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At least 937 records · Page 52Linked to original sources
PubMed1995

The neuroprotective effects of MK-801 on the induction of microgyria by freezing injury to the newborn rat neocortex.

Four-layered microgyria is associated with many developmental disorders, including mental retardation, epilepsy, and developmental dyslexia. Freezing lesions to the newborn rodent neocortex result in the formation of four-layered microgyria. Previous research had suggested this type of injury acts as an hypoxic/ischemic event to the developing cortical plate. The current study examines the effectiveness of the non-competitive N-methyl-D-aspartate receptor antagonist dizocilpine (MK-801) in protecting against freezing injury to the newborn rat cortical plate. Three groups of rats received freezing injury to the cortical plate on the first day of life (postnatal day 1). Two groups were treated with MK-801 (1 or 2 mg/kg) 0.5 h before the lesion and 6 and 14 h after, while one group received saline injections. A fourth group received MK-801 injections, but did not have a freezing lesion. The volume of neocortical abnormality was determined for all three groups in rats killed after postnatal day 7. Treatment with the higher dose of MK-801 (3 x 2 mg/kg) dramatically reduced the effects of freezing injury but also resulted in over 50% mortality in both lesioned and unlesioned groups. Animals in the lesioned group, however, had a decreased volume of abnormal cortex, and there were fewer animals with microsulci than in the untreated group. This is the first demonstration of a significant anatomical neuroprotective effect in newborns leading to a reduction of cortical malformation.

Animals↗
PubMed1993

The synaptic organization of the neocortex in Alzheimer's disease.

Alzheimer's disease (AD) is characterized by a progressive deterioration of cognitive functions. Recent studies have shown that, in addition to the classically described lesions (plaques and tangles) found in AD, this neurodegenerative disorder is characterized by neuronal and synaptic loss and by synapto-axonal pathology. Stepwise regression analysis has shown that the major correlate of cognitive deficiency is the synapse loss in the prefrontal cortex, contributing about 70% of the strength of the correlation with global psychometric tests. We review evidence that supports the theory that most of the synaptic loss in the neocortex is derived from loss of cortico-cortical associational input into the modules. This hypothesis also predicts that neuritic plaque formation in the neocortical modules could represent an aberrant sprouting reaction of associational fibers responding to abnormal growth stimuli or to local damage. On these bases, it is also proposed that the cellular substrate of AD pathology is synapto-axonal, while in certain other forms of dementia such as Creutzfeldt-Jacob disease (CJD) and HIV encephalitis (HIVE) it is primarily dendritic.

Afferent Pathways↗
PubMed1983

Long-term unilateral noradrenergic denervation: monoamine content and 3H-prazosin binding sites in rat neocortex.

Direct biochemical determinations of alpha 1 adrenoceptor sites were performed in the neocortex of rats subjected to a selective unilateral noradrenergic deafferentation, obtained by microinjecting 6-OHDA in the right dorsal noradrenergic bundle (DNB). After 3 months survival the alpha 1 sites were assayed using 3H-Prazosin (3H-PRZ), in both the denervated and the contralateral (control) cortex. The catecholamines dopamine (DA), epinephrine (EPI), norepinephrine (NE), as well as the indoleamine serotonin (5-HT) were measured using radioenzymatic assays in samples of the frontal cortex of these same animals, as well as in the septum and hippocampus in order to assess the extent and specificity of the deafferentation. The results document that unilateral NE-deafferentations of the cerebral cortex are feasable, the reduction in NE persists for at least three months, and there is an increased endogenous DA content. In the denervated cerebral cortex specific binding of 3H-PRZ showed an increase (+ 45%) in the density of receptor sites (Bmax) without any changes in the dissociation constant (KD 25 degrees C). The results have to be considered in relation both to plasticity changes in monoamine fibers and to denervation-induced alterations of the postysynaptic alpha-adrenoceptors.

