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PubMed1978

[Assessment of the functional state of the cerebral cortex in rabbits according to electroencephalographic findings using a computer diagnostic system].

Computer estimation of the current functional state of the cerebral cortex in rabbits by the EEG data permitted to distinguish its peculiarities in dark and light adaptation of different duration under the action of nembutal; individual peculiarities of the cerebral cortex activity were revealed in various rabbits. The automatic converter system and that of recording and analysis of multiprocess information (apromin system) and computer diagnostic system (mds) were used in complex for the multistage processing of the multiprocess information. Final results are presented on the plane as points reflecting multidimentional images of the current functional states of the cerebral cortex in animals.

Animals↗
PubMed1979

Anomeric preferences of D-glucose uptake and utilization by cerebral cortex slices of rats.

On aerobic incubation of rat cerebral cortex slices with anomers of D-glucose and with 2-deoxy-D-glucose (2DG) for 5 min, the disappearance of beta-D-glucose from the incubation mixture was greater than that of alpha-D-glucose and both anomers had a greater rate of disappearance than that of 2DG. In addition, there were significantly greater consumption of oxygen and production of lactate with the beta-anomer than with the alpha-anomer. In similar experiments with 3H-labeled D-glucose anomers and [1-3H]-3-O-methyl-D-glucose (3MG), the accumulation of [1-3H]-beta-D-glucose (up to 5 min) by rat cerebral cortex slices was greater than that of [1-3H]-alpha-D-glucose. Although initially lower than that of the anomers, the accumulation of [1-3H]-3MG increased at a greater rate and, by 5 min of incubation, was greater than that of both glucose anomers. This preferential accumulation was seen to disappear when the slices were preincubated with 2DG (hexokinase inhibitor) or when the temperature of incubation was reduced to 20 degrees C. Under those conditions the data with the glucose anomers were similar to those obtained with 3MG. Our data then suggested that the greater accumulation of beta-D-glucose than of alpha-D-glucose by the slices was probably not due to differences in transport through brain cell membranes but rather to the preferential metabolism of the beta-D-glucose.

Animals↗
PubMed1975

Effects of 6-hydroxydopamine and reserpine on amphetamine-induced release of norepinephrine in rat cerebral cortex.

Amphetamine released 3-H-norepinephrine from rat cerebral cortex tissue which had previously accumulated the 3-H-amine. Destruction of noradrenergic nerve endings by pretreatment of the rats with 6-hydroxydopamine inhibited the accumulation of 3-H-norepinephrine by the tissue and reduced the proportion of the 3-H-amine which was released by amphetamine. Inhibition of storage of 3-H-norepinephrine within nerve endings by pretreatment of the animals with reserpine also reduced accumulation of 3-H-norepinephrine but did not reduce the proportion of the accumulated 3-H-amine which was released by amphetamine. The addition of desipramine (an inhibitor of neuronal uptake) further reduced the accumulation of 3-H-norepinephrine in animals pretreated with reserpine but had no further effect in animals pretreated with 6-hydroxydopamine. A greater proportion of the 3-H-norepinephrine was converted to 3-H-deaminated metabolites in tissues of reserpine-treated animals than in the tissues of control or 6-hydroxydopamine-treated rats. Amphetamine-induced release of 3-H-norepinephrine was partially calcium dependent in tissues from control animals. After reserpine treatment, amphetamine-induced release of norepinephrine was independent of calcium, whereas potassium-mediated release was still markedly calcium dependent. These experiments indicate that amphetamine releases 3-H-norepinephrine primarily from storage sites within central adrenergic nerve endings. An analysis of the time course of release from tissues of rats treated with reserpine suggests that amphetamine is equally capable of releasing 3-H-norepinephrine from granular sites which are susceptible to reserpine and from reserpine-insensitive sites.

Amphetamine↗
PubMed1975

Properties of rat cerebral cortex neuronal nuclear surfaces: electrokinetic parameters.

