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At least 289 records · Page 16Linked to original sources

PubMed1997

Fast thermal waves spreading over the cerebral cortex.

Fast thermal waves spreading over the cerebral cortex were found in the white rat by infrared neuroimaging (thermoencephaloscopy) in the range of 3-5 microm. Thermal waves appeared under visual stimulation (the probability of their appearance = 0.92), and under background conditions (probability of appearance = 0.42). Typically, they moved during the period from 15 s before to 25 s after each light flash that was presented rhythmically (1.5-3 per min). The waves spread over the cerebral cortex along the limited number of typical trajectories, which are specific for the hemisphere of their origin (ipsilateral or contralateral with the side of stimulation). The waves were never recorded in a dead animal or in a thermal standard. The amplitude of the thermal waves was in the range of 0.005-0.1 degrees C, with the extent of the pathway of 2-56 mm, length of 10-15 mm, duration of 1.2-11.4 s, and velocity of 1-33 mm/s. In about half of the cases the waves appeared in the contralateral visual cortex (areas 17 and 18a), spread to the midline and crossed to the ipsilateral hemisphere (areas 17, 18a and 7). Local waves moving along a circular trajectory and rotating around the central part of the contralateral area 17 were also revealed, as well as wave rotation around the dorsal (mainly parietal) cortical fields. Possible biophysical and neurophysiological mechanisms and the functional significance of the revealed effects are discussed.

Animals↗

PubMed2001

[Development and developmental disorders of the human brain. II. Development of the cerebral cortex and major tract systems].

In the development of the cerebral cortex, two phases can be distinguished: (a) the formation of the preplate, a superficial layer essential for a normal lamination of the cerebral cortex; (b) the formation of the cortical plate. The cortical plate divides the preplate into a superficial marginal zone (the future layer I) and the subplate. The transient subplate is important for the formation of thalamocortical projections. Most cortical neurons arise in the ventricular zone of the pallium and migrate along radial glial cells (radial migration) to the cortical plate. The gamma-aminobutyric acid (GABA)ergic cortical interneurons, however, originate from the ganglionic eminences and reach the cerebral cortex through tangential migration.

Brain↗

PubMed1996

Ontogeny of somatostatin immunoreactive neurons in the medial cerebral cortex and other cortical areas of the lizard Podarcis hispanica.

The ontogeny of somatostatin immunoreactive interneurons in the cerebral cortex of the lizard Podarcis hispanica has been studied in histological series of embryos, perinatal specimens, and adults. Somatostatin immunoreactive interneurons appear in the early stages of lizard cerebral cortex ontogeny, their number increases during embryonary development, reaches a peak in early postnatal life, and decreases in adult lizards. The first somatostatin immunoreactive somata in the lizard forebrain appeared on E36, and they were located in non cortical areas. Then, on E39 and later, somatostatin immunoreactive neurons were seen in the lizard cortex in a rostral-to-caudal spatial gradient, which parallels that of the normal histogenesis of the lizard cerebral cortex. On E39, labelled somata were seen in the medial and dorsal cortex inner plexiform layers; immunoreactive puncta and dendritic processes were detectable in the inner plexiform layer of the medial cortex. On E40, labelled neurons were observed in the inner plexiform layer of the lateral cortex; labelled processes were found in the inner plexiform layers (dorsomedial, dorsal, and lateral cortices) and the outer plexiform layers (medial and dorsomedial cortices). At hatching (P0), some somatostatin immunoreactive neurons populated the external plexiform layer of the dorsomedial cortex. On P28, groups of labelled neurons appeared in the cell layer of dorsal and lateral cortices, reaching the adult-mature pattern of somatostatin immunoreactivity in the lizard cerebral cortex, i.e., labelled somata and dendritic processes populating the inner plexiform layers in addition to an axonic labelled plexus in the outermost part of the outer plexiform layers. Immunoreactive somata and processes occupied all the cortical areas, but they were especially abundant in the dorsomedial cortex. Proliferating Cell Nuclear Antigen (PCNA) immunostaining in the same histological series revealed that the number of PCNA immunoreactive nuclei in the subjacent proliferative neuroepithelium followed an inverse-complementary evolution to somatostatin, suggesting some temporal relationship between somatostatin immunoreactive cells and neurogenesis in the lizard cerebral cortex.

