SEARCH · PubMed Health

Results for “Neocortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 289 records · Page 16Linked to original sources

PubMed2004

Gamma EEG dynamics in neocortex and hippocampus during human wakefulness and sleep.

Little is known about the neurophysiological mechanisms underlying the human sleep-wake cycle. Using intracranial electrodes in humans, we investigated changes in topographic distribution of gamma power and local- and long-range gamma EEG coherence in neocortex and hippocampus during different cerebral states. We report significantly greater variability in gamma power across cortical regions during wakefulness than during either slow wave or rapid eye movement (REM) sleep. In addition, local (within cortical regions) and long-range (between cortical regions) gamma coherence was significantly higher during wakefulness than during sleep, and functional gamma-range coupling between the neocortex and hippocampus was seen during wakefulness, but not during sleep. These findings demonstrate a functional link between different stages of conscious awareness and the level of coupling of gamma-band oscillations in the human brain.

Adolescent↗

PubMed2006

P2X(7) receptors exert a permissive role on the activation of release-enhancing presynaptic alpha7 nicotinic receptors co-existing on rat neocortex glutamatergic terminals.

Adenosine triphosphate (ATP) has been reported to enhance the release of glutamate by acting at P2X presynaptic receptors. Acetylcholine (ACh) can elicit glutamate release through presynaptic nicotinic cholinergic receptors (nAChRs) of the alpha7 subtype situated on glutamatergic axon terminals, provided that the terminal membrane is weakly depolarized. Considering that ATP and ACh are co-transmitters, we here investigate on the possibility that P2X and nAChRs co-exist and interact on the same glutamatergic nerve endings using purified rat neocortex synaptosomes in superfusion. ATP evoked Ca(2+)-dependent release of pre-accumulated D-[(3)H]aspartate ([(3)H]D-ASP) as well as of endogenous glutamate; (-)-nicotine, inactive on its own, potentiated the ATP-evoked release. The ATP analogue benzoylbenzoylATP (BzATP) behaved like ATP, but was approximately 30 times more potent; the potentiation of the BzATP-evoked release was blocked by methyllycaconitine or alpha-bungarotoxin. Adding inactive concentrations of (-)-nicotine, epibatidine or choline together with inactive concentrations of BzATP resulted in significant elevation of the [(3)H]D-ASP release mediated by alpha7 nAChRs. To conclude, P2X(7) receptors and alpha7 nAChRs seem to co-exist and interact on rat neocortex glutamatergic terminals; in particular, P2X(7) receptors exert a permissive role on the activation of alpha7 nAChRs, suggesting that ATP may not only evoke glutamate release on its own, but may also regulate the release of the amino acid elicited by ACh.

Adenosine Triphosphate↗

PubMed2004

Modality- and region-specific acetylcholine release in the rat neocortex.

The basal forebrain is the major source of acetylcholine in the neocortex, and this projection has been variously described as either diffuse or highly specific. We used in vivo microdialysis to examine this discrepancy by collecting acetylcholine release simultaneously from visual, somatosensory and prefrontal cortical areas. Urethane-anesthetized rats were presented with visual and somatosensory stimulation in counter-balanced order and acetylcholine was measured using HPLC. Evoked acetylcholine release was modality-specific, i.e. visual stimulation evoked a large (75%) increase from visual cortex and little (24%) change from the somatosensory area whereas skin stimulation had the opposite effect. No increase was apparent in prefrontal cortex with either stimulation protocol. This experiment extends early studies using cortical cups to collect acetylcholine, and is consistent with the concept of functional specificity within the cholinergic basal forebrain with respect to both its sensory inputs and projections to the neocortex. This functional specificity within the cholinergic basal forebrain might be utilized in the modulation of different cortical regions during selective attention and plasticity.

Acetylcholine↗

PubMed2004

Glutamate transporters regulate excitability in local networks in rat neocortex.

