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PubMed1991

Intrinsic oscillations of neocortex generated by layer 5 pyramidal neurons.

Rhythmic activity in the neocortex varies with different behavioral and pathological states and in some cases may encode sensory information. However, the neural mechanisms of these oscillations are largely unknown. Many pyramidal neurons in layer 5 of the neocortex showed prolonged, 5- to 12-hertz rhythmic firing patterns at threshold. Rhythmic firing was due to intrinsic membrane properties, sodium conductances were essential for rhythmicity, and calcium-dependent conductances strongly modified rhythmicity. Isolated slices of neocortex generated epochs of 4- to 10-hertz synchronized activity when N-methyl-D-aspartate receptor-mediated channels were facilitated. Layer 5 was both necessary and sufficient to produce these synchronized oscillations. Thus, synaptic networks of intrinsically rhythmic neurons in layer 5 may generate or promote certain synchronized oscillations of the neocortex.

Animals↗
PubMed1975

[Morphological and histological study of neocortex of bovides (Antilopinae, Cephalophinae) and Tragulidae with comments on evolutionary development].

1. Macroscopical and histological studies on the neocortex of the cerebrum of small Artiodactyla (Tragulidae, Cephalophinae, Antilopinae) lead to some informations on the level of evolution of these animals. 2. A big part of the macroscopical investigations (pattern of sulci, relations between bodyweight and brainweight on the one hand and surface of neocortex on the other hand) already had been realized by HAARMANN and OBOUSSIER (1972). Therefore in this paper only the results for the Tragulidae and Cephalophus sylvicultor are added. The first are relatively primitive, while the latter obviously is a higher developed animal. C. sylvicultor fits into the general scheme of the brain of the Cephalophinae. 3. The investigations are complemented by microscopical investigations (histology of the neocortex: number of nerve cells per volume unit, gray cell and cortex coefficient, thickness of the neocortex). The knowledge of the evolution level obtained by macroscopical methods is confirmed. The Tragulidae are clearly separated from the other Artiodactyla as primitive animals, whereas the Cephalophinae measured with the cortex coefficient are the most developed, most "intelligent" Bovidae so far analyzed in this paper. The Antilopinae reach only lower coefficients. This subfamily may be separated into three groups (Antilopini, Neotragini, Oreotragus). The differences between the Antilopinae and the Cephalophinae are not so striking as between these Bovidae and the Tragulidae.

Animals↗
PubMedDate not supplied

[The role of the temporal neocortex in the origin of convulsive activity].

Experiments on cats with cooling capsules implanted over different areas of the neocortex have shown that cooling of different intensity applied to the temporal neocortex may result in both stimulation and switching off effects. Cold stimulation (temperature dropping to 27-33 degrees C) manifested in generalized epileptiform brain electrical activity and paroxysmal states. The functional switching off the temporal area observed during its deeper cooling (20-21 degrees C) discontinues the paroxysmal state already developed and prevents the appearance of seizures, regrardless of the localization of the epileptogenic focus. The paroxysmal state weakens and ceases after repeated cooling of the temporal neocortex. The temporal neocortex, involved in the integrated activating brain system, plays a decisive role in the emergence of paroxysmal states.

Animals↗
PubMed1990

Light and electron microscopic localization of beta I-, beta II-, and gamma-subspecies of protein kinase C in rat cerebral neocortex.

We have localized the beta I-, beta II-, and gamma-subspecies of protein kinase C in cerebral neocortex with light and electron microscopic immunocytochemistry using a monoclonal antibody against gamma-PKC and polyclonal antisera to beta I- or beta II-PKC-specific oligopeptides. The gamma-PKC-immunopositive cell bodies were seen mostly in layers II, V, and VI, and the vast majority of them were pyramidal cells. The beta II-PKC immunoreactive cell bodies were observed in layers II, III, V, and VI, and most of them seemed to be pyramidal cells. Both gamma- and beta II-PKC were colocalized in some pyramidal cells in layers II, V, and VI. The small number of beta I-PKC immunoreactive cell bodies were observed in the neocortex, and many of them were nonpyramidal cells. About 80% of the beta I-PKC-immunoreactive cells were shown to be GABAergic neurons. The gamma-PKC-immunopositive neuropils were observed in layers I, II, V, and VI, while beta II-PKC-immunoreactive neuropils were seen in layers I-III, V, and VI. The distribution of each subspecies is much the same throughout all regions of the neocortex, although with different intensities of immunoreactivity. electron microscopic studies revealed that, in the perikarya, gamma-PKC was distributed throughout the cytoplasm, beta I-PKC was just adjacent to the plasma membrane, and beta II-PKC was located around the Golgi complex. The immunoreactivity of these 3 subspecies was also seen in dendrites and axons, but no immunoreactivity of these subspecies was found in the presynaptic terminals in the present study. The discrete cellular and intracellular distributions of protein kinase C subspecies imply that each subspecies has a specific role in neuronal activity in the cerebral neocortex.

