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At least 307 records · Page 17Linked to original sources

PubMed1999

Differential expression of the small GTP-binding proteins RhoA, RhoB, Cdc42u and Cdc42b in developing rat neocortex.

Studies with cultured cells indicate that small GTPases of the Rho family may be involved in cell proliferation, differentiation, as well as migration. Therefore, we have studied the expression of four members of this protein family, i.e., RhoA, RhoB, the ubiquitous Cdc42u, and brain specific Cdc42b, during the embryonic and early postnatal development of rat neocortex. A clear isoform specificity of expression was found during the prenatal development. Thus, RhoA and Cdc42u were present in the proliferation zone while RhoB and Cdc42b were expressed only in the cortical plate where neural cells settle and differentiate. After birth, this isoform specificity quickly disappeared so that already at postnatal day 8 the adult pattern of expression was present. Our findings of a differential expression of the small GTP-binding proteins RhoA, RhoB, Cdc42u and Cdc42b in developing brain neocortex suggest isoform specific functions during neurogenesis and differentiation.

Animals↗

PubMedDate not supplied

Autoradiography of L-type and N-type calcium channels in aged rat hippocampus, entorhinal cortex, and neocortex.

The present study examined brains from 6, 17, and 32 month old male (F344x BN)F1 rats to determine whether there was any age-related change in the distribution or density of L-type and N-type Ca2+ channels in hippocampus, entorhinal cortex, and neocortex, areas commonly involved in the generation of epileptic seizures. The L-type channel antagonist PN200-110 and the N-type channel antagonist omega-conotoxin GVIA were used to determine specific binding densities and the autoradiographic distribution of ligand binding was quantified by computer-assisted densitometry. One-way ANOVA noted a significant variance in the mean value of binding density between different age groups only in neocortex laminae IV-VI for [(3)H]PN200-110 binding (P < 0.05). Post-hoc testing indicated that the mean value of the 17 month old group was significantly less than those of the 6 and 32 month old groups (P < 0.05). These results indicate no overall age-related change in the number of L-type and N-type Ca2+ channels in brain areas frequently involved in seizure activity and suggest that age-related changes in brain Ca2+ physiology may be associated with changes in voltage-gated Ca2+ channel function rather than channel number.

Age Factors↗

PubMed2001

Endogenous acetylcholine facilitates epileptogenesis in immature rat neocortex.

In the presence of the gamma-amino butyric acid-A (GABAA) antagonist bicuculline methiodide (50 microM), synchronous spontaneous and evoked potentials were recorded extracellularly from the deep layers of immature neocortex (postnatal days 10-31, P10-P31) in vitro. Addition of the anticholinesterase eserine (10 microM) depressed the amplitude (by 29.5+/-6.6%, n=13) and duration (by 26.3+/-4.7%, n=11) of the evoked field potentials in 13/19 slices (68%), and increased significantly the rates of occurrence of spontaneous epileptiform discharges or induced them in 9/19 slices (47%). All these effects were blocked by the muscarinic antagonist atropine (2.5 microM, n=3), suggesting that they were mediated by the activation of muscarinic receptors by endogenous acetylcholine. The cholinergic inhibitory effect is unlikely to terminate seizures, while the excitatory effect, could conceivably promote or aggravate their manifestation. In conclusion, these findings demonstrate that endogenous acetylcholine may contribute to epileptogenesis in immature neocortex.

Acetylcholine↗

PubMed2001

Evidence that the HIV-1 coat protein gp120 causes neuronal apoptosis in the neocortex of rat via a mechanism involving CXCR4 chemokine receptor.

