Spontaneous↗
PubMed2004

KRIT1/cerebral cavernous malformation 1 protein localizes to vascular endothelium, astrocytes, and pyramidal cells of the adult human cerebral cortex.

OBJECTIVE: Mutations in KRIT1 cause familial cerebral cavernous malformation, an autosomal dominant disorder affecting primarily the central nervous system vasculature. Although recent studies have suggested that Krev-1 interaction trapped 1 (KRIT1) is a microtubule-associated protein that interacts with integrin cytoplasmic domain-associated protein-1alpha, the function of KRIT1 remains elusive. METHODS: We used Western blotting and immunohistochemistry with specific KRIT1 polyclonal antibodies to investigate KRIT1 protein expression in diverse cerebral and extracerebral tissues. RESULTS: Immunostaining demonstrates that although KRIT1 is expressed in a broad variety of human organs, it localizes to the vascular endothelium of each, specifically to capillaries and arterioles. KRIT1 antibody fails to stain fenestrated capillaries in the kidney, the liver, or the red pulp of the spleen, where endothelial cells do not to adhere to one another. In contrast, intense staining is observed in the thymus and the white pulp of the spleen, where specialized blood-organ barriers are formed. Other cell types, including various epithelia, cardiac myocytes, and hepatocytes, also stain with KRIT1. CONCLUSION: Although KRIT1 expression is seen in every endothelium studied, cerebral cavernous malformation lesions are seen almost exclusively in the central nervous system, suggesting that additional cell type(s) contribute to the pathophysiology of cerebral cavernous malformations. Here, we demonstrate that KRIT1 is also present in cells and structures integral to the cerebral angiogenesis and formation of the blood-brain barrier, namely, endothelial cells and astrocytic foot processes, as well as pyramidal neurons in the cerebral cortex.

Adult↗
PubMed2004

Age-related changes in serum melatonin in mice: higher levels of combined melatonin and 6-hydroxymelatonin sulfate in the cerebral cortex than serum, heart, liver and kidney tissues.

Age-related changes in levels of melatonin and 6-hydroxymelatonin sulfate and effects of dietary melatonin on their levels in different tissues were determined in mice. Levels of melatonin were highest in the serum followed by liver, kidney, cerebral cortex and heart as measured by a quantitative and sensitive enzyme-labeled immunosorbent assay (ELISA). Serum melatonin levels decreased with age, and were reduced by 80% in 27-month old mice relative to 12-month old mice. Levels of 6-hydroxymelatonin sulfate were measured independently in various tissues. Levels of the melatonin metabolite, 6-hydroxymelatonin sulfate were significantly higher than free melatonin in all tissues tested. Levels of 6-hydroxymelatonin sulfate were highest in the cerebral cortex followed by the serum, heart, kidney, and liver. In 12-month old mice 6-hydroxymelatonin sulfate concentration was approximately 1000-fold greater than that of melatonin in the cerebral cortex, it was only 3-fold greater than melatonin levels in the serum. Thus only 0.1% of total melatonin in the brain was present in the free and unconjugated form but the corresponding value for serum was 27.4%. The cerebral cortex had the highest levels of combined melatonin and 6-hydroxymelatonin sulfate than other tissue tested in control mice. There was no significant change in 6-hydroxymelatonin sulfate levels between young and old mice. There was also no age-dependent change in levels of serotonin or cortisol in the serum samples. Dietary supplementation with melatonin resulted in a significant increase in levels of melatonin in the serum and all other tissue samples tested. Thus, any age-related decline of tissue melatonin can be reversed by supplementation with dietary melatonin.

Aging↗
PubMed1993

Adenosine 5'-triphosphate release from the normoxic and hypoxic in vivo rat cerebral cortex.

The release of adenine nucleotides and adenosine from the in vivo rat cerebral cortex has been measured in the presence of DL-alpha-glycerophosphate (10(-2) M), an inhibitor of non-specific phosphatases. In normoxic brains, the superfusate concentrations of adenosine and its nucleotides (in nM) were: adenosine 38.9 +/- 10.9; AMP 13.9 +/- 1.6; ADP 12.4 +/- 2.3; ATP 17.7 +/- 2.1. During 10 min episodes of hypoxia (8% oxygen inhalation) superfusate levels of adenosine doubled, but the release of nucleotides was unaltered. These findings indicate that extracellular levels of ATP in the cerebral cortex are in the range at which this compound dilates cerebral blood vessels, and that ATP may be an endogenous regulator of regional cerebral blood flow. The absence of any increase in nucleotide levels during hypoxic episodes implies that adenosine is released into the extracellular space as the nucleoside, and not as a nucleotide which would then be hydrolyzed to adenosine.

Adenine Nucleotides↗
PubMed1982

Effect of neonatal 6-hydroxydopamine treatment on alpha 1- and alpha 2-adrenoceptors in rat cerebral cortex.