Animals↗
PubMedDate not supplied

Ultrastructural changes in the mouse fetal neocortex following chronic maternal alcoholization.

Female mice (RAP strain) were alcoholized for 30-50 days before mating and during pregnancy until killing, with a 20% solution of ethanol administered instead of drinking water. From foetuses of 16, 18, 20 days and from newborn puppies on day 1 parietal neocortex fragments were excised and examined electronmicroscopically. Chronic maternal alcoholization induces in the neocortex of mouse foetuses and newborn puppies various ultrastructural changes: swelling of mitochondria with the disappearance of cristae and vacuolation, both in the capillary endothelium and in the cells of the neural tissue; enlargement of intercellular spaces; in the neocortex zones rich in neuronal processes (marginal and intermediary zone) vacuolation and structural wastage of these processes are detected. Moderate chronic alcohol intake leads to persistent ultrastructural changes in the fetal and newborn neocortex which may contribute to the appearance of some neuro-psychical and behavioral symptoms in alcohol embryo- and fetopathy. The possible pathogenetic pathways leading to the pathological changes detected are discussed.

Animals↗
PubMedDate not supplied

[Effect of the local administration of 5,7-DHT and 6-OHDA into the neocortex on the learning and exploratory behavior of rats in an open field].

On Wistar rats characteristics were studied of investigating behaviour in the open field, of learning of conditioned food-reinforced reaction and also of BA and their metabolites content in various brain structures under local intracerebral injections of specific neurotoxins; 6-hydroxydopamine (6-OHDA) and 5,7-dihydroxytryptamine (5,7-DHT), abolishing correspondingly catecholaminergic and serotoninergic terminals. Bilateral injection of 6-OHDA in the neocortex led to a weakening of rats investigating activity in the open field and to an increase of the time of fulfillment of the forming of conditioned food-reinforced reaction. Administration of 5,7-DHT was accompanied by an increase of the investigating behaviour in the open field and a reduction of the duration of the forming of conditioned reaction. Administration of 6-OHDA to the neocortex caused a lowering of catecholamines level in the frontal area of the neocortex and the hippocampus. Analogous administration of 5,7-DHT elicited simultaneously with a deep level lowering of 5-HT and its metabolite in these structures, a change of catecholamines content which testifies to a lesser specificity of the neurotoxin 5,7-DHT in comparison with 6-OHDA. Structures lesion of serotoninergic and catecholaminergic systems of the frontal cortex and the hippocampus brought about by a local administration of 6-OHDA and 5,7-DHT in the neocortex was accompanied by differently directed changes in animals behaviour.

5,7-Dihydroxytryptamine↗
PubMed1989

[Reorganization of the cortico-spinal tract after unilateral lesions of the neocortex].

By means of retrograde transport of horseradish peroxidase the left and right hemisphere connections of neocortex with right spinal cord in normal and 7-14 days after the left sensory-motor neocortex damage have been investigated. In normal brain the quantity of cross corticospinal projections was revealed. After the unilateral lesion of neocortex the atypical retrograde transport of HRP in neocortex of ipsilateral hemisphere has been observed. The role of collateral sprouting mechanisms in posttraumatic reorganization of the corticospinal tract has been discussed.

Animals↗
PubMed1987

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↗
PubMed1987

[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↗
PubMedDate not supplied

[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↗
PubMed1977

[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↗
PubMed1995

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↗
PubMed1995

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↗
PubMed2000

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↗
PubMed1999

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↗
PubMed1999

Selective block of rat and human neocortex GABA(B) receptors regulating somatostatin release by a GABA(B) antagonist endowed with cognition enhancing activity.