Rat cerebral cortex neuronal nuclei were isolated by a mild technique utilizing sucrose; citric acid was not used in the isolation of the nuclei. These nuclei in 0.0145 M NaC1, 4.5 per cent sorbitol, and 0.6 mM NaHCO3 with pH 7.2 plus or minus 0.1 at 25 degrees C had an electrophoretic morbidity of minus 2.01 mum-s(-1)-V(-1)-cm(-1). The mobility curves for the brain nuclei indicated that the surface had an acid-dissociable group of pK APPROXIMATELY 2.7. Nuclei treated with 50 mg neurominidase/mg particle protein had a mobility of minus 1.4 mum-s(-1)-V(-1)-cm(-1). DNase or RNase at 50 mug/mg protein had no effect on the mobility of the isolated nuclei. Concanavalin A at 50 mug/mg protein decreased the nuclei electrophoretic mobility to minus 1.82 mum-s(-1)-V(-1)-cm(-1). The results are interpreted to mean that the brain nuclear external surface contains terminal sialic acid residues, but it is completely devoid of nucleic acids, and it binds canavalin A.

Animals↗
PubMed1979

The aging human cerebral cortex: a stereological characterization of changes in the capillary net.

Capillaries in the cerebral cortex of six age groups, ranging between 19 and 94 years (= 34 human brains) were stereologically investigated. Capillary parameters such as diameter, volume fraction, specific surface area, mean intercapillary distances and total length per unit cortex volume in patients older than 75 years were similar to those in young ones, 19 to 44 years old. Aged subjects between 64 and 74 years revealed increased capillary diameter, volume and total length per unit cortex volume, as well as decreased specific surface area. Frequency distributions in the same age indicate a real increase of capillary diameter and volume, as also an increase of these parameters on the level of blood vessels with diamteres greater than 8 micrometer, probably arterioles. The results of this study argue against the wide-spread assumption of a decreased blood supply in the cerebral cortex during old age. On the contrary, the capillary net is able to respond to changed metabolism and blood pressure.

Adult↗
PubMed1977

Two-dimensional analysis of the redox state of the rat cerebral cortex in vivo by NADH fluorescence photography.

A photographic method for measuring two-dimensional changes in NADH fluorescence and hemoglobin distributions in the rat cerebral cortex in vivo has been developed. Intracellular NADH was excited by UV light peaking at 360 nm and the emission was observed through a window with the maximum transmission at 450 nm. The fluorescence photographs (360 leads to 450 nm) required 20-25 sec exposures at the aperture opening of f/5.6 and the reflectance photographs (360 leads to 360 nm) 10 sec exposures at f/32. The digitization of photographic images was achieved either by a PDP-8-controlled microdensitometer coupled to an A/D converter or by a combination of a manually operated microdensitometer and a computer-controlled digitizer. In the latter case, a photographic negative was scanned with a Joyce-Loebl microdensitometer in parallel lines 170 mum apart, and the densitometric tracings were digitized with a PDP-8-controlled TV digitizer. The digital data were processed by DEC PDP-10 computer and the results were displayed in 3-dimensional surfaces. Nitrogen anoxia caused increases in fluorescence at 450 nm ranging from 10 to 75% fo the normoxic fluorescence intensities (after correcting for the logarithmic characteristics of the photographic films) and decreases in reflectance intensities in the range of 10-30%. The spatial resolution of the present technique is limited to approximately 30 mum X 30 mum on the cortical surface and the time resolution to 10-25 sec. The optical properties of the cerebral cortex in vivo appear to be controlled primarily by blood vessel patterns and hemodynamic factors and secondarily by the redox state of the tissue. Evidence for a heterogeneous redox response of the cerebral cortex toward N2 anoxia was obtained.

Animals↗
PubMed1979

Selective antagonism by benzodiazepines of neuronal responses to excitatory amino acids in the cerebral cortex.

