PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cerebral Cortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 91 records · Page 5Linked to original sources
PubMed1995

Apoptotic DNA fragmentation in the rat cerebral cortex induced by permanent middle cerebral artery occlusion.

Recent investigations have demonstrated internucleosomal DNA fragmentation in ischemic neuronal tissue. This type of fragmentation is characteristic of programmed cell death or apoptosis and suggests that neuronal death in stroke may be more complex than simple necrotic death. The present experiments provide a detailed examination of the regional localization and time course for apoptotic DNA fragmentation in the cerebral cortex following focal cerebral ischemia. Spontaneously hypertensive rats were subjected to permanent right middle cerebral artery occlusion and the cerebral cortices were examined for evidence of DNA fragmentation using electrophoretic, flow cytometric, and histological approaches. An electrophoretic examination of cortical DNA at 24 h after the occlusion indicated that the majority of nucleosomal ladders were in the transition zone or penumbra and the core of the infarction, with no fragmentation apparent in the contralateral normal cortex. A flow cytometric analysis of DNA fragmentation in intact cells revealed a similar pattern, with increased fragmentation observed in ischemic cortex vs. the contralateral cortex. Saggital sections taken 1.5 mm lateral to midline were collected from animals at 1, 4, and 24 h after the infarction and DNA fragmentation was examined histologically by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) staining. Quantitative analysis of these sections indicated that DNA fragmentation can be observed in the anterior and central area of the infarctions as soon as 1 h after the occlusion and that the extent and magnitude of the fragmentation increases at 4 and 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Focal ischemia in the cerebral cortex has an effect on the neurohypophysis. I. Ultrastructural changes in capillary vessels of the neurohypophysis after focal ischemia of the cerebral cortex.

OBJECTIVES: In our investigations we have reported that photochemical reaction leading to brain ischemia can also be precipitated with visible light from a non-coherent light source. It was revealed that focal cerebral ischemia after photochemical reaction cause the alterations in the capillaries ultrastructure and perivascular spaces of the barrier-competent regions of the brain. The purpose of this study is to first characterize the ultrastructural morphological consequences of photochemically induced ischemia in the cerebral cortex on the capillaries of neurohypophysis as the barrier-free region of the brain. METHOD: We used a model of ischemic brain damage due to obliteration of microvessels following the photochemical reaction. Rats were treated with an intravenous injection of rose bengal and irradiated from a halogen lamp source through an intact cranium to precipitate microvascular damage. Material for electron microscopic studies were sampled from the neurohypophysis 1 and 4 days after irradiation (4 animals in each group) in experimental group and 1 and 4 days after a rose bengal injection in control group. RESULTS: Investigations in transmission electron microscopy revealed platelet aggregation on the endothelium preceded by its early ultrastructural damage. In the capillaries of the neurohypophysis, one and four days after irradiation, numerous microthrombi adhering to the damaged endothelium were present. The capillary vessels contained a continuous, rather than a fenestrated endothelium. The basement membrane was thickened, blurred and locally multiplicated. CONCLUSION: Our results show that experimentally-induced thrombosis of cortical microvessels leads to alterations in the capillaries of neurohypophysis.

Animals↗
PubMed2006

The role of intermediate progenitor cells in the evolutionary expansion of the cerebral cortex.

The vertebrate cerebral cortex varies from the 3-layered dorsal cortex of reptiles to the 6-layered lissencephalic cortex characteristic of rodents and to the 6-layered gyrencephalic cortex typical of carnivores and primates. Distinct developmental mechanisms may have evolved independently to account for the radial expansion that produced the multilayered cortex of mammals and for the tangential expansion of cortical surface area that resulted in gyrencephalic cortex. Recent evidence shows that during the late stages of cortical development, radial glial cells divide asymmetrically in the ventricular zone to generate radial glial cells and intermediate progenitor (IP) cells and that IP cells subsequently divide symmetrically in the subventricular zone to produce multiple neurons. We propose that the evolution of this two-step pattern of neurogenesis played an important role in the amplification of cell numbers underlying the radial and tangential expansion of the cerebral cortex.

Aging↗
PubMed2002

Involvement of reelin and Cajal-Retzius cells in the developmental formation of vertical columnar structures in the cerebral cortex: evidence from the study of mouse presubicular cortex.

