Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “neocortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

The distribution of tyrosine hydroxylase-immunoreactive fibers in primate neocortex is widespread but regionally specific.

An antiserum directed against tyrosine hydroxylase (TH), an enzyme involved in dopamine and norepinephrine synthesis, was used to visualize axons immunohistochemically in monkey neocortex. Labeled fibers were distributed throughout the entire neocortex, but they had striking patterns of regional and laminar specialization. For example, primary motor cortex contained the greatest density of TH-labeled fibers, whereas primary sensory regions were sparsely innervated. Marked heterogeneity of fiber density was also present among the association regions of the frontal, parietal, and temporal lobes. In addition, the laminar pattern of innervation in a given region was correlated with its fiber density. Sparsely innervated regions had labeled fibers only in layer I and sometimes layer VI. In regions of intermediate density, labeled fibers tended to be located in layers I-superficial III and layers V-VI, whereas in densely innervated motor cortex TH-immunoreactive fibers were present in all cortical layers. Comparison of these distribution patterns with those produced by an antiserum directed against dopamine-beta-hydroxylase (DBH), a specific marker of neocortical noradrenergic axons, revealed marked differences. DBH-immunoreactive fibers were observed in some cortical locations where few or no TH-labeled fibers were present. In other regions, the density of TH-immunoreactive processes far exceeded that of DBH-labeled fibers. These findings indicate that nearly all of the immunoreactive fibers revealed by this anti-TH antiserum are dopaminergic. This interpretation was further supported by lesions of the ascending noradrenergic fibers in the brain stem, which reduced DBH immunoreactivity, but not TH immunoreactivity, in neocortex. The distinctive innervation patterns of TH-immunoreactive fibers suggest a functional specialization of the dopaminergic projections to primate neocortex.

Animals↗

[Quantitative analysis of the mosaic formation of neurons of the neocortex and hippocampus of the mouse].

Computer analysis of the maps of distribution of intensively labelled neurons (ILN) in the frontal sections of area 6 of the frontal neocortex and area CA 1 of the dorsal hippocamp was performed in 1-day-old mice who received a single injection of 3H-thymidine on the 13th-17th day of embryogenesis (E 13-E 17). It has been revealed that ILN are distributed in rather close, vertically oriented groups. In mice exposed to isotope in E 14-E 16, the average number of ILN in a group was 4.44 +/- 0.25 for area 6 and 4.35 +/- 0.16 for area CA 1. The data available have confirmed an earlier postulated hypothesis on the discrete arrangement of neurogenesis loci in the ventricular zone of the embryonic brain. Additional calculations have allowed to conclude that in E 14-E 16 period the locus of the ventricular neocortex during one mitotic cycle produces 7-9 cells starting the neuronal differentiation, while during the whole period of neurogenesis in the neocortex the column consisting of 84-108 neurons is formed, which is close to the number of neurons in a minicolumn of the neocortex (110 cells).

Animals↗

[Dependence of the spectrum of electrical activity of the neocortex and hippocampus in rabbits on the intensity of the stimulation of the midbrain reticular formation].

Study of dominating spectral maxima in delta-, theta- and alpha-ranges of the electrical activity of rabbits' neocortex and hippocampus showed that an increase of the frequency of the mesencephalic reticular formation stimulation from 60 to 200 imp/s led in both structures to an enhancement of the theta-rhythm (up to 130% in the neocortex and 147% in the hippocampus) and suppression of delta- and alpha-activity (correspondingly up to 67 and 34% in the neocortex and 37 and 48% in the hippocampus) with subsequent weakening of this effect at frequency increase up to 1000 imp/s. In the hippocampus, the reticular stimulation was more effective with respect to the theta- and delta-rhythms, and in the neocortex--with respect to the alpha-rhythm. In both structures the theta-rhythm amplitude changed less than the amplitude of the delta- and alpha-activities. Dependence of the amplitude of dominating rhythms on intensity of reticular formation stimulation differed from the analogous frequency dependence of the same rhythms.