Afferent Pathways↗
PubMed1983

Selective noradrenergic denervation and 3H-prazosin binding sites in rat neocortex.

Biochemical determinations of alpha 1-noradrenergic binding sites were performed in the neocortex of normal rats and of rats which had been subjected to a selective noradrenergic deafferentation obtained by microinjecting 6-OHDA in the dorsal noradrenergic bundle. The extent and the specificity of the deafferentation was assessed by measuring the catecholamines dopamine, epinephrine and norepinephrine, as well as the indoleamine serotonin using radioenzymatic assays. In the denervated animals (90% reduction in NE levels) specific binding of the alpha 1-noradrenergic antagonist prazosin revealed an increase only in the number of binding sites (Bmax) without changes in the dissociation constant (Kd).

Animals↗
PubMed1988

Partial recovery of gustatory function after neural tissue transplantation to the lesioned gustatory neocortex.

The ability of homotypic cortical tissue grafts to induce recovery of function after a gustatory neocortex (GN) lesion was studied using the conditioned taste aversion (CTA) paradigm. On acquisition day, 26 GN-lesioned and 8 sham-lesioned rats were presented with a saccharin solution, followed by an injection of the illness-inducing agent lithium chloride (LiCl). On the test day, 2 days later, saccharin was presented again. The GN-lesioned rats showed significantly less aversion to saccharin on the test day, indicating that the lesion impaired their ability to form taste-illness association. Nine of the lesioned rats were then bilaterally transplanted with fetal GN tissue. Nine weeks after the transplantation, the rats were presented with a LiCl solution, which served as both a tastant and an illness-inducing agent. An NaCl solution, which tasted very similar to the LiCl solution, was used to test the CTA to salt 3 days later. The nontransplanted rats consumed significantly more LiCl than the transplanted and sham-operated rats on the acquisition day, but both transplanted and nontransplanted rats consumed more NaCl than sham-operated rats on the test day. Nissl and Golgi stainings showed numerous somata and extensive arborization of neurons within the grafts. The results indicate that fetal GN grafts can restore the ability to integrate gustatory and visceral inputs but not to form long-lasting taste-illness associations.

Animals↗
PubMed1990

Neurochemical recovery in the neocortex after colchicine lesions of the nucleus basalis magnocellularis in rats.

Neurochemical recovery was investigated in male, Fischer-344 rats up to 3 months after lesions of the nucleus basalis. Bilateral injections of colchicine (1.0 micrograms/site) into the nucleus basalis magnocellularis (NBM) resulted in a 30% decrease in choline acetyltransferase (ChAT) activity in frontal cortex 4 weeks after surgery, compared to unlesioned controls. ChAT activity in the frontal cortex gradually recovered to control levels by 12 weeks. The loss of ChAT-immunoreactive neurons in the NBM observed 4 weeks after surgery was still evident 12 weeks after surgery. These results suggest that surviving cholinergic neurons in the NBM contribute to recovery of ChAT activity in the neocortex.

Animals↗
PubMed1985

Dendritic development in the neocortex of adult rats subjected to postnatal malnutrition.

The Golgi-Cox method was used to study the maturation of the large pyramidal cells of the Vth cortical layer in two groups of adult rats, one subjected to early postnatal malnutrition and another malnourished only during the second month of life. The main alterations were observed in the pyramidal cells of cortical layer V of rats malnourished during the first month of life. They consist of a decrease in the number and span of dendritic basilar processes. In animals malnourished during the second month of life, the number and span of basilar dendritic processes in pyramidal cells of layer V, were normal. It is postulated that early postnatal malnutrition induced immediately after birth, profoundly disturbs the process of neuronal maturation in the neocortex of the rat brain, probably with permanent effects.

Age Factors↗
PubMed1988

Cytoarchitecture in cultured rat neocortex explants.