1 The recently discovered benzodiazepine receptor exists in high concentration in the cerebral cortex. We have, therefore, examined the effects of diazepam and chlordiazepoxide on cortical neurone responses to excitatory and inhibitory amino acids and acetylcholine, in the cortex of rats anaesthetized with urethane.2 Chlordiazepoxide applied by microiontophoresis reduced the responses to glutamate and aspartate but acetylcholine responses were unaffected on most cells even by much higher doses of benzodiazepine. gamma-Aminobutyric acid (GABA) and taurine responses were unaffected on most cells, but were reduced on 4 of 25 units. After intravenous diazepam, responses to GABA and taurine were reduced on 3 cells and unchanged on 11.3 On Purkinje cells in the cerebellum a number of cells (5 of 16) exhibited a substantial increase in responses to GABA and taurine following intravenous or iontophoretic application of benzodiazepines.4 It is suggested that the highly selective reduction of excitatory amino acid responses in the cerebral cortex may be of particular relevance to the behavioural effects of benzodiazepines.

Acetylcholine↗
PubMed1977

Activation of guanylate cyclase in cerebral cortex of rat by hydroxylamine.

Hydroxylamine actived guanylate cyclase in particulate fraction of cerebral cortex of rat. Activation was most remarkable in crude mitochondrial fraction. When the crude mitochondrial fraction was subjected to osmotic shock and fractionated, guanylate cyclase activity recovered in the subfractions as assayed with hydroxylamine was only one-third of the starting material. Recombination of the soluble and the particulate fractions, however, restored guanylate cyclase activity to the same level as that of the starting material. When varying quantities of the particulate and soluble fractions were combined, enzyme activity was proportional to the quantity of the soluble fraction. Heating of the soluble or particulate fraction at 55 degrees for 5 min inactivated guanylate cyclase. The heated particulate fraction markedly activated guanylate cyclase activity in the native soluble fraction, while the heated soluble fraction did not stimulate enzyme activity in the particulate. The particulate fraction preincubated with hydroxylamine at 37 degrees for 5 min followed by washing activated guanylate cyclase activity in the soluble fraction in the absence of hydroxylamine. Further fractionation of the crude mitochondrial fraction revealed that the factor(s) needed for the activation by hydroxylamine is associated with the mitochondria. The mitochondrial fraction of cerebral cortex activated guanylate cyclase in supernatant of brain, liver, or kidney in the presence of hydroxylamine. The mitochondrial fraction prepared from liver or kidney, in turn, activated soluble guanylate cyclase in brain. Activation of guanylate cyclase by hydroxylamine was compared with that of sodium azide. Azide activated guanylate cyclase in the synaptosomal soluble fraction, while hydroxylamine inhibited it. The particulate fraction preincubated with azide followed by washing did not stimulate guanylate cyclase activity in the absence of azide. The activation of guanylate cyclase by hydroxylamine is not due to a change in the concentration of the substrate GTP, Addition of hydroxylamine did not alter the apparent Km value of guanylate cyclase for GTP. Guanylate cyclase became less dependent on manganese in the presence of hydroxylamine. Thus the activation of guanylate cyclase by hydroxylamine is due to the change in the Vmax of the reaction.

Animals↗
PubMed1976

[Changes in the electric activity of the cerebral cortex in poisoning caused by Cl. perfringens toxin type A].

The electrical activity of the cerebral cortex was recorded in cats under mild nembutal anesthesia (15-20 mg/kg of body weight) during the development of Cl. perfringens, type A, toxin poisoning (the toxin was injected intramuscularly in a dose of 100 MLD per kg of body weight). Two phases of the changes in the electrical activity of the cerebral cortex were noted. The first phase was attended by the desynchronization of the electrical activity, persistence of the induced potentials and of the reaction of the rhythm reconstruction to the rhythmic light stimulus. No desynchronization occurred under conditions of preliminary section of the midbrain (on the mesencephalic preparation), this indicating the involvement of the reticular formation into the pathological process and pointing to its role in the desynchronization effect. A profound depression of the electrical activity of the brain, depression of induced potentials and disturbance of the reaction of the rhythm reconstruction occurred during the second phase.

Animals↗
PubMed1977

[Comparative study of somatic and visual projections on the cerebral cortex of the normal adult rat, the rat enucleated at birth, and the young rat].

