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PubMed2001

Two modes of radial migration in early development of the cerebral cortex.

Layer formation in the developing cerebral cortex requires the movement of neurons from their site of origin to their final laminar position. We demonstrate, using time-lapse imaging of acute cortical slices, that two distinct forms of cell movement, locomotion and somal translocation, are responsible for the radial migration of cortical neurons. These modes are distinguished by their dynamic properties and morphological features. Locomotion and translocation are not cell-type specific; although at early ages some cells may move by translocation only, locomoting cells also translocate once their leading process reaches the marginal zone. The existence of two modes of radial migration may account for the differential effects of certain genetic mutations on cortical development.

Animals↗

PubMed1986

Age-dependent day/night variations of alpha 1- and beta-adrenoceptors in the rat cerebral cortex.

Receptor binding studies in the cerebral cortex of young (2-4 months) and mature (11-12 months) rats were conducted at two points of the circadian time: 8.00 and 20.00 hr. In addition, the exploratory activity in the open field was assessed. In young rats the density of alpha 1- and beta-adrenoceptors increased at 20.00 in comparison with 8.00 hr, while no changes in the exploratory activity were observed. However, in mature rats the activity was higher at 20.00 than 8.00 hr; at the same time, a rise in the density of alpha 1- but not beta-adrenoceptors was observed. Obtained data suggest that the increased exploratory activity of mature rats at 20.00 hr may appear as a result of a higher density of alpha 1-adrenoceptors and a simultaneous lack of changes in beta-adrenoceptors.

Aging↗

PubMed1988

[Subcellular mechanisms of the action of weak extra-low frequency electromagnetic fields on the cerebral cortex].

Electron microscopic examinations of the cerebral cortex in rabbits and rats after exposure to weak extra-low electromagnetic fields has detected ultrastructural changes whose degree in different nerve tissue elements was dependent on the duration of irradiation. Single exposure to weak extra-low electromagnetic field resulted only in the glial response of the neocortex, while multiple exposure resulted alternately in the response of glial cells or neuronal bodies. Three days after a single exposure and within 15 days after multiple exposure to electromagnetic field a complete repair of the nervous tissue was observed. No destructive or pathological alterations have been found which suggests the functional character of the reactions induced. Neuro-morphological alterations are of a similar character when induced by weak extra-low electromagnetic fields or other biophysical effects which points to common subcellular mechanisms of nonspecific adaptive reactions.

Animals↗

PubMed1997

Comparison of the cortical connections of areas 4 gamma and 4 delta in the cat cerebral cortex.

Area 4 of the cat cerebral cortex has been subdivided into several regions based on cytoarchitectonic studies: areas 4 gamma, 4 delta, 4sfu, and 4fu (Hassler and Muhs-Clement [1964] J. Hirnforsch. 6:377-420). In a previous study, we found separate representations of contralateral limb movements in areas 4 gamma and 4 delta (Ghosh [1997] J. Comp. Neurol. 380:191-214). To investigate the relationship between these representations, the ipsilateral cortical connections of area 4 gamma and 4 delta were compared by the use of the retrograde neural tracers. After intracortical microstimulation of area 4, tracer was injected into one or two of the following regions: the forelimb regions of the rostral and caudal subdivisions of areas 4 gamma and 4 delta (r4 gamma, r4 delta, c4 gamma, c4 delta, separated by the cruciate sulcus) and the hindlimb regions of c4 gamma and c4 delta. Retrogradely labeled neural profiles were counted in every fourth section of the coronal series and located in cytoarchitectonic areas of the ipsilateral cortex. We found topographically organized reciprocal connections between areas 4 gamma and 4 delta; these connections were part of a rich network of interconnections between the cytoarchitectonic subdivisions of area 4. The forelimb regions of c4 gamma and c4 delta, of r4 gamma and c4 delta, and of r4 gamma and r4 delta were interconnected. These findings support the location of a secondary motor area in 4 delta. No interconnections between the forelimb regions of r4 gamma and c4 gamma, and of r4 delta and c4 gamma, could be found. Area 6 (particularly area 6a gamma) was found to project strongly to the forelimb regions of r4 gamma and r4 delta and relatively weakly to the forelimb region of c4 delta. Retrogradely labeled neurons were also detected in areas 3a, 3b, 1, 2pri, 5, 7, and insula after tracer injections in area 4.