Animals↗

PubMed2002

[Effects of lead on NO, NOS, SOD, MDA in rat cerebral cortex].

UNLABELLED: To study the effects of lead exposure on nitric oxide (NO), nitric oxide synthase (NOS), super oxide dismutase (SOD) and malondialdehyde (MDA) in cerebral cortex of rats, Wistar rats are exposed to lead from drinking 0, 18.4, 184 mg/L lead acetate solution respectively. RESULTS: Cerebral cortex NOS activity in low and high-dosed lead exposure groups are significantly increased at the time of 7 days (P < 0.05), cerebral cortex NOS activity in low-dosed group is significantly decreased after 90 days and 30 days in high-dosed group (P < 0.05) as compared with that of the controls. Cerebral cortex NO content is markedly decreased in low-dosed group after 90 days poisoning and 14 days, 60 days, 90 days in high-dosed group (P < 0.05). SOD activity in low and high-dosed group is significantly decreased after 30 days exposure. MDA content is markedly increased after 14 days exposure in high-dosed group. CONCLUSION: It is suggested that the damage of cerebral cortex may caused by lead toxicity that results from the changes of NOS activity, NO level, SOD activity and MDA content in cerebral cortex.

Animals↗

PubMed2003

Coincidental increase of leukotriene B4 between cerebral cortex and lung tissue of sensitized rats.

AIM: To explore the changes of leukotrienes (LT) in cerebral cortex and lung tissues in ovalbumin-induced rat asthma model and effects of different anti-asthma drugs on the changes. METHODS: Aerosol antigen-induced changes of inflammation in bronchoalveolar lavage fluids (BALF), pulmonary and brain histologic section in sensitized rats were investigated. Changes of LTB4 and LTC4 in lung and cerebral cortex homogenates were analyzed by reverse-phase high performance liquid chromatography (RP-HPLC). RESULTS: The number of inflammatory cells in BALF and the score of lung and brain histological examination from antigen- challenged rats were significantly higher than that from control group (P<0.05). Dexamethason (DXM, 0.5 mg/kg, ip) and ketotifen fumarate (KF, 5 mg/kg, ig) markedly reduced total leukocyte number in BALF, and inhibited eosinophil accumulation, reduced the infiltration of eosinophils, and improved mucous edema and epithelial lesion of bronchi and bronchioles. In addition, RP-HPLC results shown LTB4 in lung and cerebral cortex homogenates were increased in antigen-challenged rats [(4.1+/-2.4) ng/g and (1.5+/-0.9) ng/g, respectively] compared with control group [(1.55+/-0.21) ng/g and (0.7+/-0.3) ng/g, respectively, P<0.05], both DXM (0.5 mg/kg, ip) and KF (5 mg/kg, ig) reduced LTB4 amount in lung[(1.4+/-0.6) ng/g and (1.8+/-0.7) ng/g] and cerebral cortex homogenates [(0.5+/-0.4) ng/g and (0.7+/-0.4) ng/g] in asthma rats. LTC4 content in lung homogenates in asthma rats was increased compared with control group [(1.9+/-0.9) ng/g and (0.5+/-0.3) ng/g, respectively] (P<0.05), but it has no change in cerebral cortex homogenates. DXM (0.5 mg/kg, ip) and KF (5 mg/kg, ig) reduced LTC4 amount in lung homogenates in asthma rats [(0.8+/-0.6) ng/g and (1.0+/-0.3) ng/g, respectively] (P<0.05). CONCLUSION: The results indicate there is coincidental increase of LTB4 between central nervous system and lung tissues in asthma rats. DXM and KF can inhibit the change.