Neocortex explants obtained from 6-day-old rat pups and cultured in a serum-free medium from 5 hr to 13 days in vitro (DIV) show preservation of cytoarchitectural characteristics. Major changes in the size of the explants and their layers occur during the first 2 DIV. A radial arrangement of neurons within layer 2-3-4, which becomes apparent between 2 and 10 DIV, suggests an advance in maturation in culture. In contrast to the situation in vivo, a distinct layer 4 cannot be consistently identified. During the first 2 DIV, a transposition of cells into the pial direction can be seen. Individual degenerated cells are spotted especially in layer 5. The presence of these cells amidst healthy neurons suggests that their death has a functional cause. Neurons at the ventricular border of layer 6 become relatively large in comparison with other neurons. Within the cultured tissue there is a marked increase in GFA reactivity compared to the situation in vivo. The described results clearly indicate that in these cultured explants, both similarities and differences are of interest for studies on the formation of neuronal circuitry within the cerebral cortex.

Animals↗
PubMed1989

Cell number, tissue thickness and protein content as measures for development and variability in cultured neocortex explants.

The development of neuronal number, explant thickness and amount of protein was studied in several series of rat neocortex explants, cultured up to 21 days in vitro (DIV). In contrast to the dimensions of the explant, which rapidly stabilized, the amount of protein showed a prolonged increase with age in vitro. The number of neurons initially tended to decrease until a constant level was reached from 14 to 21 DIV. These findings are in good agreement with previously described cytoarchitectural characteristics. The present data also provided an opportunity to calculate the variance for various parameters within and between culture series obtained from different rats. Especially for the amount of protein, the variance between culture series appeared to be larger than within culture series. This difference was present already at the onset of culturing and persisted during development in vitro. Implications of these findings for experimental design are discussed.

Animals↗
PubMedDate not supplied

Alcohol preference in rats lacking gustatory neocortex.

Ingestion of alcohol solutions (in concentrations from 0.5 to 12% v/v) was examined in three experiments where rats lacking gustatory neocortex (GN) were compared with intact and control lesion rats. Two experiments tested alcohol consumption during a restricted schedule of fluid access with one or two bottle tests. The last experiment involved testing with continuous access to water and alcohol solutions in two bottle tests. Subgroups of rats in each experiment were presented with either an ascending or descending order of concentrations. In all experiments, GN rats consumed less total fluid during testing (relative to control rats). In general, GN rats exhibited similar patterns of alcohol consumption as that found in control rats. Where differences between GN rats and control rats were found, GN rats consumed more alcohol than control rats during tests with restricted fluid access. During continuous fluid access, however, no significant differences between GN rats and control rats were found.

Alcohol Drinking↗
PubMed1996

Distribution of terminal fields stained for zinc in the neocortex of the rat.

Staining for zinc in terminal fields of the rat neocortex was studied by applying the sulphide/silver histochemical method. The stain was arranged in a distinct layered pattern. Two bands of heavy reaction were found in deep layer 1 plus layers 2-3 and in upper layer 5. A band of moderate-to-heavy reaction was found in layer 6. Three bands of lighter staining were found in upper layer 1, layer 4 and deep layer 5. The layers of reaction showed variations in width and intensity of staining from area to area. In the frontal and cingulate cortices and in the association cortices, the heavily stained bands were dominant over the narrow, inconspicuous, lightly stained bands. In contrast, in primary sensory regions (Par1, Oc1 and Te1), the lightly stained bands were wide and prominent. The sulphide/silver method gives a straightforward delimitation of many cortical areas and reveals a clear distinction between (A) allocortical and isocortical areas, and (B) primary sensory areas, secondary or association areas, and prefrontal plus motor areas. The presence of vivid bands of staining for zinc appears to be linked to areas with prominent pyramidal layers.

Animals↗
PubMed1991

Control of postsynaptic Ca2+ influx in developing neocortex by excitatory and inhibitory neurotransmitters.