Animals↗

[Principles of the structural organization of the cetacean neocortex].

The investigations performed demonstrate that morphologically cetacean neocortex is organized on the same principles as that of other mammals, as it has six layer structure, layer IV including. The results of investigations done for many years gave the possibility to establish quantitative characteristics of neocortex in different zoological cetacean genera, such as volume of neocortex, total number of its nervous cells (for dolphin the data were obtained for the first time), and clarify the problem fully enough. It became clear that morphologically dolphins belong to different genera. Three quantitative gradations of morphological enrichment of the dolphin neocortex are demonstrated. The only genus of Tursiops (bottle-nosed) can be compared with man, as to on what neuromorphological criteria it is behind, equal and surpasses the man. Representatives of the two other genera investigated, according to all neuromorphological indices studied, are far behind the man.

Animals↗

Development of excitatory and inhibitory postsynaptic potentials in the rat neocortex.

The postnatal development of synaptic potentials in the rat neocortex is characterized by the sequential appearance of functional excitatory and inhibitory synapses. Morphological and electrophysiological studies provided evidence that at early stages of development, pyramidal cells are extensively coupled to each other, presumably via gap junctions. Thus, immature neurons are able to communicate through pathways that are not available or only weakly expressed in the mature neocortex. During the very early postnatal period, excitatory synaptic inputs prevail. Excitatory postsynaptic potentials (EPSPs) are characteristically long in duration and show high sensitivity to frequent stimulation. Although spontaneous inhibitory postsynaptic potentials (IPSPs) and mature responses to exogenously applied gamma-aminobutyric acid (GABA) have been described during the first postnatal week, evoked IPSPs do not develop before postnatal day 10 (P10). During the period of maximum synaptogenesis (P11 to P20), GABA-mediated synaptic inhibition develops and pyramidal cells respond to afferent activation with efficient EPSPs and IPSPs. These postsynaptic potentials gradually mature during the late postnatal period. The delayed development of synaptic inhibition in the neocortex simultaneously promotes synaptic plasticity while increasing seizure susceptibility. On the one hand, the functional lack of synaptic inhibition during early stages of development enables a period of enhanced neuronal activity and augmented synaptic plasticity necessary to form proper synaptic connections. On the other hand, the absence of inhibitory control over excitatory processes increases the vulnerability of the developing neocortex to seizure activity during postnatal ontogenesis.

Aging↗

Homology in the evolution of the cerebral hemispheres. The case of reptilian dorsal ventricular ridge and its possible correspondence with mammalian neocortex.

The present paper reviews some issues related to the evolutionary origin of distinct components of the cerebral hemispheres in vertebrates, which entails the problem of biological homology between anatomical structures. Considering that the term homology is essentially a comparative concept, making emphasis on structural correspondences between organs or body parts, I use the term evolutionary, or phylogenetic homology to denote a common evolutionary origin of two characters. In particular, the controversy of a possible phylogenetic homology between reptilian dorsal ventricular ridge (DVR) and parts of mammalian neocortex is analyzed in some detail. Although it is likely that DVR is a derived character of reptiles while neocortex is a derived character of mammals, the two structures might still originate from the same primordial anlage in the common ancestor. One main problem in the comparison of telencephalic components between reptiles and mammals is that the protrusion of reptilian DVR into the lateral ventricle causes a distortion of the topographic relations in the hemisphere. In order to determine possible homologues of DVR, it is necessary to establish clear-cut telencephalic landmarks. Since lateral cortex is similarly localized in reptiles and mammals, it is suggested that the embryonic position and timing of development of reptilian DVR in relation to lateral cortex may give special insight on the phylogenetic origins of the former. If, as implied by the work of early authors, DVR arose in evolution through an extension of the embryonic period of neuronal proliferation and migration, it may be considered as a genuine novelty in brain evolution. It is also proposed that, regardless of whether DVR and extrastriate neocortex can or cannot be considered phylogenetic homologues, some of the integrative functions performed by them might have a common evolutionary origin, that became localized in reptilian DVR and in mammalian extrastriate neocortex.