Animals↗

PubMed1991

Neurotransmitter amino acid levels in rat thalamus and cerebral cortex after cerebellectomy.

Glutamate, aspartate, GABA, glycine and taurine levels have been measured in rat thalamus and in cerebral cortex at different time intervals (3rd, 7th, 15th, 30th day) after cerebellectomy. A decrease in glutamate, aspartate and GABA was detected at the 7th day after cerebellectomy in the thalamus and at the 15th day in the cerebral cortex; at the 30th day after cerebellectomy the levels of these amino acids in the thalamus and in the cerebral cortex were observed to have recovered to control values. No statistically significant difference in glycine and taurine levels in the thalamus and in the cerebral cortex after cerebellectomy could be seen. These results show that the functional recovery process after cerebellar injury is associated with a complex modification of amino acid levels in thalamus and in cerebral cortex.

Amino Acids↗

PubMed1993

Lipid peroxidation in isolated membranes of cerebral cortex, heart and kidney.

The extent of ADP.Fe/NADPH-induced lipid peroxidation measured as production of thiobarbituric acid-reactive substances (TBARS) was determined in isolated membranes from cerebral cortex, heart and kidney of 21-days-old rats. The time course of lipid peroxidation showed higher production of TBARS in cerebral cortex than in heart and kidney. Our data indicate that high level of TBARS production is not due to high activity of NADPH oxidoreductase but due to high content of endogenous lipids in cerebral cortex membranes that could be modified. Higher production of TBARS in cerebral cortex is the result of higher content of lipids in cerebral cortex membranes because NADPH cytochrome c reductase activity in membranes of cerebral cortex is lower than that of heart and kidney.

Adenosine Diphosphate↗

PubMed1996

Capillary lesions develop in retina rather than cerebral cortex in diabetes and experimental galactosemia.

OBJECTIVE: To isolate microvessels from cerebral cortex of dogs with alloxan-induced diabetes and dogs with experimental galactosemia to compare the prevalence of microvascular lesions in cerebral cortex with that in retina. METHODS: Microvessels were isolated from cerebral cortex of experimental animals using a sieving method, and compared with the retinal vasculature isolated from the same animals using the trypsin digestion method. RESULTS: Dogs with diabetes or experimental galactosemia of 5 years' duration had retinopathy that was morphologically indistinguishable from that of humans with diabetes, including microaneurysms, acellular capillaries, and pericyte ghosts. These lesions never were seen in cerebral cortical vessels of the same animals. The only morphologic abnormality observed in cerebral capillaries of dogs with diabetes and dogs fed galactose was thickening of basement membrane. CONCLUSIONS: Local influences in the eye apparently play an important role in the development of diabetic retinopathy. Current hypotheses about the pathogenesis of the retinopathy do not account adequately for such differences in the tissue distribution of vascular lesions.

Animals↗

PubMed1989

Effect of ginseng saponins on the survival of cerebral cortex neurons in cell cultures.

The effects of nerve growth factor (NGF) and saponins isolated from Panax ginseng C.A. Mayer on the survival of chick and rat embryonic cerebral cortex neurons were examined. Ginsenoside Rg1 (GRg1) exerted a survival-promoting effect on both chick and rat cerebral cortex neurons in cell cultures. Ginsenoside Rb1 (GRb1) also had an effect in the rat and displayed some influence in the chick. NGF alone exerted no effect on both neurons, although it did potentiate the GRb1 effect on chick embryonic cerebral cortex neurons, but did not alter the GRb1 effect on rat embryonic cerebral cortex neurons. NGF did not alter the survival-promoting effect of GRg1 on either chick or rat embryonic cerebral cortex neurons. The other saponins alone or with NGF exerted no effect on the survival of cerebral cortex neurons in either the chick or rat.

Animals↗

PubMed1999

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment.