We assessed the pathways by which excitatory and inhibitory neurotransmitters elicit postsynaptic changes in [Ca2+]i in brain slices of developing rat and cat neocortex, using fura 2. Glutamate, NMDA, and quisqualate transiently elevated [Ca2%]i in all neurons. While the quisqualate response relied exclusively on voltage-gated Ca2+ channels, almost all of the NMDA-induced Ca2+ influx was via the NMDA ionophore itself, rather than through voltage-gated Ca2+ channels. Glutamate itself altered [Ca2+]i almost exclusively via the NMDA receptor. Furthermore, synaptically induced Ca2+ entry relied almost completely on NMDA receptor activation, even with low-frequency stimulation. The inhibitory neurotransmitter GABA also increased [Ca2+]i, probably via voltage-sensitive Ca2+ channels, whereas the neuromodulator acetylcholine caused Ca2+ release from intracellular stores via a muscarinic receptor. Low concentrations of these agonists produced nonperiodic [Ca2+]i oscillations, which were temporally correlated in neighbouring cells. Optical recording with Ca2(+)-sensitive indicators may thus permit the visualization of functional networks in developing cortical circuits.

Acetylcholine↗
PubMed1995

Radial and horizontal deployment of clonally related cells in the primate neocortex: relationship to distinct mitotic lineages.

To analyze cell lineage in the rhesus monkey necorotex, we used recombinant retroviruses to label individual progenitor cells in the ventricular zone (VZ), then determined histochemically the distribution of their progeny during and after the period of cortical neurogenesis. Distribution patterns of labeled cells in the VZ suggested the coexistence of asymmetrically and symmetrically dividing progenitor cells, indicating that both postmitotic and mitotic progeny are produced during cortical neurogenesis. In the cortex, several distinct patterns of clonal distribution were observed and interpreted as follows: clones aligned radially suggested that asymmetrically dividing progenitors generate sequential "siblings" that migrate, in tandem, along a common radial path to the cortex. In contrast, clones oriented horizontally within a single lamina suggested that symmetric divisions produce multiple, laterally displaced progenitors which, in turn, simultaneously generate "cousin" cells that migrate, in concert, to the same cortical layer. Thus, we propose that different mitotic lineages, which coexist in the monkey VZ, produce distinct radial or laminar patterns of clone deployment that foreshadow the cytological organization of the adult neocortex.

Animals↗
PubMedDate not supplied

A1 adenosine receptor-mediated block of epileptiform activity induced in zero magnesium in rat neocortex in vitro.

It has been suggested that endogenous chemical substances such as adenosine, released during a seizure attack, may act as anticonvulsants in vivo. To further investigate this putative role, we have tested adenosine and stable adenosine analogues for anticonvulsant activity in vitro against ictal-like epileptiform activity induced by the removal of magnesium ions from medium superfusing wedges and slices of rat neocortex. Purinoceptor agonists attenuated such burst activity with a potency profile of L-phenylisopropyl-adenosine greater than 2-chloroadenosine greater than adenosine, suggesting that their anticonvulsant actions were mediated via the A1 adenosine receptor sub-type. Adenosine exerted no apparent effect on responses to agonists acting at glutamate receptor sub-types, implying no direct postsynaptic activity at glutamatergic synapses. Adenosine receptor antagonists, the methylxanthines (3-isobutyl-1-methylxanthine greater than theophylline) markedly enhanced established epileptiform activity and reversed the anticonvulsant action of adenosine. The selectivity of this reversal was demonstrated by the lack of effect of methylxanthines on pentobarbitone-induced inhibitions of epileptiform bursts. When added to a normal medium containing 1 mM magnesium, the methylxanthines were unable to induce long-lasting ictal-like epileptiform activity.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Estradiol replacement facilitates the acquisition of seizures kindled from the anterior neocortex in female rats.

