Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neocortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 451 records · Page 25Linked to original sources

Brain neocortex modulation of mitogen-induced interleukin 2, but not interleukin 1, production.

Interleukin 2 (IL-2) production by splenic T cells stimulated by Concanavalin A was studied in mice after unilateral or bilateral brain neocortex ablation. The brain cortex was shown to modulate IL-2 production in an asymmetrical way. IL-2 levels were higher in animals with a right cortical lesion (group R) and lower in mice with a symmetrical lesion (group L) as compared to controls, differences between groups R and L being significant. Such variations of IL-2 production that were observed after unilateral lesions were abolished with bilateral cortical ablations. These results extend the immunoregulatory roles of the brain neocortex to IL-2 production by splenic T cells and may provide molecular support for neuro-immunological networks.

Animals↗

The development of cerebellar primordia transplanted to the neocortex of the rat.

Pieces of cerebellar primordia were dissected from the developing fetus at day 18 of gestation in Sprague-Dawley rats and transplanted to the neocortex of a 10- to 12-day-old rat. The histological development of 53 such transplants was analyzed at a series of survival times ranging from 5 min to 426 days. The cerebellar cortex developed much as it does in situ. However, only migratory sequences were strictly followed, while Purkinje cell differentiation and folia formation were initially retarded. In deep parts of the transplant, and throughout transplants confined to deep layers of the neocortex, the external granule layer was associated with penetrating blood vessels. An inverted cytoarchitectural pattern developed as concentric cylindrical layers around these vessels. In contrast, normal lamination and foliation were found only in transplants growing on the neocortical surface. Axons coursing between host and transplant were seen frequently and were especially pronounced at those sites beneath the internal granule layer which appeared to contain deep cerebellar nuclei. At the longest survival time there was preliminary evidence that suggested morphological deterioration of the transplant. Surface transplants, in addition to developing a normal orientation of cells and layers, have the added benefit of being accessible for further experimental manipulations after the transplant has become established.

Animals↗

A comparison of the postnatal development of post-activation potentiation in the neocortex and dentate gyrus of the rat.

The postnatal development of short-term potentiation (STP) and long-term potentiation (LTP) was examined in the neocortex and dentate gyrus of rats aged 7 days to adult. STP and LTP of the transcallosal response in the neocortex could not be demonstrated until the third postnatal week. STP and LTP of the perforant path-dentate response could not be demonstrated until the second postnatal week. In both cases, STP appeared several days before LTP. Structural and neurochemical correlates of STP/LTP development, and their implications for possible STP/LTP mechanisms, are discussed.

Aging↗

Cholinergic modulation of epileptiform activity in the developing rat neocortex.

The effects of carbachol on picrotoxin-induced epileptiform activity and membrane properties of neurons in the developing rat neocortex were examined in an in vitro slice preparation. Intracellular recordings were obtained in layer II-III neurons of slices prepared from rats 9-21 days of age. Epileptiform activity in 9- to 14-day-olds consisted of a sharply rising, sustained (10-30 s) membrane depolarization with superimposed action potentials. Bath application of carbachol (5-50 microM) raised the threshold for evoking epileptiform activity but, when such responses were evoked, their underlying depolarizations were increased in amplitude. Orthodromic stimulation in slices from 15- to 21-day-old animals evoked a prolonged epileptiform burst response that triggered an episode of spreading depression (SD). Carbachol reduced epileptiform responses and suppressed the occurrence of SD. It did not significantly affect the resting membrane potential or the height of the action potential but decreased the rheobase current needed to evoke an action potential and increased the input resistance. All effects of carbachol were antagonized by atropine (1 microM). These results indicate that carbachol has both pre- and postsynaptic effects in the developing neocortex and can significantly modulate neuronal excitability in the immature nervous system.

Action Potentials↗

Development of NADPH-diaphorase activity in the rat neocortex.

The activity of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an enzyme related to the synthesis of nitric oxide (NO), was studied histochemically in rat neocortex from the day of birth (P0) to young adulthood. At birth, NADPH-d containing neurons were already identifiable, sparsely distributed in the deep half of the pallium of the cerebrum. In addition, weakly stained bands of NADPH-d positive neuropil were detectable in layers VI and deep V and the cortical plate (CP). During the first postnatal week, NADPH-d positive neurons increased markedly, especially in CP and the superficial layers. By P7 the cells were mainly in layers VIb and II/III. Differential NADPH-d activity in the neuropil during this period appeared as higher activity gradually moving upwards until the highest intensity localised in layers II and upper III. In the caudal part of the cortex, the higher activity covered the whole of the supragranular layers. By the end of the second postnatal week, both the number and laminar distribution of NADPH-d neurons were adult-like, still mainly in layers VIb and II/III. The staining intensity in the neuropil was generally reduced but the banding pattern seen at P7 was still present. No detectable changes in the patterns of NADPH-d positive cells and neuropil in the neocortex occurred after the second postnatal week. The rostral part of the cortex matured slightly earlier than the caudal part. These results show that the development of NADPH-d activity correlates with the laminar differentiation and suggest that NADPH-d or NO may play an important role in the maturation of cortical neurons including the establishment of functional connections.