The binding characteristics of the relaxin receptor in rat atria, uterus and cortex were studied using a [33P]-labelled human gene 2 relaxin (B33) and quantitative receptor autoradiography. The binding kinetics of [33P]-human gene 2 relaxin (B33) were investigated in slide-mounted rat atrial sections. The binding achieved equilibrium after 60 min incubation at room temperature (23+/-1 degrees C) and dissociated slowly. The association and dissociation rate constants were 4.31+/-0.34x10(8) M(-1) x min(-1) and 1.55+/-0.38x10(-3) min(-1) respectively. Thus, the kinetic dissociation constant was 3.46+/-0.59 pM. Binding was saturable to a single population of non-interacting sites throughout atria, in uterine myometrium and the 5th layer of cerebral cortex. The binding affinities (pK(D)) of [33P]-human gene 2 relaxin (B33) were 8.92+/-0.09 in atrial myocardium and 8.79+/-0.04 in cerebral cortex of male rats, and 8.79+/-0.10 in uterine myometrium. Receptor densities in the cerebral cortex and atria were higher than in uterine myometrium, indicating that relaxin also has important roles in non-reproductive tissues. In male rats, treatment with 17beta-oestradiol (20 microg in 0.1 ml sesame oil s.c., 18-24 h) significantly decreased the density of relaxin receptors in atria and cerebral cortex. Identical treatment in female rats had no significant effect in atria and cerebral cortex, but it significantly increased the density of relaxin receptors in uterine myometrium. Relaxin binding was competitively displaced by porcine and rat native relaxins. Porcine native relaxin binds to the relaxin receptor in male rat atria (8.90+/-0.02), and cerebral cortex (8.90+/-0.03) and uterine myometrium (8.89+/-0.03) with affinities not significantly different from human gene 2 (B33) relaxin. Nevertheless, rat relaxin binds to the receptors with affinities (8.35+/-0.09 in atria, 8.22+/-0.07 in cerebral cortex and 8.48+/-0.06 in uterine myometrium) significantly less than human gene 2 (B33) and porcine relaxins. Quantitative receptor autoradiography is the method of choice for measurement of affinities and densities of relaxin receptor in atria, uterine myometrium and cerebral cortex. High densities were found in all these tissues. 17beta-oestradiol treatment produced complex effects where it increased the densities of relaxin receptors in uterus but decreased those in atria and cerebral cortex of the male rats, and had no effect on the atria and cerebral cortex of the female rats.

Animals↗

PubMed1998

Effects of thyroid hormone on catecholamine and its metabolite concentrations in rat cardiac muscle and cerebral cortex.

Clinical and experimental data suggest that thyroid hormone affects the actions of catecholamine (CA). However, the serum or tissue levels of CA during thyroid disorders have not been well defined. Accordingly, we investigated the levels of CA and their metabolites in the cardiac muscle, the cerebral cortex, and the plasma of rats with hyperthyroidism and hypothyroidism versus euthyroid animals. The Neurochem analyzer system (ESA, Inc., Bedford, MA) was used in such determinations. The cardiac muscles of hyperthyroid rats exhibited a 16% decrease in the levels of 1-dopa, 3-methoxytyramine (3-MT) and homovanillic acid (HVA) as compared with those in euthyroid rats. The levels of norepinephrine (NE) in cardiac muscle of these rats increased significantly (5.2-fold) relative to the levels in euthyroid rats. NE was undetectable in the cardiac muscles of the hypothyroid rats. Epinephrine (E) and dopamine (DA) were not detected in the cardiac muscles of the rats with either thyroid disorder. Levels of E and 3,4-dihydroxymandelic acid (DOPEG) were detected only in the cerebral cortex of hyperthyroid rats. The cerebral cortex levels of 3-methyoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC), metanephrine (MN), and homovanillic acid (HVA) were all significantly increased in the hyperthyroid versus the euthyroid rats. The cerebral cortex levels of DA, NE, normetanephrine (NMN), and VMA in the hyperthyroid rats all showed a significant decrease. Levels of NE, NMN, and DOPAC in the cerebral cortex increased significantly in the hypothyroid rats. The level of VMA was undetectable in cerebral cortex of such animals. Data from studies on cardiac muscle and cerebral cortex indicate that the changes in CA and CA metabolites are responsible in part for the cardiovascular and the central nervous system symptoms observed in hyperthyroidism and hypothyroidism.