A comparative study of somatic and visual projections on the cerebral cortex of the adult of the normal rat or of the rat enucleated at birth, and of the young rat. This study was first designed to examine the developmental features of somate, sensory and visual projections to the rat cerebral cortex, together with their alteration as a consequence of early sensory deafferentation. We were led to a reevaluation of these projectins in the normal adult rat. This study specifically shows that topical projections exist, for both the somatic and the visual system. However, projections that are highly convergent in nature are present over most of the superolateral aspect of the cerebral cortex and we were unable to demonstrate any simple change resulting from early visual deafferentation.

Afferent Pathways↗
PubMed1979

Agonist-induced changes in beta adrenergic receptor density and receptor-mediated responsiveness in slices of rat cerebral cortex.

Incubation of slices of rat cerebral cortex with the beta adrenergic receptor agonist (-)-isoproterenol led to a 30 to 50% decrease in the number of binding sites for [125I]iodohydroxybenzylpindolol and to a 60 to 80% decrease in isoproterenol-stimulated cyclic AMP accumulation. The density of beta adrenergic receptors was also decreased following incubation with (-)-norepinephrine but not with (+)-isoproterenol or dopamine and the decrease in receptor density was blocked by co-incubation with the beta adrenergic receptor antagonist sotalol. The half-time for loss of receptors was approximately 3 min and recovery was observed during a 1 hr reincubation of tissue slices or following exposure to guanine nucleotides. A decrease in beta adrenergic receptor density was also observed following chronic treatment with desmethylimipramine which blocks norepinephrine reuptake and thus potentiates the effects of neurally released norepinephrine at adrenergic receptors. The loss of receptors induced in vitro could be reversed by reincubation or by exposure to guanine nucleotides. In contrast, the loss of receptors induced in vivo was not affected by these procedures.

Adrenergic beta-Agonists↗
PubMed2024

A conserved molecular logic for neurogenesis to gliogenesis switch in the cerebral cortex.

During development, neural stem cells in the cerebral cortex, also known as radial glial cells (RGCs), generate excitatory neurons, followed by production of cortical macroglia and inhibitory neurons that migrate to the olfactory bulb (OB). Understanding the mechanisms for this lineage switch is fundamental for unraveling how proper numbers of diverse neuronal and glial cell types are controlled. We and others recently showed that Sonic Hedgehog (Shh) signaling promotes the cortical RGC lineage switch to generate cortical oligodendrocytes and OB interneurons. During this process, cortical RGCs generate intermediate progenitor cells that express critical gliogenesis genes Ascl1, Egfr, and Olig2. The increased Ascl1 expression and appearance of Egfr+ and Olig2+ cortical progenitors are concurrent with the switch from excitatory neurogenesis to gliogenesis and OB interneuron neurogenesis in the cortex. While Shh signaling promotes Olig2 expression in the developing spinal cord, the exact mechanism for this transcriptional regulation is not known. Furthermore, the transcriptional regulation of Olig2 and Egfr has not been explored. Here, we show that in cortical progenitor cells, multiple regulatory programs, including Pax6 and Gli3, prevent precocious expression of Olig2, a gene essential for production of cortical oligodendrocytes and astrocytes. We identify multiple enhancers that control Olig2 expression in cortical progenitors and show that the mechanisms for regulating Olig2 expression are conserved between the mouse and human. Our study reveals evolutionarily conserved regulatory logic controlling the lineage switch of cortical neural stem cells.

Animals↗
PubMed1979

Studies on synaptic vesicles in mammalian brain characterization of highly purified synaptic vesicles from bovine cerebral cortex.

Synaptic vesicles have been isolated from bovine cerebral cortex by sequential differential and density gradient centrifugations followed by chromatography on a Sepharose 6B column. We have studied the morphology, enzymatic markers, neurotransmitter and ATP contents and protein composition of the vesicles. The specific contents of acetylcholine, gamma-aminobutyric acid, aspartate, glutamate and catecholamines were 4--8-fold higher in the vesicle fraction compared to the crude synaptosomal pellet. Electron micrographs of the vesicle preparation showed enrichment of vesicular material with an average diameter of 50 nm. The purity of the preparation was assessed by the very low activities of enzymatic markers of cellular membranes and cytosol components. Some Ca--Mg-activated ATPase activity was detected in the vesicle preparations, but its content relative to the neurotransmitters fell on chromatography, suggesting that this activity may be partially contributed by non-synaptic vesicle components, such as small microsomes. The isolated synaptic vesicles were solubilized with 1% sodium dodecyl sulfate and subjected to polyacrylamide gel electrophoresis. The major Coomassie blue stained bands observed with apparent molecular weights of 160,000 and 55,000 were enriched in parallel to the increase in purity of the preparation.