Neonatal 6-hydroxydopamine (6-OHDA) treatment was used to destroy the noradrenergic nerve endings in rat cerebral cortex and thus give some insight into the development and regulation of alpha-adrenoceptor subtypes, which in turn provides information concerning the anatomical localization of alpha 1- and alpha 2-adrenoceptors. In cerebral cortex of rats treated in the neonatal period with 6-OHDA, we have observed an irreversible decrease in noradrenaline levels. Differences in 3H-clonidine and 3H-prazosin binding occurred which varied depending upon the time between denervation and the binding assay. In 7-14 day-old rats we observed a 20% decrease in the number of alpha 2-adrenoceptors and a marked increase in alpha 1-adrenoceptors. In older rats (45-50 day-old) both types of alpha-adrenoceptors were increased. Results of this study indicate that alpha 2-adrenoceptors located on presynaptic noradrenergic terminals represent only a minor fraction of the total alpha 2- adrenoceptors in rat cerebral cortex that are lost after denervation. Conversely, noradrenergic denervation resulted in supersensitivity of the alpha 1-adrenoceptors and nonnoradrenergic terminals located on alpha 2-adrenoceptors.

Aging↗
PubMed1998

beta-adrenergic receptor-induced activation of nerve growth factor gene transcription in rat cerebral cortex involves CCAAT/enhancer-binding protein delta.

Stimulation of beta-adrenergic receptors (BAR) by clenbuterol (CLE) increases nerve growth factor (NGF) biosynthesis in the rat cerebral cortex but not in other regions of the brain. We have explored the transcription mechanisms that may account for the cortex-specific activation of the NGF gene. Although the NGF promoter contains an AP-1 element, AP-1-binding activity in the cerebral cortex was not induced by CLE, suggesting that other transcription factors govern the brain area-specific induction of NGF. Because BAR activation increases cAMP levels, we examined the role of CCAAT/enhancer-binding proteins (C/EBP), some of which are known to be cAMP-inducible. In C6-2B glioma cells, whose NGF expression is induced by BAR agonists, (i) CLE increased C/EBPdelta-binding activity, (ii) NGF mRNA levels were increased by overexpressing C/EBPdelta, and (iii) C/EBPdelta increased the activity of an NGF promoter-reporter construct. Moreover, DNase footprinting and deletion analyses identified a C/EBPdelta site in the proximal region of the NGF promoter. C/EBPdelta appears to be responsible for the BAR-mediated activation of the NGF gene in vivo, since CLE elicited a time-dependent increase in C/EBPdelta-binding activity in the cerebral cortex only. Our data suggest that, while AP-1 may regulate basal levels of NGF expression, C/EBPdelta is a critical component determining the area-specific expression of NGF in response to BAR stimulation.

Animals↗
PubMed1997

Cholinergic synapses in human cerebral cortex: an ultrastructural study in serial sections.

Cholinergic axons in the human cerebral cortex were analyzed by electron microscopy. Choline acetyltransferase (ChAT) immunoreactivity was used to identify cholinergic axons in samples of anterior temporal lobe removed at surgery. A systematic survey of labeled axon varicosities, visualized in complete serial sections, showed that 67% of all varicosities formed identifiable synaptic specializations. These synapses were usually symmetric and quite small, often present in only one to two serial sections. However, an occasional synapse was asymmetric and larger, seen in five to seven serial sections. The postsynaptic processes at cholinergic synapses were often identified as spiny dendrites or spines. The existence of cholinergic axons in the human cerebral cortex has been demonstrated in numerous studies. Our findings provide the first ultrastructural evidence that these axons make synaptic contact with cortical neurons in the human brain.

Adult↗
PubMed1999

Regional expressions of Fos-like immunoreactivity in rat cerebral cortex after stress; restraint and intraperitoneal lipopolysaccharide.

To demonstrate regional activation in the rat cerebral cortex related to stress-evoked neuroendocrine response, Fos expression in both the cerebral cortex and hypothalamic paraventricular nucleus (PVN) was immunohistochemically examined in two experimental groups; a lipopolysaccharide (LPS) intraperitoneally injected group for inflammatory stress and a restraint group for emotional stress. The LPS injection (100 microg/100 g b.w.) and restraint (for 30 min) had similar effect on Fos-like immunoreactivity (Fos-LI) in PVN with regard to the number of immunoreactive nuclei and their distribution pattern, while the times to maximize Fos-LI were different. Numerical analysis of cortical Fos-LI in untreated rats showed a distinct region-specific pattern. Statistical analysis revealed no significant increase in Fos-LI density in any cortical regions in the LPS group, but restraint resulted in a dramatic and region-specific increase. A significant increase was detected in the prefrontal cortex (the cingulate, orbital and agranular insular cortex), the frontal area 2, the agranular retrosplenial cortex, the parietal cortex, and the medial and lateral occipital area 2. These results indicate that cortical activation relevant to specific functions may be involved in stress-specific neural circuitry.

Animals↗