The HIV-1 coat protein, gp120 (100 ng given intracerebroventricularly (i.c.v.) daily for seven consecutive days) causes DNA fragmentation in the brain neocortex of rat. In neocortical cells bearing ultrastructural features typical of apoptosis, electron microscopy revealed specific immunopositivity for neurofilament cytoskeletal proteins, suggesting the neuronal nature of dying cells. Neuronal apoptosis by gp120 implicates CXCR4 chemokine receptors; in fact, in rats receiving a single daily, non-neurotoxic, dose of SDF-1alpha (0.25 pmoles given i.c.v. for 7 days before gp120), the natural ligand of CXCR4 receptor, apoptosis was significantly hindered. The mechanism of SDF-1alpha protection involves inhibition of gp120-enhanced expression of IL-1beta, a cytokine implicated in the mechanisms of apoptosis induced by the viral protein in the neocortex of rat.

AIDS Dementia Complex↗

PubMed1998

Dysplastic neocortex and subcortical heterotopias in methylazoxymethanol-treated rats: an intracellular study of identified pyramidal neurones.

Intracellular recordings were obtained using biocytin-filled electrodes from 78 neurones located in both dysplastic neocortex and subcortical heterotopic aggregates in a model of neuronal migration disorder induced in rats by means of a double methylazoxymethanol injection given on embryonic day 15. Both regular spiking and intrinsically bursting pyramidal neurones were found in all of the examined structures and were synaptically activated by subcortical stimulation. In a neuronal subpopulation (22%) located in the neocortex as well as in the subcortical heterotopic aggregates, the injection of depolarising current pulses elicited aberrant firing patterns, consisting of repetitive bursts of APs that gradually increased in duration and eventually merged in a long-lasting discharge. The gradual development of this 'excessive' bursting behaviour suggests a progressive run-down of the slow components of the hyperpolarising afterpotential.

Animals↗

PubMed1998

Evidence for the activity of five adenosine-3',5'-monophosphate-degrading phosphodiesterase isozymes in the adult rat neocortex.

In the present study, the expression of the activity of adenosine-3',5'-monophosphate-degrading phosphodiesterases (cAMP-PDEs) was analyzed in rat neocortex homogenates. Following separation by anion-exchange chromatography, the isozymes were characterized by their sensitivity to modulators and by their kinetic properties. We identified the activity of five distinct cAMP-PDE isozymes: two calcium/calmodulin-dependent forms (PDE 1), one PDE 2 isozyme stimulated by guanosine-3',5'-monophosphate (cGMP), one cGMP-inhibited form (PDE 3) and a cAMP-specific, rolipram-sensitive form (PDE 4). Our study provides, for the first time, evidence for the existence of PDE 3 enzyme activity in rat neocortex and predicts the expression of at least two isoforms (splice variants) of PDE 1A in this brain area. The existence of different cAMP-degrading phosphodiesterases modulated by different intracellular second messengers (calcium and cGMP) suggests that the activity of neocortical neurons and glia cells is regulated, inter alia, by a 'crosstalk' between calcium-, cGMP- and cAMP-dependent second messenger pathways.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1998

Chronic elevation of amyloid precursor protein expression in the neocortex and hippocampus of rats with selective cholinergic lesions.

Overexpression or aberrant processing of the beta-amyloid precursor protein (APP) and loss of cortical cholinergic function represent two hallmark pathological features of Alzheimer's disease, although it is still unclear whether these alterations take place independently or in an inter-related manner. In the present study, the possible relationships between altered APP expression and cholinergic hypofunction in the neocortex and hippocampus were addressed histologically following selective and complete (90-95%) removal of the basal forebrain cholinergic neurons by the 192 IgG-saporin immunotoxin, at a dose (5.0 microg, intraventricularly) producing profound and permanent cognitive deficits. Computer-aided densitometric analyses revealed, at 6 months post-lesion, a virtually complete loss of terminal cholinergic innervation in various neocortical and hippocampal regions (up to 80%), which correlated highly with the marked (up to 71%) increases in APP expression measured in the same territories. The present results indicate that the integrity of ascending basal forebrain cholinergic inputs to the neocortex and hippocampus may be required for the maintenance of physiological levels of APP expression in the same regions, thus providing a novel rationale for interventions aimed at restoring or enhancing cortical cholinergic neurotransmission.