Animals↗

PubMedDate not supplied

Thermodynamic study of iodocyanopindolol beta-adrenoceptors interactions with rat lung and cerebral cortex.

(+/-)125 I-cyanopindolol ((+/-) I CYP) was used to characterize beta-adrenoceptors on rat lung and cerebral cortex membranes. The affinity of (+/-) ICYP was higher for lung (Kd = 64.3 pM) at 37 degrees C. The association reaction of (+/-) ICYP was faster with lung (k+1 = 1.52 X 10(9) M-1.min-1) than with cerebral cortex beta-adrenoceptors (k+1 = 1.75 X 10(8) M-1.min-1). In both tissues, the dissociation reaction followed a biphasic process with a fast (t 1/2 = 15.4 min and 5.6 min for lung and cerebral cortex respectively) and a slow component (t 1/2 = 474 min and 255 min for lung and cerebral cortex respectively). The thermodynamic parameters for (+/-) ICYP - beta-adrenoceptors binding have been determined from kinetics and equilibrium studies, for the two tissues, at several temperatures between 0 degrees and 44 degrees C. For lung and cerebral cortex, Arrhenius plots were linear with different energies of activation. Van't Hoff plot was not linear for lung and the standard enthalpy and entropy changes of (+/-) ICYP - beta-adrenoceptors interaction decreased linearly with temperature: the binding occurred with a negative heat capacity change (delta Cp degrees = -368.9 cal. moles-1.K-1) at 25 degrees C. Thermodynamic and kinetic results show that binding of (+/-) ICYP to lung beta-adrenoceptors could involve two successive equilibria with a conformational change of the beta-adrenergic receptor.

Animals↗

PubMed1986

Congenital Pick cell encephalopathy: a distinct disorder characterized by diffuse formation of Pick cells in the cerebral cortex.

Diffuse degeneration of the cerebral cortex and claustrum was found in the brain of a 7-week-old baby with profound psychomotor retardation, multiple ankyloses, seizures, and hypothalamic dysfunction. There was ubiquitous Pick cell formation and gliosis in the affected gray matter. The cortex was not atrophic; in fact, the brain was moderately enlarged. The clinical and pathological findings suggest that the disorder should be distinguished from Pick's disease, as well as from other congenital encephalopathies.

Cerebral Cortex↗

PubMed1998

Middle cerebral artery occlusion in the rat causes a biphasic production of immunoreactive interleukin-1beta in the cerebral cortex.

Interleukin-1beta (IL-1beta) has been implicated in the sequence of events leading to neuronal cell death. We have used an ultrasensitive, highly specific immunometric assay for rat IL-1beta to determine the pattern of protein expression in the rat cerebral cortex following middle cerebral artery occlusion. In the ipsilateral cerebral cortex there was a biphasic pattern of production with a rapid early phase of IL-1beta expression followed by a delayed phase at 4 h which was sustained for up to 72 h. There was a similar but smaller expression of IL-1beta in the contralateral cortex. Sham operated animals showed no IL-1beta expression. These results provide further evidence to show that IL-1beta is expressed in the rat cerebral cortex following cerebral ischaemia.

Animals↗

PubMed1999

Dopamine D4-like binding sites labeled by [3H]nemonapride include substantial serotonin 5-HT2A receptors in primate cerebral cortex.