The mammalian cerebral cortex is organized into horizontal and vertical arrays of neurons and their fiber connections that form anatomically and physiologically distinct laminar and columnar compartments. However, the developmental mechanism(s) underlying this dichotomous pattern remains a mystery. We provide anatomical evidence suggesting that reelin, a diffusible protein produced and secreted by Cajal-Retzius cells, is involved in the developmental formation of the vertical cell structures in the mouse presubicular cortex, the unique site where the vertical columnar arrays of cortical plate neurons and their dendritic branches are clearly identified during the early postnatal period. Our results also suggest that reelin plays a role in the formation of these vertical structures by acting as an inhibitory or stop signal for cortical plate neurons and their dendritic extensions. In addition to having perturbed horizontal laminae, reeler mutant mice, lacking reelin, display disruption of these vertical structures. Based on the present findings, we hypothesize that reelin and Cajal-Retzius cells regulate the developmental formation of not only horizontal laminations, but also vertical columnar structures in the cerebral cortex.

Animals↗
PubMed2001

Functional nicotinic acetylcholine receptor expression in stem and progenitor cells of the early embryonic mouse cerebral cortex.

The adult cerebral cortex contains nicotinic acetylcholine (ACh) receptors vital to cortical function. However, little is known about the assembly of embryonic nicotinic receptor subunits into functional receptors or whether they play an active role in cortical development. We now report evidence of functional nicotinic acetylcholine receptor channels in fetal mouse cerebral cortex as early as embryonic day 10 (E10), when the cortex consists of dividing stem and progenitor cells. Patch-clamp electrophysiological measurements indicate that nicotine and ACh evoke sizable inward currents characteristic of nicotinic receptors, that are strongly rectifying with a reversal potential near 0 mV. Three different nicotinic agonists, ACh, nicotine, and dimethylphenylpiperazinium, evoked cytosolic Ca(2+) signals. Agonist-evoked Ca(2+) signals and electrophysiological responses were found in greater than 70% of all E10-E11 cells tested and were blocked by nicotinic receptor antagonists. The Ca(2+) response to nicotinic agonists was markedly prolonged in cells from early embryonic stages relative to later stages of development. alpha3, alpha4, and alpha7 receptor subunit proteins were detected immunocytochemically in cortical cells from E10 to birth. The incidence of each subunit declined with embryonic age, suggesting a role in early development. We discuss the possible function of nicotinic receptors in early cortical development and their role as a target for nicotine in the developmental pathologies associated with the fetal tobacco syndrome.

Acetylcholine↗
PubMed1998

Induction of tyrosine hydroxylase gene expression in human foetal cerebral cortex.

Human foetal cerebral cortex (9-14 weeks gestational age) was dissected out and cultured in microwell plates. It was then treated with brain-derived neurotrophic factor (BDNF, 50 ng/ml), dopamine (10 mM) or their combination. After 5 weeks of this treatment tyrosine hydroxylase (TH)-immunopositive neurones were detected at a level of 0.73% of total neurones present. This represented 300-500 TH + neurones per microwell. None were seen in untreated cultures. This correlates with induction of the entire dopaminergic phenotype in foetal rat cerebral cortex (E1214) by the same co-treatment applied for a much shorter time period (7 days), which implies that the complete dopaminergic phenotype is also induced in cultured human foetal tissue over a longer period, reflecting the 5-fold longer neuronal gestational period.

Animals↗
PubMed1999

Molecular gradients and compartments in the embryonic primate cerebral cortex.

The mature cerebral cortex is divided into morphologically distinct, functionally dedicated and stereotypically connected cortical areas. How might such functional domains arise during development? To investigate possible intrinsic programs within the embryonic cerebral cortex we examined patterns of gene expression early in corticogenesis. We performed these studies using the developing macaque monkey because of the size, complexity, areal make-up and the extended nature of its cortical development. Here, we present results for two types of molecules. (i) Transcription factors -- gene products that bind DNA and activate transcription, directing cellular fates through cascades of gene expression. We find that the transcription factors TBr-1, Lhx-2, Emx-1 and a novel POU domain-containing gene are differentially expressed within the forming primate forebrain, and are present in gradients across the neocortex. (ii) The EphA receptor tyrosine kinases -- gene products that mediate cellular recognition in many embryonic systems. Individual members of this family are expressed during primate corticogenesis in pronounced gradients and/or well-defined compartments with distinct boundaries. Together, these results suggest that at least two modes of grouping cells within the neocortex exist: the graded patterning of cells across its full anteroposterior extent and the parcellation of cells into defined domains. Moreover, emergence of molecular differences between regions of the cortical plate, prior to the arrival of afferent and formation of efferent connections, suggests that the initial cellular parcellation in the telencephalon is cell-autonomously regulated. This initial independence from peripheral influences supports the existence of an intrinsic protomap that may function both to differentially attract and respond to specific afferents, thus predicting the functional map of the mature cortex.

