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PubMed1997

Development of proenkephalin gene expression in rat neocortex: a non-radioactive in situ hybridization study.

Products of the proenkephalin gene are not only neurotransmitters but may also influence brain development. The ontogeny of the expression of the proenkephalin gene in neocortex was studied in embryonic and postnatal rats with in situ hybridization. At embryonic day 14, the proliferating cells in the ventricular zone strongly expressed the gene. Thereafter, the expression decreased and was hardly detectable up to embryonic day 21. At the day of birth and during the subsequent week, proliferating cells in the subventricular zone were labelled. The expression of the proenkephalin gene in proliferating neuronal and glial progenitors indicates that gene products may affect proliferation and/or commitment. In the neocortex, cells which strongly expressed the gene were first seen at postnatal day 7 in the outer part of the neocortex. Seven days later, a second band of positive cells had appeared in the inner part of the cortex, i.e. the adult pattern of distribution had been established. Thus, in rat neocortex the expression of the proenkephalin gene developed in an outside-first, inside-last mode.

Animals↗
PubMed1997

Colocalization of parvalbumin and calbindin D-28k in neurons including chandelier cells of the human temporal neocortex.

Chandelier cells are cortical GABAergic interneurons with a unique synaptic specificity enabling them to exert a strong inhibitory influence on pyramidal cells. By using immunocytochemistry for the calcium-binding protein calbindin D-28k in the human temporal neocortex, we have found numerous immunoreactive processes that were identified as chandelier cell axon terminals. This was a striking find since in previous immunocytochemical studies of the primate neocortex, chandelier cell axon terminals had been shown to be immunoreactive for another calcium-binding protein, parvalbumin, and colocalization studies indicate that parvalbumin and calbindin are present in almost completely separate neuronal populations. Here, we present double-label immunofluorescence experiments showing that parvalbumin and calbindin immunoreactivities are colocalized in certain neurons that include a subpopulation of chandelier cells whose cell bodies are located mainly in layers V and VI of the human temporal neocortex. The results suggest a selective laminar distribution of neurochemical subtypes of chandelier cells which is a peculiar feature of the organization of the human neocortex.

Adolescent↗
PubMed1977

Absence of differential associative responses to novel and familiar taste stimuli in rats lacking gustatory neocortex.

Rats lacking gustatory neocortex (n = 24) and normal rats (n = 24) were familiarized to either hydrochloric acid (10(-1.6) M) or quinine hydrochloride (10(-4) M) solutions during free-drinking trials. They were trained subsequently to avoid either the familiar or the novel taste stimulus, using a balanced design, by pairing the to-be-associated taste with ip injections of apomorphine hydrochloride. Balanced, nonpaired presentations of the other taste solution and water were presented also. Normal rats more efficiently learned to avoid the novel compared with the familiar taste. Rats with gustatory neocortex lesions did not differentiate novel from familiar tastes. They learned aversions to both in a manner highly similar to the aversion learning of familiar tastes by the normal group. Therefore, rats lacking gustatory neocortex displayed an associative deficiency, relative to normal, only when they were trained on novel stimuli. This observation supports an earlier suggestion that gustatory neocortex lesions disrupt the conditionability of taste stimuli by reducing or eliminating responses to taste novelty. This suggestion is supported further by the absence of a "neophobic" response in the operated rats to the first presentation of a taste stimulus.

Animals↗
PubMed1997

Threshold effects in synaptosomal and nonsynaptic mitochondria from hippocampal CA1 and paramedian neocortex brain regions.

After a brief period of global ischemia, the hippocampal CA1 region is more susceptible to irreversible damage than the paramedian neocortex. To test whether primary differences in bioenergetic parameters may be present between these regions, respiration rates and respiratory control activities were measured. In synaptosomal and nonsynaptic mitochondria isolated from the hippocampal CA1 region, state 3 respiration rates and complex IV activities were significantly lower than those present in synaptosomal and nonsynaptic mitochondria from the paramedian neocortex. These results suggest that mitochondria from the CA1 hippocampal area differ in some properties of metabolism compared with the neocortex area, which may render them more susceptible to a toxic insult such as that of ischemia. In addition, when complex I and IV activities were titrated with specific inhibitors, thresholds in ATP synthesis and oxygen respiration became apparent. Complex I and IV activities were decreased by 60% in nonsynaptic mitochondria from the hippocampal CA1 region and paramedian neocortex before oxidative phosphorylation was severely compromised; however, in synaptosomes from these regions, complex I activities had a threshold of 25%, indicating heterogenous behaviour for brain mitochondria. Reduced complex I thresholds in mitochondria, in association with other constitutive defects in energy metabolism, may induce a decreased ATP supply in the synaptic region. The implications of these findings are discussed in relation to delayed neuronal death and processes of neurodegeneration.