Acetylcholinesterase↗
PubMed1979

The isolation and lipid composition of subcellular fractions derived from neuronal perikarya isolated in bulk from rabbit cerebral cortex.

(1) Neuronal perikarya were isolated from rabbit cerebral cortex and were homogenized and separated into a number of subcellular membrane fractions using differential and discontinuous density gradient centrifugation. (2) The efficiency of homogenizing the nerve cell bodies could be greatly increased by the preliminary passage of the cell body fraction through a micropipet tip. (3) Of a number of density media, a discontinuous gradient of metrizamide gave the best resolution of the mitochondrial and lysosomal marker enzymes found in the crude mitochondrial fraction. This yielded a purified mitochondrial fraction and several lighter membrane fractions. (4) The lighter membrane fractions in metrizamide contained a degree of mitochondrial contamination which could be removed by a second gradient spin on 1.2 M sucrose, producing a second mitochondrial fraction and two light membrane fractions. (5) Based on marker analyses, fractions enriched in nuclei, mitochondria, microsomes and plasma membrane/lysosomes were produced. (6) The two mitochondrial fractions showed the highest, and the nuclear fraction the lowest specific phospholipid content. Cholesterol: phospholipid molar ratios showed a gradient of values from a low (0.2) for the mitochondria and nuclei to an intermediate value (0.4) for the microsomes to a high (0.6) for the light membrane fractions. (7) Phospholipid distributions indicated that for the nuclear and mitochondrial fractions phosphatidylinositol was more abundant than sphingomyelin or phosphatidylserine, while for the microsomes and the two light membrane fractions these three phospholipids were present in almost equal amounts.

Acetylglucosaminidase↗
PubMed1978

Brain alpha-adrenergic receptors: comparison of [3H]WB 4101 binding with norepinephrine-stimulated cyclic AMP accumulation in rat cerebral cortex.

The ability of a series of adrenergic agents to displace the binding to brain membranes of [3H]WB 4101, a potent alpha-adrenergic antagonist (WB 4101 = 2-[2-(2,6-dimethoxyphenoxy)ethylaminomethyl]-1,4-benzodioxane hydrochloride), has been compared with the potency of these agents in stimulating or inhibiting the alpha-adrenergic component of cyclic AMP accumulation in rat cerebral cortex slices. [3H]WB 4101 rapidly bound to a high affinity site (KD = 2.7 nM) in membranes from cerebral cortex. Binding came to equilibrium by 2 min at 37 degrees C and was rapidly reversed in the presence of phentolamine. The potencies of adrenergic agents (WB 4101 greater than phentolamine greater than naphazoline) in displacing binding of [3H]WB 4101 were comparable to the potencies of these agents as inhibitors of the alpha-adrenergic component of norepinephrine-stimulated cyclic AMP accumulations. Phenoxybenzamine, clonidine, chlorpromazine and haloperidol were about 10--30 times more potent in inhibiting cyclic AMP accumulation than in displacing [3H]WB 4101 binding. The potency of classical alpha-adrenergic agonists in displacing WB 4101 (epinephrine greater than norepinephrine greater than methoxamine) correlated with the ability of these agonists to increase cyclic AMP levels. Overall a significant correlation (r = 0.87, P less than 0.005) was found between WB 4101 binding and alpha-adrenergically mediated cyclic AMP accumulation in brain. Several ligands bind to specific sites in brain membranes with alpha-adrenergic receptor properties. The identification of these binding sites as receptors depends on a correlation of binding with a known alpha-adrenergic receptor-mediated response in brain. These data demonstrating that WB 4101 correlates with norepinephrine-stimulated cyclic AMP accumulation suggest that WB 4101 may bind to the membrane receptor sites mediating the alpha-adrenergic accumulation of cyclic AMP in rat cerebral cortex.