Animals↗

PubMed1974

The projection of the vestibular nerve to the cerebral cortex in the cat.

1. The cerebral cortex in the cat has been examined for responses to contra-lateral vestibular nerve shocks and to natural stimuli.2. Stimulation of the nerve produces short latency (3.5 msec) surface positive responses in very restricted areas. Within these areas, unitary discharges occur during the equivalent negative phase below the surface.3. It has not been possible to evoke unitary activity in these areas by natural stimulation during light anaesthesia with pentobarbitone, chloralose or urethane.4. The distribution and properties of the shock evoked responses have been studied with special attention to the problem of stimulus spread. They are shown to be overlapped by somato-sensory and auditory projections, but to be distinguishable from them. Evidence is presented that previously reported longer latency responses were probably due to stimulus spread.5. Reasons are discussed for the extreme sensitivity of the vestibulocortical pathway to anaesthesia.

Anesthesia, General↗

PubMed1983

The effect of p-chloromercuribenzoate on structure-binding relationships of muscarinic receptors in the rat cerebral cortex.

Muscarinic receptors in the rat cerebral cortex, reacted with p-chloromercuribenzoate (PCMB) under different conditions (Phase I and II), have modified binding sites. These exhibit remarkable changes in the structural dependence of the binding of drugs. In Phase I, the structure-binding profile of agonists for both the high and low affinity agonist sites are altered. In Phase II, the structure-binding profile of antagonists is also observed. In Phase II, the ability of potent agonists to discriminate between sub-classes of agonist binding sites is eliminated. There is also a loss of heterogeneity in the binding of the selective antagonist pirenzepine. Of the 16 agonists examined, only pilocarpine has a heterogeneous binding profile in Phase II, the dispersity of binding being increased. The changes in binding properties of the receptors are discussed in terms of general theories of drug-receptor interactions.

Animals↗

PubMed1990

Induction of ornithine decarboxylase in cerebral cortex by excitotoxin lesion of nucleus basalis: association with postsynaptic responsiveness and N-methyl-D-aspartate receptor activation.

The major cholinergic innervation of the rat cerebral cortex arises from the nucleus basalis in the basal forebrain. Introduction of the excitotoxins kainate or ibotenate into the nucleus basalis by stereotaxic injection results in degeneration of the cholinergic cells. We have investigated the effect of this excitotoxic action on ornithine decarboxylase (ODC) activity and cholinergic responsiveness in the cerebral cortex. A massive and rapid induction of ODC activity was seen in ipsilateral cortex after injection of excitotoxin. A maximal increase in ODC activity of 268 times the control value was seen in ipsilateral cerebral cortex 8 h after lesioning. Thereafter, ODC activity declined but remained significantly greater than control levels for 32 h. Pretreatment of animals with the irreversible ODC inhibitor difluoromethylornithine prevented the induction of ODC by kainate. Tissue content of the ODC product putrescine showed a marked increase in cerebral cortex ipsilateral to the lesion, increasing sevenfold at 24 h, the maximal concentration reached. After 24 h, the level of putrescine decreased but remained significantly elevated above control values for 5 days. Levels of the polyamines spermidine and spermine were unaffected by lesioning. Increases on ODC activity of much smaller magnitude were also seen in brain regions not directly innervated from the ipsilateral nucleus basalis. However, the response in ipsilateral cortex was found to be dependent on an intact projection from nucleus basalis to cortex. The induction of ODC was shown to be prevented by treatment of rats with MK-801, a result indicating the involvement of N-methyl-D-aspartate (NMDA) receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

4-Hydroxy-trans-2-nonenoic acid is a gamma-hydroxybutyrate receptor ligand in the cerebral cortex and hippocampus.