Excitatory postsynaptic currents (EPSCs) in the neocortex are principally mediated by glutamate receptors. Termination of excitation requires rapid removal of glutamate from the synaptic cleft following release. Glutamate transporters are involved in EPSC termination but the effect of uptake inhibition on excitatory neurotransmission varies by brain region. Epileptiform activity is largely mediated by a synchronous synaptic activation of cells in local cortical circuits, presumably associated with a large release of glutamate. The role of glutamate transporters in regulating epileptiform activity has not been addressed. Here we examine the effect of glutamate transport inhibition on EPSCs and epileptiform events in layer II/III pyramidal cells in rat neocortex. Inhibiting glutamate transporters with DL-threo-beta-benzyloxyaspartic acid (TBOA; 30 microM) had no effect on the amplitude or decay time of evoked, presumably alpha-amino-3-hydroxyl-5-methyl-isoxazolepropionic acid-mediated, EPSCs. In contrast, the amplitude and duration of epileptiform discharges were significantly enhanced. TBOA resulted also in a decreased threshold for evoking epileptiform activity and an increased probability of occurrence of spontaneous epileptiform discharges. TBOA's effects were not inhibited by the group I and II metabotropic glutamate receptors antagonist (S)-alpha-methyl-4-carboxyphenylglycine or the kainate receptor antagonist [(3S,4aR, 6S, 8aR)-6-((4-carboxyphenyl)methyl-1,2,3,4,4a,5,6,7,8,8a-decahydroisoquinoline-3-carboxylic acid]. D-(-)-2-amino-5-phosphonovaleric acid could both prevent excitability changes by TBOA and block already induced changes. Dihydrokainate (300 microM) had effects similar to TBOA suggesting involvement of the glial transporter GLT-1. Inhibiting glutamate transport increases local network excitability under conditions where there is an enhanced release of glutamate. Our results indicate that uptake inhibition produces an elevation of extracellular glutamate levels and activation of N-methyl-D-aspartate receptors.

2-Amino-5-phosphonovalerate↗

PubMed2006

Neuronal production and precursor proliferation defects in the neocortex of mice with loss of function in the canonical Wnt signaling pathway.

To better understand the function of the Wnt pathway in the developing telencephalon, we analyzed neocortical development in low density lipoprotein receptor-related protein (LRP) 6 mutants. LRP6 mutant mice are hypomorphic for the canonical Wnt signaling pathway and have hypoplasia of the developing neocortex. While early telencephalic morphogenesis is largely intact in these mice, probably due to compensation by LRP5, the mutant mice develop a dramatically thinner cortical plate. There is a prominent reduction of neurogenesis leading to a thin cortical plate. Reduced proliferation late in gestation probably also contributes to the hypoplasia. Although there are marked decreases in the numbers of layer 6 and layers 2-4 neurons all laminar identities are generated and there is no evidence of compensatory increases in layer 5 neurons. In addition, LRP6 mutants have partial penetrance of a complex of cortical dysmorphologies resembling those found in patients with developmental forms of epilepsy and mental retardation. These include ventricular and marginal zone heterotopias and cobblestone lissencephaly. This analysis demonstrates that canonical Wnt signaling is required for a diverse array of developmental processes in the neocortex in addition to the previously known roles in regulating precursor proliferation and patterning.

Animals↗

PubMed2004

Quantitative MR imaging of the neocortex.

This article provides an overview of novel MR image analysis methods applied to the quantitative assessment of the neocortex in various forms of epilepsy. Postacquisition processing methods, such as voxel-based morphometry and texture analysis, involve the use of computer software to manipulate, enhance, and classify image information in a digital format. These techniques have the potential to demonstrate subtle abnormalities that are not identified by eye because of anatomic variability. Information provided by quantitative MR imaging of the neocortex may be important for the identification of accurate predictors of surgical outcome and may refine the selection of surgical candidates, particularly those with "nonlesional" neocortical epilepsy.

Epilepsies, Partial↗

PubMed2004

The rhinal cortices: a wall of inhibition between the neocortex and the hippocampus.

Anatomical data indicate that the parahippocampal region, comprised of the perirhinal (PRC), postrhinal (POR) and entorhinal (ERC) cortices, is an essential link between neocortex and hippocampus. Lesion studies demonstrated that memory functions previously ascribed to the hippocampus depend on the integrity of the rhinal cortices. This review will consider recent data suggesting that the ERC and PRC, far from being passive relay stations, actively gate impulse traffic between neocortex and hippocampus, because they are endowed with a powerful intrinsic inhibitory system. It is proposed that the cross-talk between PRC and ERC is not organized to unrestrictedly transfer information, but to select relevant inputs. The implication of these new evidences for the propagation of epileptiform activity will be considered.