Adrenergic alpha-Antagonists↗
PubMed1977

Microiontophoretic studies of the effects of cylic nucleotides on excitability of neurones in the rat cerebral cortex.

1. Responses of cerebral cortical neurones to the microiontophoretic application of acetylcholine, noradrenaline, cyclic adenosine 3',5'-monophosphate (cyclic AMP) and cyclic guanosine 3',5'-monophosphate (cyclic GMP) were examined.2. The application of acetylcholine and cyclic GMP to identified pyramidal tract neurones resulted in an increased frequency of firing in a large number of cells. Upon application of both substances to cells which could not be identified as pyramidal tract cells, a reduction in the frequency of spontaneous firing was sometimes observed.3. Careful current controls had no effect on the cells discussed here, indicating that the observed responses were not due to the iontophoretic currents. Also, the electro-osmotic ejection of cyclic GMP (outward current) produced similar changes of cell firing to those which followed iontophoretic application (inward current).4. The microiontophoretic application of atropine resulted in a blockade of acetylcholine responses while leaving responses to cyclic GMP unaffected. This suggests that cyclic GMP was not acting indirectly by releasing acetylcholine from presynaptic endings.5. Ejection of cyclic GMP from solutions containing calcium ions produced responses comparable to those produced by cyclic GMP alone. It is unlikely therefore that cyclic GMP was causing excitation by chelating calcium.6. Applications of noradrenaline and cyclic AMP produced a reduction in the spontaneous discharge rate of most neurones tested.7. Phosphodiesterase inhibitors such as ICI 63,197 caused a potentiation of the noradrenaline responses of pyramidal tract neurones.8. 5'-adenosine monophosphate produced a powerful depression of all cells to which it was applied. This action was blocked by aminophylline, suggesting the effect was mediated through an adenosine receptor. Responses to cyclic AMP were usually not abolished, but were reduced by about 50% in amplitude.9. These results are consistent with the hypothesis that cyclic AMP may mediate some neuronal effects of noradrenaline and cyclic GMP may mediate some effects of acetylcholine. The results are also consistent with the suggestion that the two nucleotides may sometimes mediate opposite cellular responses to humoral stimuli.

Acetylcholine↗
PubMed1976

Guanylate cyclase. Subcellular distribution in cardiac muscle, skeletal muscle, cerebral cortex and liver.

1. Guanylate cyclase of every fraction studied showed an absolute requirement for Mn2+ ions for optimal activity; with Mg2+ or Ca2+ reaction was barely detectable. Triton X-100 stimulated the particulate enzyme much more than the supernatant enzyme and solubilized the particulate-enzyme activity. 2. Substantial amounts of guanylate cyclase were recovered with the washed particulate fractions of cardiac muscle (63-98%), skeletal muscle (77-93%), cerebral cortex (62-88%) and liver (60-75%) of various species. The supernatants of these tissues contained 7-38% of total activities. In frog heart, the bulk of guanylate cyclase was present in the supernatant fluid. 3. Plasma-membrane fractions contained 26, 21, 22 and 40% respectively of the total homogenate guanylate cyclase activities present in skeletal muscle (rabbit), cardiac muscle (guinea pig), liver (rat) and cerebral cortex (rat). In each case, the specific activity of this enzyme in plasma membranes showed a five- to ten-fold enrichment when compared with homogenate specific activity. 4. These results suggest that guanylate cyclase, like adenylate cyclase, and ouabain-sensitive Na+ + K+-dependent ATPase (adenosine triphosphatase), is associated with the surface membranes of cardiac muscle, skeletal muscle, liver and cerebral cortex; however, considerable activities are also present in the supernatant fractions of these tissues which contain very little adenylate cyclase or ouabain-sensitive Na+ + K+-dependent ATPase activities.

Adenylyl Cyclases↗