Animals↗

The development of parvalbumin-immunoreactivity in the neocortex of the mouse.

In the present study the postnatal development of parvalbumin-immunoreactivity was examined in the neocortex of the mouse. Postnatal mice were processed at different developmental stages using a well-characterized monoclonal antibody against parvalbumin, and immunocytochemistry. The first immunoreactive neurons appeared in the first parietal and retrosplenial cortices at postnatal day 10 (P10). From P11 to P12, immunoreactivity emerged in the second parietal, cingular, frontal, hindlimb-forelimb, first temporal, primary and secondary occipital and gustatory cortices, and at P14, parvalbumin-positive cells were present in the remaining regions. In general, parvalbumin-immunoreactivity appeared first in the primary sensory/motor areas, and then in second sensory/motor or associative areas. The maturation of parvalbumin-immunoreactivity, however, was a long-lasting process, which was not completed until adult stages. In all cortical regions, parvalbumin-immunoreactive cells were present first in layer V, from which immunoreactivity expanded to the upper and inner cortical layers at subsequent developmental stages. This pattern of maturation differed from the usual 'inside-out' gradient of neocortical neurogenesis and maturation. At the cellular level, parvalbumin-immunoreactivity appeared first in cell somata, and staining of dendrites and boutons was apparent two days later. From the second postnatal week onwards, an immunoreactive axonal system was observed in the neocortical white matter and the corpus callosum. We conclude that the emergence and maturation of parvalbumin-immunoreactivity in the mouse neocortex shows marked area-specific differences, but proceeds following a similar center-to-outside radial gradient. These features may reflect the acquisition of certain physiological properties by a subset of GABAergic inhibitory neurons.

Animals↗

Effect of prior experience on bar-pressing in rats without neocortex.

Rats in which all neocortex had been surgically removed produced similar patterns of performance to those previously established for rabbits with total neocortical ablations in a bar-pressing task for food reward. The animals deprived of neocortex developed inefficient patterns of food-tray related behaviours and a limit to their bar-pressing performance for intermittent rewards in the region of 4-10 presses per reward. The lesioned animals were also unable to form a sequential brightness discrimination on a GO-NOGO schedule using a bar-press response. Neither prior experience of other instrumental learning situations nor experience of working in the same apparatus and using the same instrumental response were sufficient to improve subsequent bar-press performance for intermittent reward in the neocortically lesioned animals. Previous success in improving such performance by pretraining procedures designed to facilitate identification of the part of the apparatus to be manipulated by the animal cannot easily be explained, therefore, on the basis of such incidental factors as increased behavioural sophistication or of increased familiarity with the apparatus and the instrumental response itself. The data are consistent with the view that the neodecorticate's difficulty in the bar-pressing situations for intermittent rewards is due to inadequate identification of cues associated with the object to be manipulated rather than to an associative learning deficit.

Animals↗

Accumulation of a 50 kDa N-terminal fragment of beta-APP695 in Alzheimer's disease hippocampus and neocortex.

Proteolytic processing of beta-amyloid precursor protein (beta-APP) is a key event in the formation of beta-amyloid deposits in Alzheimer's disease (AD) brains and is likely to be accompanied by the accumulation of cleavage products other than the beta/A4 protein. Using a beta-APP695-specific monoclonal antibody in quantitative immunoblotting, a 50 kDa N-terminal fragment of beta-APP695 was detected in neocortex, hippocampus and cerebellum of AD patients and control individuals. The mean level of this fragment was higher in AD hippocampus and neocortex as compared to controls, suggesting that beta-APP695 fragments are generated in various brain regions but that the proteolytic processing is increased in pathologically affected brain areas.

Adult↗

Postnatal development of parvalbumin immunoreactivity in axon terminals of basket and chandelier neurons in monkey neocortex.