Animals↗
PubMed2002

Localization and functional role of hepatocyte growth factor (HGF) and its receptor c-met in the rat developing cerebral cortex.

Development of the cerebral cortex is a series of precisely timed proliferative, migratory, and maturational processes. Hepatocyte growth factor (HGF) is a pleiotrophic cytokine, which plays important roles in the organogenesis and regeneration of various tissues, both during development and in the adult, due to its mitogenic, motogenic and morphogenic activities. In the present study, we examined expression and functional roles of HGF and c-Met during development of the rat cerebral cortex. Quantitative competitive reverse transcription-polymerase chain reaction (RT-PCR) revealed that expression levels of c-met and HGF mRNAs were increased in the cerebral cortex during late embryonic development and peaked at E18. Immunohistochemical analyses revealed that c-Met-immunoreactivity (IR) was localized to the preplate (PP), with weaker-IR in neuroepithelial layer (NE) at embryonic day 14 (E14). At E16, c-Met-IR was present in the cortical plate (CP) and the intermediate zone (IZ), with a weak presence in the ventricular zone (VZ). On the other hand, HGF-IR was present in NE and VZ at E14 and E16, respectively. HGF-IR appeared in cortical plate tissue from E16 onward. Double labeling immunofluorescent cytochemical studies revealed that c-Met-IR was localized both in TuJ-1-IR- and non-TuJ-1-IR-cells, purified from E18 cerebral cortex in vitro, suggesting the presence of c-Met-IR in postmitotic neurons as well as in neuroepithelial cells. c-Met-IR was strong in cell bodies and neurites shortly after in vitro culture, while at 7DIV c-Met-IR decreased in neurites and was evident in growth cones. HGF dose dependently supported neuronal survival in vitro under serum-deprived conditions. In a transwell culture chamber, HGF increased neuronal migration, and co-incubation with functional blocking antibody against HGF abrogated this motogenic effect of HGF. These lines of evidence suggest that HGF is involved in the development and maintenance of cortical neurons during differentiation, motogenesis, neuritogenesis and neuronal survival.

Animals↗
PubMed1989

Studies on the vasculogenesis in rat cerebral cortex.

The cerebral cortices are nourished by blood circulating through a capillary network branching from parent arteries. In this paper, vasculogenesis of the cerebral cortices in developing rats (11-18 days after birth) was studied by light and electron microscopy after intravenous administration of horseradish peroxidase (HRP). In the first phase of vasculogenesis, tentacles grew out from the distal end of the vascular cord (tip cells), and in the second phase, they extended to the afferent blood vessel. The reaction product of HRP was distributed not only in the primitive vascular lumen, but also in the peripheral extravascular space of the vascular cord. Most tentacles were free from reaction product, but, in some cases where reaction product was detected, the intercellular spaces had spread into the tip cells and reached the root of the tentacles. After the tentacles contacted the afferent vascular cord, the two vascular cords approached and fused with each other. Blood serum was able to circulate between the two vascular cords via the irregular interstices formed among the endothelial cells, cytoplasmic processes, and tentacles. Later, the primitive vascular lumen developed to a sufficient size to allow for the circulation of blood cells. The sequential events in the process of fusion between two vascular cords are illustrated. The following two points were also noticed in this study: 1) during cerebral vasculogenesis, degeneration and vacuolization in primitive endothelial cells occurred only in some of the serial sections and did not play a significant role in the formation of vascular lumen, and 2) cerebral pericytal macrophages (CPM) (classified as fluorescent granular perithelial cells by the authors) appeared close to the vascular cord, although the biological meaning of it remained unknown in the present investigation.

Animals↗
PubMed1985

Involvement of benzodiazepine recognition sites in the foot shock-induced decrease of low affinity GABA receptors in the rat cerebral cortex.