Amyloid beta-Protein Precursor↗

PubMed2000

Morphological and electrophysiological properties of atypically oriented layer 2 pyramidal cells of the juvenile rat neocortex.

We used whole-cell patch clamp recordings combined with intracellular dye-filling to examine the morphological and electrophysiological properties of atypically oriented pyramidal cells located at the layer 1/2 border of the juvenile rat neocortex. Orientation of the apical dendrite varied from oblique (>20 degrees from vertical) to truly horizontal (90 degrees from vertical). The length of the apical dendrite ranged from 150 to 400 microm. The total horizontal domain of the dendritic tree (including basal dendrites) of the longest horizontal pyramids exceeded 500 microm, but we also found short horizontal cells with horizontal dendritic domains of less than 300 microm. In addition, atypically oriented pyramids had long horizontal axon collaterals in layer 1/2. Electrophysiologically, atypically oriented pyramidal cells had intrinsic membrane properties similar to regularly oriented pyramids that have been described in the superficial layers at this age in the rat. Cells that fired repetitively were all regular spiking. In addition, we identified a subgroup of neurons (20%) in this sample, which were unable to fire more than a few spikes at the beginning of the current pulse. We suggest that the unique orientation and size of their dendritic trees and the length and arrangement of their local axons collaterals make atypically oriented pyramids in layer 2 ideally suited to perform horizontal integration of synaptic inputs in the neocortex.

Animals↗

PubMed2000

Kainic acid induces distinct types of epileptiform discharge with differential involvement of hippocampus and neocortex.

Systemic administration of kainic acid (KA), an excitatory amino acid agonist, provides a model of epilepsy due to increased neural excitation. We examined discharges using multi-channel EEG recording and spectral analysis in rats implanted with neocortical and hippocampal electrodes after intravenous infusion of KA (10 mg/kg), until and including the first convulsive seizure. Gamma activity (30-80 Hz) increased in hippocampus from 3-9 min after KA administration. Two types of preconvulsive bilateral rhythmic discharges were observed, both consisting of generalised high voltage sharp waves at low frequencies (<10 Hz) mixed with fast oscillations (<20 Hz): (1) generalised non-convulsive discharges (GNCD) occurred in all animals and (2) spike-wave discharges (SW), predominantly localised in neocortex, occurred in 45% of animals. Convulsive seizure evolved out of a GNCD. Spectral profiles of epileptiform discharges were characterised by an increase in power of low (<10 Hz) and high (beta and gamma range, 20-80 Hz) frequencies which were differently expressed in neocortex and hippocampus. Thus, in this model of convulsive epilepsy caused by increased excitation, there is an early increase in gamma activity, a process that might contribute to synchronisation, and two distinct types of bilateral discharges, hippocampal-neocortical (GNCD) and preferentially neocortical (SW). Neocortical, not hippocampal, changes in EEG power correlated with development of convulsive behaviours.

Animals↗

PubMed2000

Ontogeny of the dopamine D2 receptor mRNA expressing cells in the human hippocampal formation and temporal neocortex.

The study details the cellular expression of the dopamine D2 receptor mRNA in the human temporal lobe during prenatal development. At 13 embryonic weeks (E13) D2 mRNA was widely expressed in the temporal lobe. At this time point in the dentate gyrus D2 mRNA positive cells first appeared at the outer border of the granular layer and their number increased with development. The CA1 exhibited the highest level of D2 mRNA expression. By E19-25 the hippocampal formation underwent rapid morphological maturation. D2 mRNA expression became more uniform and dense in the ammonic subfield. At all ages the subiculum appeared more mature morphologically but less intensely stained for D2 mRNA than the ammonic fields. In the entorhinal cortex D2 mRNA expression was most conspicuous in the future layer II at all ages. In the temporal neocortex D2 mRNA-positive cells were detected in the subplate and cortical plate. Differentiation of the cortical plate was accompanied by concentration of D2 mRNA-positive cells in layer V. The most conspicuous cells expressing D2 mRNA were found in the marginal zone of all regions and resembled Cajal-Retzius cells in morphology and location. Density of putative Cajal-Retzius cells expressing D2 mRNA decreased with development. They all but disappeared from the hippocampal areas by mid gestation, but in the temporal neocortex occasional cells were seen even at term. Early and widespread but region and cell type specific expression of D2 receptor mRNA suggests an important role of this DA receptor subtype in prenatal development of the human temporal lobe.