Animals↗

Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease.

CONTEXT: Amyloid plaques, a major pathological feature of Alzheimer disease (AD), are composed of an internal fragment of amyloid precursor protein (APP): the 4-kd amyloid-beta protein (Abeta). The metabolic processing of APP that results in Abeta formation requires 2 enzymatic cleavage events, a gamma-secretase cleavage dependent on presenilin, and a beta-secretase cleavage by the aspartyl protease beta-site APP-cleaving enzyme (BACE). OBJECTIVE: To test the hypothesis that BACE protein and activity are increased in regions of the brain that develop amyloid plaques in AD. METHODS: We developed an antibody capture system to measure BACE protein level and BACE-specific beta-secretase activity in frontal, temporal, and cerebellar brain homogenates from 61 brains with AD and 33 control brains. RESULTS: In the brains with AD, BACE activity and protein were significantly increased (P<.001). Enzymatic activity increased by 63% in the temporal neocortex (P =.007) and 13% in the frontal neocortex (P =.003) in brains with AD, but not in the cerebellar cortex. Activity in the temporal neocortex increased with the duration of AD (P =.008) but did not correlate with enzyme-linked immunosorbent assay measures of insoluble Abeta in brains with AD. Protein level was increased by 14% in the frontal cortex of brains with AD (P =.004), with a trend toward a 15% increase in BACE protein in the temporal cortex (P =.07) and no difference in the cerebellar cortex. Immunohistochemical analysis demonstrated that BACE immunoreactivity in the brain was predominantly neuronal and was found in tangle-bearing neurons in AD. CONCLUSIONS: The BACE protein and activity levels are increased in brain regions affected by amyloid deposition and remain increased despite significant neuronal and synaptic loss in AD.

Aged↗

Fetuin in the developing neocortex of the rat: distribution and origin.

Immunocytochemical distribution of the fetal protein fetuin in the neocortex of developing rat brain and the presence of its mRNA, as detected by using reverse transcriptase-polymerase chain reaction analysis, was studied in fetuses at embryonic day 15 (E15) through E22, in neonates at postnatal day 0 (P0) through P20, and in adults. Quantitative estimates of fetuin in cerebrospinal fluid (CSF) and plasma were obtained over the same period. Exogenous (bovine) fetuin injected intraperitoneally into fetal and postnatal rats was used to study the uptake of fetuin into CSF and brain and its distribution compared with endogenous fetuin; bovine albumin was used as a control. Fetuin was identified immunocytochemically in the cortical plate and subplate cells of the developing neocortex. In the rat fetus, fetuin first was apparent at E17, mainly in cell processes, but a few subplate cells also were positive. By E18, there was strong staining in subplate neurons and in inner cells of the cortical plate. At E21, these inner cells of the cortical plate were beginning to differentiate into layer VI neurons, many of which were positive for fetuin. By P0-P1, more layer VI neurons and some layer V neurons had become positive for fetuin. Fetuin immunoreactivity generally was weaker at P1, and, by P2-P3, it had disappeared from all of the layers of the developing neocortex. Bovine fetuin (but not albumin), probably taken up through CSF over the neocortical dorsal surface, had a cytoplasmic distribution; endogenous rat fetuin was both cytoplasmic and membrane bound. Thus, much of this fetuin can be accounted for by uptake, although the presence of fetuin mRNA indicates that in situ synthesis may also contribute.

Animals↗

Global analysis of gene expression patterns in developing mouse neocortex using serial analysis of gene expression.