Dopamine D4-like binding sites are abundant in human cerebral cortex as detected by [3H]nemonapride. The extremely low density of D4 mRNA in human cerebral cortex is inconsistent with the high amount of D4-like binding sites. To investigate the nature of the D4-like receptors, [3H]nemonapride binding sites in the nonhuman primate cerebral cortex were characterized. Although [3H]nemonapride binding sites were D4-like, displaceable by clozapine but not raclopride, [3H]nemonapride binding was not displaced by selective D4 antagonists but was displaced by the selective 5-HT2A antagonist MDL100907. Using [3H]ketanserin as a 5-HT2A ligand, nemonapride showed high affinity for monkey (Ki = 10.4 nM) and cloned human (Ki = 9.4 nM) 5-HT2A receptors, while its affinity for rat receptors was lower (Ki = 140 nM). The present study demonstrates that cerebral cortical D4-like binding sites labeled by [3H]nemonapride in nonhuman primates consist of a very small portion of D4, but a substantial portion of 5-HT2A receptors. The unexpectedly high affinity of nemonapride for primate 5-HT2A receptor suggests reconsidering previous data from other studies using [3H]nemonapride, particularly those on D4-like receptors.

Animals↗

PubMed1989

Hundred-fold increase in neuronal vulnerability to glutamate toxicity in astrocyte-poor cultures of rat cerebral cortex.

In cultures of rat cerebral cortex in which astrocyte proliferation was stringently suppressed, glutamate neurotoxicity occurred at glutamate concentrations similar to those which are normally found in the extracellular space in the hippocampus. Concentrations of glutamate one hundred-fold higher were required to produce neurotoxicity in the presence of abundant astrocytes. This suggests that the sensitivity of central neurons to glutamate toxicity may be dependent upon astrocyte function.

2-Amino-5-phosphonovalerate↗

PubMed1966

Effects of lower alcohols on potassium transport and microsomal adenosine-triphosphatase activity of rat cerebral cortex.

1. Slices of rat cerebral cortex, incubated anaerobically at 37 degrees , lost K(+) from an initial concentration of 102m-equiv./kg. to a concentration of 57m-equiv./kg. after 10min. On subsequent aerobic incubation they regained K(+) rapidly at a rate that varied with the K(+) concentration of the medium. 2. Lower aliphatic alcohols, present at equal thermodynamic activity, produced approximately equal degrees of inhibition of K(+) uptake during the aerobic incubation. This inhibition was reduced by an increase in K(+) content of the medium. Ethanol did not affect the rate of K(+) loss during anaerobic incubation. 3. Li(+), in concentrations of 1-10mm, also inhibited K(+) uptake by brain-cortex slices, the degree of inhibition varying with the Li(+) concentration. Ouabain also inhibited K(+) uptake. 4. The same series of alcohols, at equal thermodynamic activity, produced comparable degrees of inhibition of Na(+),K(+),Mg(2+)-stimulated adenosine-triphosphatase activity in brain microsomes. 5. It is suggested that inhibition of cation transport is an important, but not a primary, mechanism in the production of central nervous depression by alcohols and other substances.

Adenosine Triphosphatases↗

PubMed2003

Dominant events that modulate mass transfer coefficient of oxygen in cerebral cortex.

Recently, a model of cerebral oxygen delivery was described (J Appl Physiol 85:554) which yields a relationship similar to that used to depict substrate transport across the endothelium. Because the endothelium is not a diffusion barrier for oxygen, the permeability surface area product was replaced by an effective mass transfer coefficient term for oxygen, D. The cerebral metabolic rate of oxygen utilization (CMRO2) was linked to cerebral blood flow (CBF) and volume (CBV) through properties that modify the vessel-to-tissue oxygen tension giving rise to changes in D. Changes in the value of D were correlated with changes in CBF, CMRO2, and CBV as measured using NMR methods in a 48 microL volume of the cerebral cortex of anesthetized rats at different levels of activity. We conclude that the changes in total vascular volume (i.e., swelling or shrinking of the capillary bed) contributes < 5% to changes in D, whereas variations in the number of hematic vs. plasmatic capillaries, or intra-capillary stacking vs. unpacking of erythrocytes, or increase vs. decrease of dissolved oxygen in the tissue (i.e., processes which modify vessel-to-tissue oxygen tension) contribute(s) > 95% to changes in D.

Animals↗