Elevated production of 4-hydroxy-trans-2-nonenal (HNE) occurs in numerous neurological disorders involving oxidative damage. HNE is metabolized to the non-toxic 4-hydroxy-trans-2-nonenoic acid (HNEAcid) by aldehyde dehydrogenases in the rat cerebral cortex. Based upon the structural similarity of HNEAcid to ligands of the gamma-hydroxybutyrate (GHB) receptor, we hypothesized that HNEAcid is an endogenous ligand for the GHB receptor. HNEAcid displaced the specific binding of the GHB receptor ligand (3)H-NCS382 (30 nm) in membrane preparations of human frontal cerebral cortex and whole rat cerebral cortex with IC(50s) of 3.9 +/- 1.1 and 5.6 +/- 1.2 micro m, respectively. Inhibition was attenuated when the carboxyl group of HNEAcid was replaced with an aldehyde or an alcohol. HNEAcid (300 micro m) did not displace the binding of beta-adrenergic receptor and GABA(B) receptor antagonists, demonstrating the selectivity of HNEAcid for the GHB receptor. HNEAcid is formed in homogenates of human frontal cortical gray matter in an NAD(+)-dependent (V(Max), 0.71 nmol/min/mg) and NADP(+)-dependent (V(Max), 0.12 nmol/min/mg) manner. Lastly, (3)H-NCS382 binding is elevated 2.7-fold with age in the cerebral cortex of rats. Our data demonstrate that an HNE metabolite, formed in rat and human brain, is a signaling molecule analogous to other bioactive lipid peroxidation products.

Adrenergic beta-Antagonists↗

PubMed1999

Age-related alteration of intracellular ATP maintenance in the cell suspensions of mice cerebral cortex.

Neurological alteration in the aging brain has been suggested to be due to, in part, a declined cellular energy metabolism. In order to understand age-related alteration of intracellular ATP maintenance, the present in vitro study measured change of intracellular adenosine triphosphate (ATP) content in cell suspensions of cerebral cortex isolated from male ICR mice aged 2 days (infant), 8 weeks (young adult) and 12 months (aged) under several different conditions, using the chemiluminescence technique. Among the three different ages, significant decrease of intracellular ATP content by oxygen deprivation for 15 min was observed in the cell suspensions of cerebral cortex from 12-month-old mice (P < 0.05). When cell suspensions of 8-week cerebral cortex were incubated with or without glucose (0-60 min), intracellular ATP content decreased in a time-dependent manner under both conditions, but depletion rate was significantly high in the glucose-free condition. This decrease was maximally restored by adding 1 mM glucose as tested. In addition, the ability for intracellular ATP maintenance in the presence or absence of glucose was age-dependently different. The rank order of difference of intracellular ATP content between with and without glucose was 3 months > 12 months > 2 days. The highest decrease of intracellular ATP content by incubation without glucose was observed in the 12-month samples. Sodium cyanide (100 microM) produced a gradual ATP depletion in cerebral cortex suspended from 2-day-old mice, but rapid change in both 8-week and 12-month samples. Combination of cyanide and iodoacetate (3.5 mM) rapidly depleted the intracellular ATP content in all age groups tested. These results suggest that the aging process in the cerebral cortex of mice is accompanied by alteration of maintenance of intracellular ATP homeostasis under a given condition, and this may be associated with pathological change of overall mechanisms involved in the development of neuronal disease in the senescent brain.

Adenosine Triphosphate↗

PubMed2000

A metabolic path for the degradation of lysophosphatidic acid, an inhibitor of lysophosphatidylcholine lysophospholipase, in neuronal nuclei of cerebral cortex.