Molecular inventories of the developing mouse neocortex before and after birth were generated using the global gene expression profiling tool serial analysis of gene expression (SAGE). Libraries were generated from embryonic day 15 and postnatal day 1 mouse neocortex and more than 40,000 tags were collected (20,211 and 22,001 tags, representing 11,706 and 12,402 transcripts, respectively). Comparison of the two libraries resulted in the identification of 321 transcripts that were differentially expressed (P < 0.05). Differential expression was independently verified for selected genes by Northern blotting, and in situ hybridization revealed spatial expression patterns in the neocortex. Differentially expressed transcripts included genes known to be important in neocortical development (e.g., brain factor 1, neuroD2, and Id2), genes not previously associated with neocortical development (such as brahma-related gene 1, receptor for activated C-kinase I, hypermethylated in cancer 2, and Evi9), and genes of unknown identity or function.

Animals↗

Stimulation of GABAB receptors increases the expression of the proenkephalin gene in slice cultures of rat neocortex.

In rat neocortex the proenkephalin gene is expressed in GABAergic interneurons. Immunocytochemistry and in situ hybridisation show only a small number of cells in layers II to VI which express the gene. In organotypic slices of rat neocortex, the GABAA receptor inhibitor bicuculline methiodide enhances the expression of the gene in numerous cells. In the present study, we have investigated how GABA regulates the expression of the proenkephalin gene. The GABAA receptor antagonist bicuculline methiodide and the inhibitor of ligand-gated Cl- channels picrotoxin strongly enhanced the expression of the gene in numerous cells which were arranged in neocortical layers II/III and V/VI. Since bicuculline methiodide can also block Ca(++)-activated K+ channels, the possible involvement of such channels was tested. However, apamin which blocks only Ca(++)-activated K+ channels had no effect on the expression of the proenkephalin gene indicating that the effect of bicuculline methiodide was due to inhibition of GABAA receptors. In addition, the GABAB receptor agonist baclofen increased the neocortical expression of the proenkephalin gene mainly in cells located in layers V/VI of the neocortex. The effect of baclofen was inhibited by the GABAB receptor antagonists CGP35348 and CGP52432. Also muscimol, an agonist at GABAA receptors, enhanced the expression of the proenkephalin gene. This effect was blocked by CGP52432 confirming previous observations that muscimol can also stimulate GABAB receptors. Our results indicate that GABA can regulate the expression of the opioid peptide in neocortical neurons in a bidirectional manner. The expression is suppressed via GABAA and enhanced via GABAB receptors.

Animals↗

Evaluation of autoreceptor-mediated control of [(3)H]acetylcholine release in rat and human neocortex.

In order to assess the autoinhibitory control of endogenous acetylcholine (ACh) in rat and human neocortex, slices of these tissues were prelabelled with [(3)H]choline, superfused continuously and stimulated electrically using various frequencies in the presence or absence of drugs. The autoinhibitory feedback control of [(3)H]ACh release was operative - despite the absence of blockers of ACh esterase - at stimulation frequencies >/= 3 Hz in rat and >/= 6 Hz in human neocortex tissue. At these frequencies the muscarinic antagonist atropine (0.1 microM) disinhibited the release of [(3)H]ACh in both species. Estimation of the biophase concentration of ACh near the autoreceptor in the rat neocortex from concentration-response curves of the muscarinic agonist oxotremorine revealed that at 3 Hz about 25% of the autoreceptors were activated by endogenously released ACh. This estimation is consistent with an increase in [(3)H]ACh release to about 120% of control values by complete blockade of autoreceptors with atropine. The observation that in human neocortical tissue presynaptic autoinhibition of [(3)H]ACh release is operative at stimulation frequencies >/= 6 Hz suggests that selective blockade of autoinhibition may also increase ACh release in the cortex of Alzheimer's disease patients, without additional blockade of the enzyme acetylcholinesterase.

Acetylcholine↗

The fate of Nissl-stained dark neurons following traumatic brain injury in rats: difference between neocortex and hippocampus regarding survival rate.