1. Two classes of GABAergic inhibitory interneurons, chandelier and basket cells, are known regulators of pyramidal neurons. Parvalbumin (PV) a calcium binding protein, has been shown to be a marker for axon terminals of subpopulations of these interneurons. 2. Immunohistochemical methods were used in this study to examine changes in the distribution of PV-immunoreactive (IR) chandelier and basket axon terminals during postnatal development of monkey neocortex. 3. Our results indicate a differential effect of postnatal development on PV-IR axon terminals of chandelier and basket neurons that is region-specific. 4. The differential regional, laminar and developmental pattern of PV-IR axon terminals of chandelier and basket cells may provide insight into the functional role of these classes of inhibitory neurons in primate neocortex.

Aging↗

Horseradish peroxidase pellets implanted into infant neocortex: some technical considerations.

This study was undertaken to examine whether implanting pellets of horseradish peroxidase (HRP), rather than injecting an aqueous solution, would improve the sensitivity of the retrograde tracing method as applied to infant rat neocortex. From 1 to 10 pellets, each containing approximately 10 microgram of HRP, were implanted into somatosensory cortex of 6-day-old rats. Implantation of one pellet labeled 4 neuronal groups; 5 pellets, 37 groups. Higher doses of injected HRP (20--50 microgram and 200-400 microgram) are needed to label the same number of groups. Also, individual neurons of a group generally contain more granules/cell after pellets than following injections of much higher doses of HRP. The pellet implant technique offers a high degree of reproducibility and is technically simpler than injections. We conclude that HRP pellet implants offer advantages over injections in identifying potential afferents to immature neocortex.

Animals↗

Basal forebrain neurons provide major cholinergic innervation of primate neocortex.

In 3 monkeys, lesions were made in the basal forebrain by microinjections of ibotenic acid into the nucleus basalis. Bilateral samples of multiple neocortical gyri were assayed for the activity of choline acetyltransferase. Compared to control hemispheres, enzyme activity was reduced up to 69% in the neocortex ipsilateral to the lesion; in addition, acetylcholinesterase staining was decreased at the lesioned site and in the ipsilateral cortex. These results support the concept that the principal cholinergic innervation of the primate neocortex is derived from axons and nerve terminals of neurons whose perikarya are located in the basal forebrain, particularly the nucleus basalis.

Animals↗

Excitatory synaptic transmission mediated by NMDA and non-NMDA receptors in the superficial/middle layers of the epileptogenic human neocortex maintained in vitro.

Conventional intracellular recordings were made from regular-spiking cells located in layers II-IV to examine the involvement of excitatory amino acid receptors in synaptic transmission in epileptogenic human neocortical slices maintained in vitro. Extracellular stimuli that were below the threshold for generating action potentials evoked an excitatory postsynaptic potential (EPSP) with short latency to onset (0.8-4 ms). When suprathreshold stimuli were delivered, 95% of the neurons fired a single action potential. In 5% of the population, however, an all-or-none bursting discharge was observed. The EPSP and the bursting discharge were tested with the N-methyl-D-aspartate (NMDA) antagonist 3-((+/-)-2-carboxypiperazin-4-yl)propyl-1-phosphonate (CPP, 5 microM) or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 4 microM). In the presence of CNQX the peak amplitude of the EPSP was reduced by 85% and the bursting discharge was abolished completely. By contrast, CPP reduced the peak amplitude of the EPSP by 52%, attenuated the late phase of the bursting discharge and increased its threshold. These results indicate that excitatory amino acids function as excitatory transmitters in the human brain. While the involvement of non-NMDA receptors in the EPSP is in line with data from normal neocortical slices of other mammals, the participation of NMDA-mediated conductances to the EPSP appears peculiar to the epileptogenic human neocortex. This evidence, together with the contribution of NMDA and non-NMDA receptors to the all-or-none bursting discharge suggests that excitatory amino acid-mediated transmission might be modified in the epileptogenic human neocortex.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Metabotropic glutamate receptor activation decreases epileptiform activity in rat neocortex.

Intracellular and extracellular recordings were obtained from layers II-III of slices of adult rat neocortex maintained in vitro. Excitatory postsynaptic potentials (EPSPs) and epileptiform discharges (paroxysmal depolarizing shifts, PDSs) were evoked in the presence of bicuculline methiodide. Responses were monitored before, during, and after bath application of the putative metabotropic glutamate receptor agonists, 1S, 3R-ACPD and L-AP4. Peak EPSP amplitude and both PDS amplitude and duration were reduced during 1S,3R-ACPD application. Area measurements indicate that PDSs were reduced to 51.7 +/- 19.9% of control. Stimulus threshold for evoking a PDS was increased in the presence of 1S,3R-ACPD or L-AP4. Pretreatment of slices with 1S.3R-ACPD did not prevent the generation of epileptiform events when bicuculline subsequently was applied. These results indicate that mGluR activation by 1S,3R-ACPD has significant suppressive effects on evoked epileptiform activity in the adult rat neocortex in vitro.