Brain Chemistry↗

PubMed2002

Neurofilament triplet proteins are restricted to a subset of neurons in the rat neocortex.

The cellular localisation of neurofilament triplet subunits was investigated in the rat neocortex. A subset of mainly pyramidal neurons showed colocalisation of subunit immunolabelling throughout the neocortex, including labelling with the antibody SMI32, which has been used extensively in other studies of the primate cortex as a selective cellular marker. Neurofilament-labelled neurons were principally localised to two or three cell layers in most cortical regions, but dramatically reduced labelling was present in areas such as the perirhinal cortex, anterior cingulate and a strip of cortex extending from caudal motor regions through the medial parietal region to secondary visual areas. However, quantitative analysis demonstrated a similar proportion (10-20%) of cells with neurofilament triplet labelling in regions of high or low labelling. Combining retrograde tracing with immunolabelling showed that cellular content of the neurofilament proteins was not correlated with the length of projection. Double labelling immunohistochemistry demonstrated that neurofilament content in axons was closely associated with myelination. Analysis of SMI32 labelling in development indicated that content of this epitope within cell bodies was associated with relatively late maturation, between postnatal days 14 and 21. This study is further evidence of a cell type-specific regulation of neurofilament proteins within neocortical neurons. Neurofilament triplet content may be more closely related to the degree of myelination, rather than the absolute length, of the projecting axon.

Animals↗

PubMed1997

Double bouquet cell axons in the human temporal neocortex: relationship to bundles of myelinated axons and colocalization of calretinin and calbindin D-28k immunoreactivities.

We have examined the distribution of double bouquet cell axons, immunocytochemically stained for the calcium-binding proteins calretinin and calbindin D-28k in the human temporal neocortex, in relation to bundles of myelinated axons (originating from pyramidal cells) and the colocalization of these calcium-binding proteins. The large number and regularity of distribution of double bouquet cell axons was clearly visualized in tangential sections from cortical layers III--V. In these sections, we estimated that the mean number +/- standard deviation of double bouquet cell axons per 10,000 microns2 was 11.65 +/- 0.44 with a mean diameter of 12.10 +/- 0.63 microns and a mean center-to-center spacing of 29.8 +/- 0.91 microns. These values are very similar to those previously reported in the monkey neocortex. The distribution of double bouquet cell axons was closely related to bundles of myelinated axons; there was overlapping with basically a one-to-one correspondence. Finally, double-label immunofluorescence experiments revealed that the vast majority of double bouquet cell axons immunoreactive for calbindin were also stained for calretinin. Since relatively few cell somata were double-labeled in the human temporal cortex, we concluded that double bouquet cells may represent a significant subpopulation of neurons that colocalize these calcium-binding proteins.

Adult↗

PubMedDate not supplied

Prenatal administration of nicotine results in dopaminergic alterations in the neocortex.

This study examined the effect of two high doses (3 or 6 mg/kg/day) of nicotine administrations via injections to pregnant rats on the dopaminergic, serotonergic, and noradrenergic systems in six brain regions in young adult male rats. The 3 mg/kg/day and 6 mg/kg/ day nicotine exposure resulted in significant decreases in dihydroxyphenylacetic acid (DOPAC) content in the neocortex and in both the neocortex and in the midbrain plus pons medulla, respectively, without any effects on the other brain regions such as the hypothalamus or striatum. No significant effects of prenatal nicotine were found on norepinephrine, serotonin, or 5-hydroxy-3-indolacetic acid levels. These data demonstrated that prenatal nicotine induced disturbances in the dopaminergic system in the young adult period. Furthermore, the region-specific reductions in the DOPAC content suggests that the exposure to a high dose of nicotine in utero might cause a predisposition to diseases related to a dopaminergic dysfunction in the frontal cortex.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1999

Cellular and molecular guidance of GABAergic neuronal migration from an extracortical origin to the neocortex.