Estradiol replacement facilitates kindling from a limbic region, the amygdala. This study determined if estradiol also interacts with kindling from a non-limbic region, the anterior neocortex. Ovariectomized female rats with estradiol replacement required 24 +/- 1.6 trials to kindle and accumulated 434 +/- 28 sec of afterdischarge (AD), significantly less than the 38 +/- 2.2 trials and 840 +/- sec in rats without estradiol. Estradiol replacement did not significantly alter the long series of focal cortical seizures preceding generalized seizures in spite of the early appearance of AD in the contralateral amygdala. Estradiol significantly advanced the onset of generalized seizures compared to rats without estradiol (19 +/- 0.6 versus 24 +/- 1.9 trials). Following secondary seizure generalization, estradiol rats rapidly completed late kindled seizure acquisition. In contrast, late kindling in rats without estradiol was slower as reflected by a 3-fold greater number of AD trials and AD seconds to complete kindling compared to rats with estradiol. One factor in the slower late kindling of rats without estradiol was the instability of generalized seizures which frequently regressed to focal or partial responses. The results provide further experimental evidence for a role for estradiol in catamenial epilepsy and suggest that the process of secondarily generalization of seizures is especially sensitive to estradiol.

Animals↗
PubMedDate not supplied

Zinc and glycine do not modify low-magnesium-induced epileptiform activity in the immature neocortex in vitro.

Exposure of neocortical slices from immature rats to saline containing no added magnesium induced spontaneous epileptiform activity that consisted of bursts of low-amplitude isolated discharges lasting 50-90 sec, recurring every 90-300 sec. Bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-7-phosphonoheptanoic acid led to a rapid, reversible suppression of epileptiform activity, indicating involvement of NMDA receptors. Perfusion with zinc or glycine, putative modulators of the NMDA receptor, with suppressive and enhancing properties, respectively, had no effect on the frequency or duration of the epileptiform discharges. These results indicate that in the immature neocortex in vitro, application of zinc or glycine does not modulate NMDA receptor-mediated, low-magnesium-induced epileptiform discharges.

2-Amino-5-phosphonovalerate↗
PubMed1991

Changes in seizure activity of the neocortex during the early postnatal development of the rat: an electrophysiological study on slices in Mg(2+)-free medium.

NMDA receptor-mediated process of rat neocortex slices prepared from 2-24-day-old rats were studied in Mg(2+)-free solution. The response to NMDA application as well as the susceptibility to epileptiform discharges showed age-dependent changes during the first 4 weeks. Slices from the youngest age group seemed to be the most sensitive to NMDA, whereas epileptic activity developed most readily at around the third week.

Aging↗
PubMed2004

Cell proliferation correlates with the postconceptual and not with the postnatal age in the hippocampal dentate gyrus, temporal neocortex and cerebellar cortex of preterm infants.

BACKGROUND: In previous studies, lower IQ scores and educational difficulties of preterm children were correlated with the reduced size of several brain areas, including the cerebellum and the hippocampus. The most plausible reason for reduction would be the reduced cell formation following premature birth. However, no data are available about the rate of postnatal cell proliferation in the different brain areas of preterms. METHODS: Cytoarchitectonics and cell proliferation were examined in the cerebellum, hippocampal formation and temporal neocortex of preterm infants who lived for several weeks or months. Cell proliferation was detected with Ki-67 immunostaining and proliferating cells were identified with vimentin as glial and with CD31 and periodic acid-Schiff (PAS) reaction as endothelial elements. RESULTS: The rate of cell formation and the width of the cytoarchitectonic layers of the cerebellum of preterm infants corresponded to that of the age-matched controls. In the hippocampal dentate gyrus, the rate of cell formation and the density of proliferating cells were slightly higher in the preterm infants than in the full-term age-matched controls. Endothelial cell proliferation and the surface area of the capillaries were larger in the dentate gyrus of preterms than in age-matched controls. CONCLUSION: Rate of cell proliferation that correlates with the postconceptual age is not reduced in preterms, therefore the reduced size of the cerebellum and hippocampal formation is unlikely to be the result of decreased cell formation.

Aging↗