Aminobutyrates↗

Neurons dissociated from neocortex fire with 'burst' and 'regular' trains of spikes.

Neurons acutely dissociated from neocortex slices of 14-16-day-old rats were patch-clamped in physiological conditions. Different pyramidal cells, spontaneously or in response to current steps, generate regular spiking and intrinsically bursting behaviour during long periods of time. We show that typical firing properties recorded in somatosensory neocortex slices are preserved in dissociated pyramidal neurons originating from the slices themselves, thus, providing a way for the related characterization of biophysical properties of currents in identified subtypes of pyramidal neurons.

Action Potentials↗

An increased intensity of N-methyl-D-aspartate (NMDA) but not non-NMDA receptor activation may be responsible for the enhancement of excitatory processes in the neocortex of two-week-old rats: a brain slices study.

During the brain maturation a critical period is detectable when the sensitivity of the neocortex is high. Enhanced excitatory activity is characteristic at that time while the inhibitory processes are underdeveloped. The goal of this study was to determine the effectiveness of different types of excitatory amino acid antagonists reducing the electrically evoked excitatory synaptic responses of the somatosensory cortex. Effects of the specific competitive N-methyl-D-aspartate (NMDA) antagonist 4-amino-phosphono-valerate (APV), and the specific non-competitive, non-NMDA antagonist 1-(4-aminophenyl)-3-methylcarbamoyl-7,8-methylenedioxy-5H-2,3-benz odiazepine (GYKI 53655) were analysed on neocortex slices prepared from 2-week-old and adult rats. APV caused a partial inhibition of the electrically evoked response more effectively in young animals than in adults, while the effective IC50 values were similar. In contrast, the non-NMDA antagonist had a similar effect on the slices of both age-groups.

Action Potentials↗

5-HT1D-like receptors inhibit the release of endogenously formed [3H]GABA in human, but not in rabbit, neocortex.

Both human and rabbit brain contain the 5-hydroxytryptamine (5-HT)1D subtype of 5-HT1 receptors. We studied the effects of 5-HT1D receptor stimulation on neocortical [3H] gamma-aminobutyric acid (GABA) release from GABAergic neurons in these species. The 5-HT1D receptor agonist sumatriptan depressed [3H]GABA release in human neocortex and the 5-HT1 receptor antagonist metitepin prevented this depression with potencies suggesting mediation by 5-HT1D-like receptors. In rabbit neocortex, however, 5-HT1D agonists did not affect the release of [3H]GABA. Since 5-HT and GABA seem to function antagonistically in anxiety disorders their neocortical interaction may be (patho)physiologically relevant.

3-Mercaptopropionic Acid↗

Hibernators' brain: protein synthesis in the neocortex and the hippocampus.

[3H]leucine incorporation into 16 electrophoretic protein fractions from the neocortex and the hippocampus and their relative content have been estimated in various physiological states of ground squirrels: in torpor, in 3 transition phases, in long-term wakefulness and a fortnight after forced arousal in winter. The changes are greater in the neocortex than in the hippocampus. Incorporation is not the same in naturally awake animals and forced awake animals.

Animals↗

Transplantation of embryonic ventral forebrain neurons to the neocortex of rats with lesions of nucleus basalis magnocellularis--I. Biochemical and anatomical observations.

Unilateral ibotenic acid lesions of the rat nucleus basalis magnocellularis produce approximately 60% depletion of choline acetyltransferase activity in ipsilateral frontal and frontoparietal neocortex. This depletion, which represents the loss of most of the extrinsic neocortical cholinergic input, is stable for at least 6 months. Embryonic ventral forebrain neurons survive transplantation to such cholinergically denervated neocortex. Cholinergic cells abound within these transplants and appear able to reinnervate the cholinergically depleted host cortex, as assessed histochemically and by measurement of choline acetyltransferase activity. Outgrowing fibres may extend beyond 2 mm from the grafts and often appear to be organized in an appropriate laminar pattern within the host cortex. Peptidergic neurons are sparse within the grafts and their fibres frequently appear unable to grow into the host tissue. Control grafts of non-cholinergic embryonic hippocampal cells survive well but have no effect on cortical depletions of acetylcholinesterase or choline acetyltransferase activity. Reconstruction of the extrinsic cholinergic input to the cortex by transplantation provides a useful tool for understanding the functions of this pathway.

Animals↗