Neuronal nuclei isolated from rabbit cerebral cortex were found to be enriched in an NEM-insensitive lysophosphatidic acid (lysoPA) phosphohydrolase activity. LysoPA is an inhibitor of the nuclear lysophosphatidylcholine (lysoPC) lysophospholipase, and by preserving lysoPC levels, lysoPA boosted the nuclear production of the acyl analogue of platelet-activating factor by promoting the acetylation of lysoPC (Baker and Chang, Mol. Cell Biochem., 1999, in press). The nuclear phosphohydrolase converts lysoPA to 1-monoacylglycerol, and thus eliminates this lysoPA inhibition of lysoPC lysophospholipase. The nuclear lysoPA phosphohydrolase specific activity was more than three times that observed for the nuclear lysoPA lysophospholipase (Baker and Chang, Biochim. Biophys. Acta 1438 (1999) 253-263) and represents a more active route for nuclear lysoPA removal. The neuronal nuclear lysoPA phosphohydrolase was inhibited at acidic pH, and also inhibited by calcium ions. The 1-monoacylglycerol product of the phosphohydrolase is rapidly degraded by neuronal monoacylglycerol lipase, an enzyme some sevenfold more active than the phosphohydrolase and sensitive to inhibition by arachidonoyl trifluoromethyl ketone (AACOCF(3)). Both acidic pH and free fatty acid inhibited the lipase. In the absence of AACOCF(3), production of fatty acid from lysoPA substrate could be largely attributed to the sequential actions of the nuclear phosphohydrolase and lipase. This facilitates fatty acid recycling back into phospholipid by lysophospholipid acylation when ATP levels are restored following periods of brain ischemia. At relatively low concentrations, sphingosine-1-phosphate, and alkylglycerophosphate were the most effective phosphohydrolase inhibitors while phosphatidic acid, alkylacetylglycerophosphate and ceramide were without effect. LysoPA is an interesting regulatory molecule that can potentially preserve lysophosphatidylcholine within the nuclear membrane for use in acetylation reactions. Thus conditions relevant to brain ischemia such as falling pH, falling ATP concentrations, rising fatty acid and intracellular calcium levels may, by slowing this metabolic path for lysoPA loss, promote the production of acyl PAF and contribute to the increased levels of the acetylated lipids noted in ischemia.

Animals↗

PubMed2002

The lizard cerebral cortex as a model to study neuronal regeneration.

The medial cerebral cortex of lizards, an area homologous to the hippocampal fascia dentata, shows delayed postnatal neurogenesis, i.e., cells in the medial cortex ependyma proliferate and give rise to immature neurons, which migrate to the cell layer. There, recruited neurons differentiate and give rise to zinc containing axons directed to the rest of cortical areas, thus resulting in a continuous growth of the medial cortex and its zinc-enriched axonal projection. This happens along the lizard life span, even in adult lizards, thus allowing one of their most important characteristics: neuronal regeneration. Experiments in our laboratory have shown that chemical lesion of the medial cortex (affecting up to 95% of its neurons) results in a cascade of events: first, massive neuronal death and axonal-dendritic retraction and, secondly, triggered ependymal-neuroblast proliferation and subsequent neo-histogenesis and regeneration of an almost new medial cortex, indistinguishable from a normal undamaged one. This is the only case to our knowledge of the regeneration of an amniote central nervous centre by new neuron production and neo-histogenesis. Thus the lizard cerebral cortex is a good model to study neuronal regeneration and the complex factors that regulate its neurogenetic, migratory and neo-synaptogenetic events.

Animals↗

PubMed1996

Early appearance of abnormality of microperoxisomal enzymes in the cerebral cortex of senescence-accelerated mouse.