Animals↗

PubMed2006

Role of Sox2 in the development of the mouse neocortex.

The mammalian neocortex is established from neural stem and progenitor cells that utilize specific transcriptional and environmental factors to create functional neurons and astrocytes. Here, we examined the mechanism of Sox2 action during neocortical neurogenesis and gliogenesis. We established a robust Sox2 expression in neural stem and progenitor cells within the ventricular zone, which persisted until the cells exited the cell cycle. Overexpression of constitutively active Sox2 in neural progenitors resulted in upregulation of Notch1, recombination signal-sequence binding protein-J (RBP-J) and hairy enhancer of split 5 (Hes5) transcripts and the Sox2 high mobility group (HMG) domain seemed sufficient to confer these effects. While Sox2 overexpression permitted the differentiation of progenitors into astroglia, it inhibited neurogenesis, unless the Notch pathway was blocked. Moreover, neuronal precursors engaged a serine protease(s) to eliminate the overexpressed Sox2 protein and relieve the repression of neurogenesis. Glial precursors and differentiated astrocytes, on the other hand, maintained Sox2 expression until they reached a quiescent state. Sox2 expression was re-activated by signals that triggered astrocytic proliferation (i.e., injury, mitogenic and gliogenic factors). Taken together, Sox2 appears to act upstream of the Notch signaling pathway to maintain the cell proliferative potential and to ensure the generation of sufficient cell numbers and phenotypes in the developing neocortex.

Animals↗

PubMed2000

Nicotinic acetylcholine receptor-mediated synaptic potentials in rat neocortex.

In the neocortex, fast excitatory synaptic transmission can typically be blocked by using excitatory amino acid (EAA) receptor antagonists. In recordings from layer II/III neocortical pyramidal neurons, we observed an evoked excitatory postsynaptic potential (EPSP) or current (EPSC) in the presence of EAA receptor antagonists (40-100 microM D-APV+20 microM CNQX, or 5 mM kynurenic acid) plus the GABA(A)-receptor antagonist bicuculline (BIC, 20 microM). This EAA-antagonist resistant EPSC was observed in about 70% of neurons tested. It had a duration of approximately 20 ms and an amplitude of 61.5+/-6.8 pA at -70 mV (n=35). The EAA-antagonist resistant EPSC current-voltage relation was linear and reversed near 0 mV (n=23). The nonselective nicotinic acetylcholine receptor (nAChR) antagonists dihydro-beta-erythroidine (DH beta E, 100 microM) or mecamylamine (50 microM) reduced EPSC amplitudes by 42 (n=20) and 33% (n=9), respectively. EPSC kinetics were not significantly changed by either antagonist. Bath application of 10 microM neostigmine, a potent acetylcholinesterase inhibitor, prolonged the EPSC decay time. EAA-antagonist resistant EPSCs were observed in the presence of antagonists of metabotropic glutamate, serotonergic (5-HT(3)) and purinergic (P2) receptors. The EAA-antagonist resistant EPSC appears to be due in part to activation of postsynaptic nAChRs. These results suggest the existence of functional synaptic nAChRs on pyramidal neurons in rat neocortex.

2-Amino-5-phosphonovalerate↗

PubMed2001

Glutamine is the major precursor for GABA synthesis in rat neocortex in vivo following acute GABA-transaminase inhibition.