We studied the fate of Nissl-stained dark neurons (N-DNs) following traumatic brain injury (TBI). N-DNs were investigated in the cerebral neocortex and the hippocampus using a rat lateral fluid percussion injury model. Nissl stain, acid fuchsin stain and immunohistochemistry with phosphorylated extracellular signal-regulated protein kinase (pERK) antibody were used in order to assess posttraumatic neurons. In the neocortex, the number of dead neurons at 24 h postinjury was significantly less than that of the observed N-DNs in the earlier phase. Only a few N-DNs increased their pERK immunoreactivity. On the other hand, in the hippocampus the number of dead neurons was approximately the same number as that of the N-DNs, and most N-DNs showed an increased pERK immunoreactivity. These data suggest that not all N-DNs inevitably die especially in the neocortex after TBI. The fate of N-DNs is thus considered to differ depending on brain subfields.

Analysis of Variance↗

PTEN-mediated Akt activation in human neocortex during prenatal development.

Akt is a crucial factor for cell survival and migration. Phosphatase and tensin (PTEN) negatively regulates cell growth and survival by inhibiting PI3K-dependent signaling. PTEN also blocks Akt phosphorylation, a main downstream molecule of PI3K cascade. So far, no studies have shown PTEN expression and Akt phosphorylation levels in the developing human neocortex. Our hypothesis is that spatial and temporal expression of PTEN is likely to modulate developing human brain cortical modeling by regulating Akt activation. Therefore, our aim is to analyze the expression pattern of PTEN and phospho-Akt levels using immunohistochemistry, Western blot, and semiquantitative analysis in the developing human neocortex (n=13 fetuses from first, second, and third trimesters). PTEN expression was decreased parallel to development, but some cells revealed strong nuclear immunoreactivity in the developing neocortex while the active Akt level was increased. Double immunohistochemistry was performed for proliferating cell nuclear antigen (PCNA)-Tuj1 (as neuronal marker) and PCNA-GFAP (Glial marker) to the subsequent sections of PTEN and Akt-stained slides. PCNA (+) cells were mostly positive for glial fibrillary acidic protein (GFAP) and correlated with active-Akt immunoreactivity. Our results suggest that Akt-mediated signaling plays an active role in cell migration, survival, and cerebral cortical modeling throughout prenatal life and that PTEN is the most likely protein to regulate this signaling.

Blotting, Western↗

Isolation of neuronal progenitor cells from the adult human neocortex.

BACKGROUND: The reliability of harvesting neuronal progenitor cells (NPCs) from the adult human neocortex has not been established, with respect to preparing autologous cell cultures for transplantation in stroke and traumatic brain injured patients. METHOD: Enriched NPC cultures have been generated from nonneurogenic regions of the adult rodent brain by buoyancy-dependent fractionation, but the feasibility of using such a method to isolate NPCs from the adult human cortex has not been reported previously. To determine if a starter population of human adult cortical NPCs could be isolated for in vitro expansion using this method, tissue samples from five patients undergoing cortical resection for either epilepsy or trauma were assayed. FINDINGS: Cultured cells generated from all patients predominately expressed both the NPC marker nestin and neuron-specific beta-tubulin III. The presence of NPCs was verified by in vitro BrdU/beta-tubulin III co-labeling and increasing beta-tubulin expression in differentiating conditions. Despite the formation of aggregates in monolayer culture, cell proliferation as measured by BrdU incorporation was not as prevalent as that reported from rodent cultures generated by this protocol. CONCLUSIONS: NPCs isolated from the adult human neocortex using this method expressed beta-tubulin III in larger percentages than has been previously reported for NPCs isolated using other methods. As such, these data suggest the possibility of culturing dividing neuroblasts from the adult neocortex for further manipulation as transplantable cells.

Adolescent↗

Glial fibrillary acidic protein in astrocytes in the human neocortex.