SAMP8, a substrain of senescence-accelerated mouse (SAM), has been characterized by several age-related deficits in the brain. Previously, we reported that the contents of lipid peroxides and protein carbonyl, and net generation of H2O2 were increased in the cerebral cortex of SAMP8 at 4-8 weeks of age in comparison with those in age-matched SAMR1 substrain used as a control. To study the cause of these increases, we compared the activities of antioxidative enzymes in the cerebral cortex between the two substrains. The catalase activity was decreased by 75% in SAMP8 at 4-8 weeks of age, whereas neither superoxide dismutase nor glutathione peroxidase activities were changed. The change in the catalase activity was seen only in the cerebral cortex where oxidative stress was increased in SAMP8. On the contrary, the activity of acyl-CoA oxidase, a microperoxisomal H2O2-producing enzyme, in the cerebral cortex of SAMP8 was increased 1.6 fold in comparison with that in age-matched SAMR1 without change in the activity of D-amino acid oxidase. Furthermore, the changes in the activities of catalase and acyl-CoA oxidase with age were paralleled with those observed in oxidative stress in SAMP8. These results suggest that the abnormality of activities in two microperoxisomal enzymes, catalase and acyl-CoA oxidase, may be one of the cause of the early increase in oxidative stress observed in the cerebral cortex of 4-8 weeks old SAMP8.

Acyl-CoA Oxidase↗

PubMed2002

Astroglial interlaminar processes in human cerebral cortex: variations in cytoskeletal profiles.

Among mammalian species, astroglial interlaminar processes are unique features of the primate cerebral cortex. The morphological diversity in the immunocytochemical expression of their cytoskeleton was analyzed. For this purpose, samples from normal human cerebral cortex from autopsy cases were used. While Fractal dimension failed to represent the actual complexity of interlaminar processes, Compression analysis allowed classification of these profiles according to their relative tortuosity. Conversion of Compression values into estimates of membrane surface suggested that profile changes could not only affect the directionality of dynamic events, but also the amount of glial cell membrane exposed to the local neuropil. Terminal segments of interlaminar processes were usually more tightly twisted than the cytoskeleton stalk, and enlarged in aged individuals. If not aberrant structures, these so-called 'terminal masses' may provide an additional means to increase local membrane availability. Based on Compression analysis, categories of the geometric variability of the cytoskeleton of cerebral cortex interlaminar glial processes are presented.

Aging↗

PubMed1997

Age-related change in the neuropeptide Y and NADPH-diaphorase-positive neurons in the cerebral cortex and striatum of aged rats.

Age-related changes of neuropeptide Y (NPY) and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) were examined in the rat cerebral cortex and striatum by immunohistochemical and histochemical methods. Double labeling for NPY and NADPH-d showed that about 30-70% of NPY-immunoreactive (NPY-IR) neurons in the cerebral cortex of the control (4-month-old) rats contained NADPH-d and that 50-75% in the aged (24-month-old) rats. The aged rats showed a significant increase in percentage of colocalization of NPY and NADPH-d in comparison with the control rats in the temporal cortex, occipital cortex, cingulate cortex, insular cortex, retrosplenial cortex and caudatoputamen. However, colocalization percentage between control and aged rats in the frontal cortex, parietal cortex, perirhinal cortex, entorhinal cortex and nucleus accumbens were practically identical. In the aged group, the number of NPY-IR/NADPH-d-positive neurons was not significantly decreased in the cerebral cortex and striatum compared to the control group. However, the number of NPY-IR/NADPH-d-negative neurons was significantly decreased in all cerebral cortical areas and caudatoputamen in the aged group except in the nucleus accumbens. Major loss of NPY-IR/NADPH-d-negative neurons in the aged group were observed in the neurons of layer II/III and V/VI. These results demonstrate that the NADPH-d containing NPY-IR neurons are less influenced by aging than the control group in the cerebral cortex and striatum of rats.

Aging↗

PubMed2004

[Effect of microwave irradiation on neurocyte mitochondrial ultrastructure and mtTFA mRNA expression in rats cerebral cortex and hippocampus].