The objective of the present study was to assess the degree to which astrocytic glutamine provides carbon for net synthesis of GABA in the rat neocortex in vivo. Isotopic labeling of GABA and glutamate from astrocytic glutamine was followed in halothane anesthetized and ventilated rats during an intravenous infusion of [2-(13)C]glucose. A net increase in GABA was achieved by administration of the GABA-transaminase inhibitor, gabaculine to suppress catabolism of GABA and recycling of (13)C label. (13)C Percentage enrichments of GABA, glutamate and glutamine were assessed in tissue extracts using (13)C-edited (1)H nuclear magnetic resonance at 8.4 T. GABA levels increased 2.6 micromol/g at 2 h and 6.1 micromol/g at 5 h after gabaculine, whereas glutamate and glutamine decreased in toto by 5.6 micromol/g at 2 h and 3.1 micromol/g at 5 h. Selective enrichment of glutamine, glutamate, and GABA C3's over other carbon positions was observed consistent with a precursor role for astrocytic glutamine. Between 1 h (control) and 3 h (gabaculine-treated) of [2-(13)C]glucose infusion, (13)C percentage enrichment increased in glutamine C3 (from 3.2+/-0.5 to 7.0+/-0.9%), glutamate C3 (from 1.8+/-0.5 to 3.4+/-0.9%), and GABA C3 (from 2.7+/-1.6 to 4.8+/-0.4%). The measured incremental [3-(13)C]GABA concentration (0.15 micromol/g) was close to the predicted value (0.13 micromol/g) that would be expected if the increase in GABA were produced entirely from glutamine compared to glutamate (0.07 micromol/g) based on the average precursor enrichments between 1 and 3 h. We conclude that glutamine is the major source of GABA carbon in the rat neocortex produced acutely following GABA-T inhibition by gabaculine in vivo.

4-Aminobutyrate Transaminase↗

PubMed2002

Agonist-specific maturation of GIRK current responses in acutely isolated pyramidal neurons of rat neocortex.

We performed whole-cell recordings from acutely isolated pyramidal cell somata of rat neocortex to measure and compare G protein-activated, inwardly rectifying K+ (GIRK) currents induced by adenosine, serotonin and baclofen at different postnatal stages (postnatal days 3-19). In about two thirds of neurons, baclofen-induced GIRK currents were already detected at postnatal days 3 and 4 (P3-P4) and almost all neurons between P5 and P19 were responsive. This robust response suggests that postsynaptic effects of baclofen occur much earlier than previously thought. Sensitivity to adenosine was around 70% during the first two postnatal weeks. Given the late maturation of functional synaptic inhibition in neocortex, we propose that phasic and/or tonic activation of GIRK current by baclofen and adenosine might serve as a mechanism to control neuronal excitability during early postnatal development. In marked contrast to the pronounced early sensitivity to baclofen and adenosine, only 20% of the neurons displayed a GIRK current response to serotonin during the first postnatal week. After that, about half of the neurons tested positive for serotonin. GIRK current densities for baclofen and adenosine attained a maximum at the end of the second postnatal week, whereas the serotonin-induced current showed a linear increase during the second and third week of life. Set in relationship with previous data on the postnatal expression of receptor protein and GIRK channel mRNA, our findings suggest that the maturation of GIRK current responses is determined predominantly by the different postnatal patterns of receptor expression.

Adenosine↗

PubMed2003

Constructing the mammalian neocortex: the role of intrinsic factors.

The mammalian neocortex is subdivided into regions that are specialised for the processing of particular forms of information. These regions are distinct in terms of their cytoarchitecture, electrophysiology, and connectivity. How this regional diversity is generated through development is currently a topic of considerable interest and has centered upon two main issues. First, to what extent are these regions prespecified by intrinsic genetic mechanisms? Second, what is the influence of extrinsic activity in transmitting signals that ultimately shape functional regions? Historically, experimental evidence has tended to emphasise the role of extrinsic influences, but the identification and analysis of several genes that are expressed asymmetrically in the developing neocortex have tempered this viewpoint. We review current literature from the standpoint that intrinsic influences act early in neocortical development to generate molecular patterning whose main role is the guidance of long-range projections from the dorsal thalamus. Extrinsic influences appear to generate receptive fields for peripheral input, the summation of which determines the areal extent of particular neocortical region.

Animals↗

PubMed2002

Gabapentin inhibits presynaptic Ca(2+) influx and synaptic transmission in rat hippocampus and neocortex.