Previously, we have shown that presynaptic GABA(B) receptors regulating the release of various transmitters from CNS terminals can be differentially blocked by GABA(B) antagonists suggesting the existence of pharmacologically distinct GABA(B) receptor subtypes. We here examined the ability of CGP 36742 [(3-aminopropyl)n-butylphosphinic acid], a selective GABA(B) antagonist endowed with cognition enhancing activity, to block release-regulating GABA(B) receptors. In particular, CGP 36742 was tested against the inhibition of the depolarization-evoked release of GABA, glutamate, cholecystokinin and somatostatin produced by (-)baclofen in rat and human neocortex axon terminals. CGP 36742 potently antagonized (IC50 = 0.14 microM) the inhibition by (-)baclofen of somatostatin release from superfused rat neocortex synaptosomes. In contrast, the effects of (-)baclofen on GABA, glutamate and cholecystokinin release were insensitive to CGP 36742, at concentrations of up to 100 microM. In human neocortex synaptosomes CGP 36742 exhibited a pattern of selectivity identical to that in rat synaptosomes, although the antagonist was at least 10-fold less potent in human than in rat brain. CGP 36742 is the first compound displaying great selectivity for the GABA(B) presynaptic receptors regulating somatostatin release. Considering the proposed implication of the neuropeptide in cognitive processes, disinhibition of somatostatin release merits consideration as one of the mechanisms possibly involved in the behavioral activity of CGP 36742.

Adult↗
PubMed2000

Time-related changes in connexin mRNA abundance in the rat neocortex during postnatal development.

Gap junction coupling between neurons is important for the temporal and spatial co-ordination of neocortical development and can be visualised by dye-coupling. Neuronal dye-coupling in the rat neocortex is extensive during the first 2 postnatal weeks and diminishes rapidly thereafter. We used RT (reverse transcriptase)-PCR to investigate the time-related changes in mRNA expression for the connexins (Cx) Cx 26, Cx 30, Cx 32, Cx 36, Cx 37, Cx 40, Cx 43, Cx 45 and Cx 46 as well as for beta-actin and GAPDH in rat neocortex during the first 6 postnatal weeks. The time courses for mRNA expression for GAPDH, Cx 30, Cx 36 and Cx 43 were also investigated by northern blotting. Cx 30 and Cx 45 mRNA abundance showed no time-dependent changes during the early postnatal period. The relative abundance of Cx 32, Cx 43 and Cx 46 mRNA increased significantly during the first 2-3 weeks and then remained relatively constant during weeks 3-6. The relative abundance of Cx 26, Cx 36, Cx 37 and Cx 40 mRNA also increased significantly during the first 10-15 postnatal days but then declined significantly from their peak values during weeks 3-6. beta-actin mRNA expression showed no time-related changes but GAPDH mRNA expression increased significantly during the first postnatal week, then remained constant. The time-dependent changes in mRNA relative abundance for GAPDH, Cx 36 and Cx 43 determined by northern blotting corroborate the results from the RT-PCR study. None of the Cx exhibited time-dependent changes in mRNA expression in homogenates of rat neocortex which parallel the changes in neuronal dye-coupling during postnatal development.

Actins↗
PubMedDate not supplied

delta 1-Opioid receptor-mediated control of acetylcholine (ACh) release in human neocortex slices.

In slices of human neocortex, prelabelled with [3H]-choline, the release of [3H]-acetylcholine reflects the evoked release of endogenous acetylcholine which was elicited by the same electrical stimulation paradigm. [3H]-Acetylcholine release was depressed by the delta-opioid receptor agonist D-Pen2-D-Pen5-enkephalin. When the nerve endings were depolarized by elevating extracellular potassium the evoked [3H]-acetylcholine release was similarly depressed by D-Pen2-D-Pen5-enkephalin in the absence, but not in the presence, of tetrodotoxin which blocks action potential propagation. Therefore, the delta-opioid receptor inhibiting [3H]-acetylcholine release should not be located to cholinergic nerve terminals, but rather to interneurons. The somatostatin2 receptor partial agonist octreotide per se did not influence action potential-evoked [3H]-acetylcholine release, but prevented the inhibition of release of [3H]-acetylcholine by D-Pen2-D-Pen5-enkephalin. Similarly, the delta 1-opioid receptor antagonist 7-benzylidenenaltrexon per se did not influence [3H]-acetylcholine release, but prevented of the inhibition of release by D-Pen2-D-Pen5-enkephalin. From the present findings we conclude: (1) The evoked release of [3H]-acetylcholine from human neocortex slices reflects the release of endogenous acetylcholine. (2) It is inhibited in an indirect manner by opioid receptors of the delta 1-subtype, which (3) are not localized on cholinergic axon terminals but on soma and dendrites of somatostatin-containing interneurons, where they inhibit somatostatin release. (4) These interneurons innervate cholinergic nerve endings in the human neocortex and appear to facilitate acetylcholine release via somatostatin2 receptors.

Acetylcholine↗