Glial fibrillary acidic protein (GFAP), expressed in the brain by astrocytes, is one of the major immunocytochemical markers of these cells. The aim of the present work was to study the structure of GFAP-positive astrocytes in the human neocortex. Immunocytochemical confocal laser microscopy was used to characterize the main types of GFAP-immunoreactive astrocytes in the human neocortex. These were astrocytes of layer I, forming the superficial glial delimiting membrane, along with transmembrane astrocytes of layer I, with very long processes penetrating several layers of the cortex, astrocytes of the middle layers of the neocortex, mostly of the protoplasmic type and involved in forming perivascular delimiting membranes, and typical white matter fibrous astrocytes. These data may help unify assessments of histopathological processes seen in various types of gliosis in the CNS.

Adolescent↗

Gaba- and serotonin-immunoreactive structures and ca(2+)-binding protein in the neocortex of the reeler mouse mutant.

The transmitter organization of anomalously formed neocortex was studied in reeler mutant mice by immunohistochemical studies of GABA- and serotoninergic structures and Ca(2+)-binding protein. GABAergic structures were identified in terms of the localization of glutamate decarboxylase (GDC) within them, this being an enzyme involved in GABA synthesis. The neocortex of reeler mutant mice was found to contain an unusual distribution of cells morphologically and chemically identical to Cajal-Retzius cells - beneath layer I rather than in its upper third, as seen in normal animals. GDC-immunoreactive label accumulated in the neuropil of the intermediate and deep layers, layer I containing only occasional granules. Serotonin-immunoreactive fibers did not form superficial or deep plexuses, as seen in normal animals, though they did reach their innervation targets. Thus, the anomalously formed neocortex which lacks the typical cytoarchitectonic organization, showed abnormalities in the structure of both intrinsic and projectional transmitter systems.

Animals↗

Receptor-like protein tyrosine phosphatase zeta/RPTP beta is expressed on tangentially aligned neurons in early mouse neocortex.

Protein tyrosine phosphatase zeta (PTPzeta)/RPTPbeta is a chondroitin sulfate proteoglycan predominantly expressed in the brain. In this study, we examined immunohistochemical localisation of PTPzeta in the mouse telencephalon from embryonic day 9.5 (E9.5) to E15.5. During E10.5-E12.5, immunoreactivities for PTPzeta are specifically observed on the tangentially aligned neurons at the preplate (PP) of the neocortex, as well as on the neurons at the mantle layer (ML) of the ganglionic eminences (GEs). Likewise, neurons immunoreactive for CR50, a marker for Cajal-Retzius neurons, are aligned from the ML of the ganglionic eminences to the PP of the neocortex and co-express PTPzeta. During E13.5-E15.5, PTPzeta-positive neurons are present at the subplate (SP) as well as at the marginal zone (MZ) of the neocortex. These results indicate that PTPzeta is a useful marker for early-generated neocortical neurons in mice: Cajal-Retzius neurons as well as the subplate neurons.

Aging↗

Behavioural state affects saccades elicited electrically from neocortex.

Reviewed is how behavioural context influences saccadic eye movements elicited electrically from the neocortex of monkeys. Factors found to affect stimulation-evoked saccades include (1) motor state, i.e. whether stimulation is delivered during free-viewing, or during or after active fixation, or before an animal is about to execute a saccade to a target location, and (2) reward delivery, i.e. the characteristics and timing of reward, which can promote or inhibit the evocation of saccades. We conclude that anyone using electrical stimulation in neocortex to study sensory and cognitive processes must control for the possibility that stimulation of cortex is merely generating a saccade vector whose expression is being obscured by the behavioural paradigm in use. Areas of neocortex from which saccades can be evoked using low currents (<100 microA) are surprisingly widespread and include regions traditionally considered within the sensory domain (e.g. V1, V2, V4, and MT), in addition to visuomotor regions such as the lateral intraparietal area, the dorsomedial frontal cortex, the frontal eye fields, and the prefrontal cortex. This is especially true once the behavioural state of a stimulated animal is put under experimental control.

Animals↗