OBJECTIVE: To explore molecular controlling mechanism of mitochondrial injury induced by different density of microwave irradiation. METHODS: Rats were exposed to microwave irradiation for 1 hour at average power density of 3 mW/cm(2) or 30 mW/cm(2). After microwave irradiation, the changes of pathological ultrastructure of rat cerebral cortex and hippocampus were observed by electron microscope, and mitochondrial transcription factor A (mtTFA) mRNA expression level were determined by RT-PCR. RESULTS: After 3 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure and mtTFA mRNA expression level didn't significantly change in rat cerebral cortex and hippocampus. After 30 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure obviously changed, mtTFA mRNA expression in rat hippocampus significantly increased by 67.00%, 80.00%, 30.00% respectively, and in rat cerebral cortex by 133.00%, 86.00%, 233.00% respectively. There were significant differences between the corresponding groups of hippocampus and cerebral cortex (P < 0.01). CONCLUSION: No obvious change in mitochondria was found after 3 mW/cm(2) microwave irradiation, but it was found after 30 mW/cm(2) microwave irradiation. Mitochondria injury in cerebral cortex was more severe than that in hippocampus. mtTFA mRNA may have certain regulation in mitochondrial energy metabolism.

Animals↗

PubMed2001

Patterning the mammalian cerebral cortex.

When and how is the area map of the cerebral cortex set up during development? Recent studies indicate that regional pattern emerges early in cortical neurogenesis, and that this pattern does not require cues from extrinsic innervation. Studies of mutant mice indicate a role for embryonic signaling centers and for specific transcription factors in regionalizing the cortex. Thus, it is increasingly probable that the cortex is partitioned using the same types of mechanisms--and in some cases, the same gene families--that are used in patterning other parts of the embryo. This emerging model is likely to be the basis for many future studies. However, new evidence also confirms the special nature of the cerebral cortex, in that cues from developing connections appear to modify and refine the final area map.

Animals↗

PubMed1998

Cholecystokinin innervation of the cerebral cortex in a reptile, the lizard, Psammodromus algirus.

We used light and electron microscopic and immunohistochemical methods to map the distribution of cholecystokinin (CCK) in the cerebral cortex of a lizard, Psammodromus algirus. At light microscopy, the CCK immunoreactivity was limited to fibers and terminals densely innervating all cortical regions except for the lateral (pyriform) cortex which was very slightly immunostained. The CCK-positive terminals were almost restricted to the cell layers in every cortical region where they surrounded immunonegative cell bodies and proximal dendrites of neurons within the layer. No CCK-containing neurons were observed within the cerebral cortex. At the electron microscopic level, most positive structures were presynaptic boutons contacting cell bodies and proximal dendrites. All contacts appeared to form symmetric junctions, both the distribution and type of synaptic contacts of CCK fibers in the cerebral cortex of Psammodromus are very similar to the corresponding features in the hippocampus of mammals, although in this lizard the CCK cortical innervation, unlike that in mammals, is probably of extrinsic origin. Double HRP-retrograde labeling and CCK immunohistochemistry show that part of the CCK in the cerebral cortex of Psammodromus arises from the hypothalamic supramammillary nuclei.

Animals↗

PubMed2002

Hyperexcitability of hippocampal CA1 neurons after fluid percussion injury of the rat cerebral cortex.

Effects of fluid percussion injury (FPI) of the parietal cerebral cortex on the neuronal activity in the temporal region of the rat hippocampal CA1 area were investigated by using optical and extracellular recording techniques. Application of moderate impact (1.5-2.0 atm) to the parietal cerebral cortex enhanced the optical signal of the neuronal activity in the ipsilateral hippocampal CA1 area. The field potential evoked by the Schaffer collaterals had multiple population spikes in the ipsilateral hippocampal CA1 pyramidal cell layer. Bicuculline (15 microM) increased the amplitude and the number of population spikes of the field potential even after the brain injury. These results suggest that FPI produces hyperexcitability of hippocampal CA1 neurons, probably by increasing the activity of the Schaffer collaterals of hippocampal CA3 neurons.

Action Potentials↗