Animals↗
PubMed1995

Abnormal expression of microtubule-associated protein 2 (MAP-2) in neocortex in Rett syndrome.

Immunocytochemical evaluations of the neocortex of three classical Rett syndrome (RS) individuals revealed a selective abnormality in the expression of microtubule-associated protein 2 (MAP-2). MAP-2 immunoreactivity (ir) was reduced throughout the neocortex of all three RS cases with a reversal of the normal pattern of more intense staining in deep cortical layers. This anomaly was selective for MAP-2 because nonphosphorylated neurofilament (SMI-32) labeling of deep pyramidal neurons and calbindin (CaBP)-stained GABAergic cells remained unchanged. Moreover, MAP-2 ir was virtually undetected in white matter while GABAergic and, particularly, peptidergic (neuropeptide Y: NPY) profiles were easily recognized. These results demonstrate a marked disruption of a major cytoskeletal component in neocortex in RS which seems to affect, predominantly, pyramidal projection and white matter neurons. MAP-2 expression appears early in neuronal maturation of the neocortex, particularly in the subplate region, the future superficial white matter, suggesting that these reported abnormalities in RS represent a developmental disturbance. Considering that MAP-2 expression is regulated by several neurotransmitter systems in adult cerebral cortex, particularly dopaminergic and cholinergic afferents that are deficient in RS, these neurochemical alterations could be related to this anomalous MAP-2 expression.

Adult↗
PubMed1987

Effects of maternal dietary restriction in vitamin B-6 on neocortex development in rats: B-6 vitamer concentrations, volume and cell estimates.

Influence of the time of maternal restriction in dietary vitamin B-6 on vitamer concentrations and morphological development of neocortex was examined. Rats were fed ad libitum a vitamin B-6-free diet supplemented with 0.0 or 0.6 mg pyridoxine X hydrochloride (PN X HCl)/kg diet during gestation followed by a control diet (7.0 mg PN X HCl/kg) during lactation or were supplemented with 0.6 or 7.0 mg PN X HCl/kg diet throughout gestation and lactation. During postweaning offspring received the maternal diets fed during lactation. Neocortices of offspring were examined at 30 d of age by liquid chromatography and light microscopy. Vitamin restriction during gestation and 30 d postnatal was the only vitamin B-6-restricted treatment of the three administered that altered B-6 vitamer levels in neocortex; all vitamers were depressed equally. Brain weight and volume of neocortex were not changed significantly by the maternal restrictions imposed. However, each restriction adversely affected neurogenesis and neuron longevity of the neocortex and when expressed as percent reduction from control, neuron longevity was affected more severely than neurogenesis.

Animals↗
PubMed1990

Effects of maternal restriction in vitamin B-6 on neocortex development in rats: neuron differentiation and synaptogenesis.

Effects of maternal restrictions in vitamin B-6 on neuron differentiation and synaptogenesis in developing neocortex were examined. Rats were fed ad libitum a vitamin B-6-free diet supplemented with 0.0 or 0.6 mg pyridoxine hydrochloride (PN.HCl)/kg diet during gestation followed by a control level of 7.0 mg/kg diet during lactation, or they were fed the vitamin B-6-free diet supplemented with 0.6 or 7.0 mg PN.HCl/kg diet throughout gestation and lactation. Neocortices of the offspring were examined at 30 d of age by light and electron microscopy. All maternal restrictions in vitamin B-6 reduced the number of higher order dendrites on stellate neurons in layer II and on pyramidal neurons in layer V of the neocortex and decreased synaptic density in the neuropil of the neocortex. The findings indicated that vitamin B-6 restriction during gestation, either marginal or severe, was the critical treatment factor that adversely affected synaptogenesis and at least one event in neuron differentiation in the neocortex, the arborization of dendrites.

Animals↗
PubMed1996

Neocortex size and behavioural ecology in primates.

The neocortex is widely held to have been the focus of mammalian brain evolution, but what selection pressures explain the observed diversity in its size and structure? Among primates, comparative studies suggest that neocortical evolution is related to the cognitive demands of sociality, and here I confirm that neocortex size and social group size are positively correlated once phylogenetic associations and overall brain size are taken into account. This association holds within haplorhine but not strepsirhine primates. In addition, the neocortex is larger in diurnal than in nocturnal primates, and among diurnal haplorhines its size is positively correlated with the degree of frugivory. These ecological correlates reflect the diverse sensory-cognitive functions of the neocortex.

Animals↗
PubMed1992

Characterization of the 5-hydroxytryptamine receptor modulating the release of 5-[3H]hydroxytryptamine in slices of the human neocortex.