The cerebral cortices of rats habituated to the handling manipulation that precedes sacrifice by guillotine (unstressed rats) have a higher number of low affinity GABA receptors than naive rats (stressed rats). Foot shock stress delivered to handling-habituated rats 5 min before sacrifice decreased the number of low affinity GABA receptors to the level found in naive animals, while leaving almost unchanged the [3H]GABA binding in the latter group. Since benzodiazepine (BZ) recognition sites are the target through which benzodiazepines modulate the emotional states of the animals, we investigated whether these receptors were involved in the action of foot shock stress on GABA binding. The in vitro addition of diazepam (5 X 10(-6) M) to cortical membranes from foot-shocked handling-habituated rats brought back the number of low affinity GABA receptors to the level found in cortical membranes from handling habituated rats. Moreover, the effect of foot shock on low affinity GABA receptors was completely antagonized in vivo by pretreatment with the specific benzodiazepine antagonist Ro15-1788 (30 mg/kg per os). Since the effect of foot shock on [3H]GABA binding is mimicked by the in vitro addition of beta-carbolines to cortical membranes from handling habituated rats, our working hypothesis is that an endogenous ligand for BZ recognition sites, possessing beta-carboline-like properties, is released during foot shock stress.

Animals↗
PubMed1988

Layer VII of rodent cerebral cortex.

The cerebral isocortex is usually considered to be a 6-layered structure. Our anatomical findings suggest that layer VII be recognized as a distinct entity in rodent isocortex. This conclusion is based on cytoarchitectural, fiberarchitectural, connectional and developmental data.

Animals↗
PubMed1994

Synaptic pathology and glial responses to neuronal injury precede the formation of senile plaques and amyloid deposits in the aging cerebral cortex.

The cerebral cortices of macaques (ranging in age from 10 to 37 years; n = 17) were analyzed by immunocytochemistry and electron microscopy to determine the cellular and subcellular localizations of the amyloid precursor protein and beta-amyloid protein, the cellular participants in the formation of senile plaques and parenchymal deposits of the beta-amyloid protein, and the temporal/spatial development of these lesions. Amyloid precursor protein was enriched within the cytoplasm of pyramidal and nonpyramidal neuronal cell bodies in young and old monkeys. In the neuropil, amyloid precursor protein was most abundant within dendrites and dendritic spines; few axons, axonal terminals, and resting astrocytes and microglia contained the amyloid precursor protein. At synapses, amyloid precursor protein was found predominantly within postsynaptic elements and was enriched at postsynaptic densities of asymmetrical synapses. The earliest morphological change related to senile plaque formation was an age-related abnormality in the cortical neuropil characterized by the formation of dense bodies within presynaptic terminals and dendrites and an augmented localization of the amyloid precursor protein to astrocytes and microglia. In most monkeys > 26 years of age, the neocortical parenchyma exhibited neuritic pathology and plaques characterized by swollen cytoplasmic processes, interspersed somata of neurons, and reactive glia within or at the periphery of senile plaques. Neurites and reactive astrocytes and microglia within these plaques were enriched with the amyloid precursor protein. In diffuse plaques, nonfibrillar beta-amyloid protein immunoreactivity was visualized within cytoplasmic lysosomes of neuronal perikarya and dendrites and the cell bodies and processes of activated astrocytes and microglia. In mature plaques, beta-amyloid protein immunoreactivity was associated with extracellular fibrils within the parenchyma; some cytoplasmic membranes of degenerating dendrites and somata as well as processes of activated glia showed diffuse intracellular beta-amyloid protein immunoreactivity. We conclude that morphological abnormalities at synapses (including changes in both pre- and postsynaptic elements) precede the accumulation of the amyloid precursor protein within neurites and activated astrocytes and microglia as well as the deposition of extracellular fibrillar beta-amyloid protein; neuronal perikarya/dendrites and reactive glia containing the amyloid precursor protein are primary sources of the beta-amyloid protein within senile plaques; and nonfibrillar beta-amyloid protein exists intracellularly within neurons and nonneuronal cells prior to the appearance of extracellular deposits of the beta-amyloid protein and the formation of beta-pleated fibrils.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1986

[Dendritic action potentials of pyramidal neurons of the sensomotor cortex of the cerebral cortex of the cat].

The intracellular activity of pyramidal tract neurons during electrical stimulation of ventro-lateral and ventro-postero-lateral nuclei of thalamus was studied in acute experiments on cats immobilized by myorelaxants. Both somatic and presumably dendritic spikes (d-spikes) were observed. The latter were characterized by relatively low and variable (5-60 mV) amplitude; d-spikes occurred both spontaneously and in response to single shock and tetanic (8-14/s) stimulation of the thalamus. They were also induced by intracellular depolarizing current pulses and thalamic stimulation following iontophoretic application of strychnine. Simultaneously generated somatic and d-spikes revealed no collision between each other. Intracellular hyperpolarizing current pulses abolished only somatic spikes, while d-spikes were not affected. Dendritic origin with multiple generation zones of these variable spikes is suggested. Possible functional role of d-spike is discussed.

Action Potentials↗