Formation of the normal mammalian cerebral cortex requires the migration of GABAergic inhibitory interneurons from an extracortical origin, the lateral ganglionic eminence (LGE). Mechanisms guiding the migratory direction of these neurons, or other neurons in the neocortex, are not well understood. We have used an explant assay to study GABAergic neuronal migration and found that the ventricular zone (VZ) of the LGE is repulsive to GABAergic neurons. Furthermore, the secreted protein Slit is a chemorepellent guiding the migratory direction of GABAergic neurons, and blockade of endogenous Slit signaling inhibits the repulsive activity in the VZ. These results have revealed a cellular source of guidance for GABAergic neurons, demonstrated a molecular cue important for cortical development, and suggested a guidance mechanism for the migration of extracortical neurons into the neocortex.

Animals↗

PubMed2001

Embryonic regionalization of the neocortex.

Understanding the development of the vertebrate brain and in particular that of the neocortex, where high brain functions reside, remains one of the most difficult and exciting tasks in biology. In this review, we discuss recent experimental evidence as well as different possibilities for the intrinsic regionalization of the embryonic dorsal telencephalon, which may be related to the formation of distinct functional areas in the adult neocortex.

Animals↗

PubMed2001

Place- and time-dependent expression of mouse sFRP-1 during development of the cerebral neocortex.

Wnts are a family of secreted proteins involved in multiple developmental mechanisms during nervous system development, including cell proliferation, cell migration, axon guidance and specification of cell positional information. We report here the expression of sFRP-1 mRNA, encoding a putative inhibitor of Wnt, in the developing mouse neocortex during the entire period when neurons for the neocortex are born. We show that sFRP-1 mRNA expression is spatially restricted to the proliferative zones during the period, when neurons are known to be generated in large numbers for the enlarging cortical plate.

Animals↗

PubMedDate not supplied

Anatomical and functional differentiation of glutamatergic synaptic innervation in the neocortex.

Pyramidal neurons are the principal neurons of the neocortex and their excitatory impact on other pyramidal neurons and interneurons is central to neocortical dynamics. A fundamental principal that has emerged which governs pyramidal neuron excitation of other neurons in the local circuitry of neocortical columns is differential anatomical and physiological properties of the synaptic innervation via the same axon depending on the type of neuron targeted. In this study we derive anatomical principles for divergent innervation of pyramidal neurons of the same type within the local microcircuit. We also review data providing circumstantial and direct evidence for differential synaptic transmission via the same axon from neocortical pyramidal neurons and derive some principles for differential synaptic innervation of pyramidal neurons of the same type, of pyramidal neurons and interneurons and of different types of interneurons. We conclude that differential anatomical and physiological differentiation is a fundamental property of glutamatergic axons of pyramidal neurons in the neocortex.

Animals↗

PubMed2006

Canadian Association of Neurosciences review: postnatal development of the mammalian neocortex: role of activity revisited.

The mammalian neocortex is the largest structure in the brain, and plays a key role in brain function. A critical period for the development of the neocortex is the early postnatal life, when the majority of synapses are formed and when much of synaptic remodeling takes place. Early studies suggest that initial synaptic connections lack precision, and this rudimentary wiring pattern is refined by experience-related activity through selective elimination and consolidation. This view has been challenged by recent studies revealing the presence of a relatively precise pattern of connections before the onset of sensory experience. The recent data support a model in which specificity of neuronal connections is largely determined by genetic factors. Spontaneous activity is required for the formation of neural circuits, but whether it plays an instructive role is still controversial. Neurotransmitters including acetylcholine, serotonin, and gamma-Aminobutyric acid (GABA) may have key roles in the regulation of spontaneous activity, and in the maturation of synapses in the developing brain.

Action Potentials↗