In the rat brain, the presynaptic 5-hydroxytryptamine (5-HT) autoreceptors located on 5-HT terminals correspond to the 5-HT1B subtype. The presence of a 5-HT receptor probably located on 5-HT nerve endings and modulating transmitter release in the human neocortex has been reported, but its detailed pharmacological characterization is not yet available. On the other hand, receptor binding and autoradiographic results indicate that the 5-HT1B receptor subtype is not present in the human brain. We, therefore, studied the modulation of the electrically evoked release of [3H]5-HT by various 5-HT receptor agonists and antagonists in preloaded slices of human neocortex obtained from 18 patients undergoing neurosurgery. The nonselective 5-HT1A/1B/1D receptor agonist 5-carboxamidotryptamine produced a potent inhibition (70% at 0.03 microM) of the electrically evoked release of [3H]5-HT which was blocked by 5-HT receptor antagonists with the following relative order of potency: methiothepin greater than metergoline = methysergide greater than propranolol. The selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin at 0.1 microM did not modify the electrically evoked release of [3H]5-HT. The 5-HT1A/1B receptor agonist RU 24969 was 10 times more potent at inhibiting [3H]5-HT overflow in the rat frontal cortex than in the human neocortex. The potent 5-HT1B receptor antagonist cyanopinodolol did not modify the 5-carboxamidotryptamine-induced inhibition of the electrically evoked release of [3H]5-HT in slices of the human neocortex, but produced by itself a small inhibition of [3H]5-HT overflow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Effects of 5-HT receptor agonists on depolarization-induced [3H]-noradrenaline release in rabbit hippocampus and human neocortex.

1. The present study attempted to determine whether noradrenaline (NA) release in rabbit hippocampus and human neocortex is modulated by presynaptic 5-hydroxytryptamine (5-HT) receptors. 2. Slices of rabbit hippocampus and human neocortex, loaded with [3H]-noradrenaline ([3H]-NA) were superfused and the effects of 5-hydroxytryptamine (5-HT) receptor ligands on electrically evoked [3H]-NA release were investigated. 3. In rabbit hippocampus, 5-HT, 5-carboxamidotryptamine (5-CT; 32 microM) and 2-CH3-5-HT (32 microM) increased [3H]-NA release elicited with 360 pulses/3 Hz. Facilitation of transmitter release was not influenced by the 5-HT3 receptor antagonist, tropisetron but was prevented by the alpha 2-adrenoceptor antagonist, rauwolscine. When autoinhibition was avoided by stimulating the tissue with 4 pulses/100 Hz (pseudo-one pulse-(POP) stimulation), 2-CH3-5-HT decreased evoked transmitter release, whereas 5-HT and 5-CT had no effect. Inhibition caused by 2-CH3-5-HT was not affected by tropisetron but counteracted by the alpha 2-adrenoceptor ligands, clonidine and rauwolscine. Inhibition caused by clonidine was diminished in the presence of 5-CT or 2-CH3-5-HT. 4. In human neocortex, [3H]-NA release elicited with 360 pulses/3 Hz was increased by 10 microM 5-HT and 32 microM 5-CT, whereas 2-CH3-5-HT was ineffective. [3H]-NA release evoked with a modified POP stimulation (2 bursts of 4 pulses/100 Hz, 3.5 min apart) was not affected by 2-CH3-5-HT or 5-CT. 5. The present results indicate that 5-HT, 2-CH3-5-HT and 5-CT can act on presynaptic alpha 2-autoreceptors as partial agonists (2-CH3-5-HT; in rabbit hippocampal tissue) or antagonists (5-HT and 5-CT; in tissue of rabbit hippocampus and human neocortex). Furthermore the existence of autoinhibition dictates whether these drugs cause facilitation of release, inhibition or have no effect.

Age Distribution↗
PubMed1996

Long-term effect of postnatal alcohol exposure on the number of cells in the neocortex of the rat: a stereological study.

Behavioral and morphological studies suggest that exposure to alcohol during development may cause damage in the neocortex. In this study, rat pups were exposed to alcohol during the brain growth spurt and examined at adulthood to ascertain the long-term effect of alcohol exposure on the neocortex. Four-day-old rat pups were surgically implanted with an intragastric cannula while under ether anesthesia and artificially reared from postnatal day (PN) 4 through PN11. Two of the consecutive 12 daily feeds contained either alcohol (4.5 g/kg; alcohol-exposed) or an isocaloric maltose/dextrin solution (gastrostomy control) from PN4 through PN9. On PN115, animals were perfused intracardially and the brains removed. Unbiased stereological methods were used to determine the neocortical volume, the total number of neurons and glial cells in the entire neocortex and in layer V, and the mean cell volume of neurons or mean nuclear volume of glial cells in layer V. No effect of alcohol was seen in the neuronal population on either cell number or mean cell volume, nor was there any difference in the total number or mean nuclear volume of glial cells in layer V. These findings suggest that neither the entire neocortex nor layer V alone are vulnerable to permanent alcohol-induced cell death.

Animals↗
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↗