Gabapentin is a widely used drug with anticonvulsant, antinociceptive and anxiolytic properties. Although it has been previously shown that Gabapentin binds with high affinity to the alpha(2)delta subunit of voltage-operated Ca(2+) channels (VOCC), little is known about the functional consequences of this interaction. Here, we investigated the effect of Gabapentin on VOCCs and synaptic transmission in rat hippocampus and neocortex using whole-cell patch clamp and confocal imaging techniques. Gabapentin (100-300 microM) did not affect the peak amplitude or voltage-dependency of VOCC currents recorded from either dissociated or in situ neocortical and hippocampal pyramidal cells. In contrast, Gabapentin inhibited K(+)-evoked increases in [Ca(2+)] in a subset of synaptosomes isolated from rat hippocampus and neocortex in a dose-dependent manner, with an apparent half-maximal inhibitory effect at approximately 100 nM. In hippocampal slices, Gabapentin (300 microM) inhibited the amplitude of evoked excitatory- and inhibitory postsynaptic currents recorded from CA1 pyramidal cells by 30-40%. Taken together, the results suggest that Gabapentin selectively inhibits Ca(2+) influx by inhibiting VOCCs in a subset of excitatory and inhibitory presynaptic terminals, thereby attenuating synaptic transmission.

Acetates↗

PubMed1998

Post-activation potentiation in the neocortex of awake freely moving rats.

The search for the cellular processes that underlie information storage within neuronal systems lead to the development of two models of post-activation potentiation, long-term potentiation (LTP) and kindling. Both models give rise to a long-lasting increase in synaptic strength and altered unit discharge patterns. The present paper reviews synaptic plasticity in the neocortex of awake freely moving rats following both single and multiple sessions of activation with high-frequency, tetanic electrical stimulation. The phenomenology of neocortical post-activation potentiation and some possible underlying mechanisms are discussed. We speculate that the functional significance of potentiated responses may reflect a reorganization of the neocortex in a manner similar to those that create and define receptive fields.

Animals↗

PubMed1998

In vivo detection of experimentally induced cortical dysgenesis in the adult rat neocortex using optical coherence tomography.

Imaging cerebral structure in vivo can be accomplished by many methods, including MRI, ultrasound, and computed tomography. Each offers advantages and disadvantages with respect to the others, but all are limited in spatial resolution to millimeter-scale features when used in routine applications. Optical coherence tomography (OCT) is a new, high resolution imaging technique which uses light to directly image living tissue. Here, we investigate the potential use of OCT for structural imaging of the fully developed mammalian cerebral cortex. In particular, we show that OCT can perform in vivo detection of neocortex and differentiate normal and abnormal cortical anatomy. We present the results of detailed optical coherence tomographic (OCT) observations of both normal and abnormal rat neocortex obtained in vivo. Comparative histologic analysis shows excellent correlation with the OCT tomograms.

Animals↗

PubMed2000

Unchanged total number of neurons in motor cortex and neocortex in amyotrophic lateral sclerosis: a stereological study.

Modern stereological methods provide precise and reliable estimates of the number of neurons in specific regions of the brain. The total number of neurons in the neocortex and motor cortex from eight patients suffering from amyotrophic lateral sclerosis (ALS) and nine controls was estimated. No attempt was made to estimate subpopulations of neurons such as the number of giant pyramidal cells of Betz. No difference was found in the average number of neurons in neocortex in ALS and controls, 21.7 and 22.3 x 10(9), respectively, and 1.33 and 1.29 x 10(9) in motor cortex, respectively. In the light of our stereological measurements, results obtained from in-vivo proton magnetic resonance spectroscopy (1H-MRS), suggesting neuronal loss in ALS, may instead be due to neuronal metabolic dysfunction and/or alteration in the size or the volume fraction of the neurons.

Aged↗

PubMed1998

A critical period for reduced brain vulnerability to developmental injury. II. Volumetric study of the neocortex and thalamus in cats.

Groups of young adult cats with a left hemineodecortication at postnatal (P) ages (in days) 5-15 (P10), 30 (P30) 60 (P60), 90 (P90), 120 (P120) and in adulthood, were used to measure the volume of the thalamus, bilaterally, and of the remaining neocortex (right hemisphere). The same subjects were employed for the behavioral studies reported in the preceding paper. There was a bilateral, age-dependent, thalamic volume decrease. Ipsilateral to the resection, the thalamic shrinkage was the largest for the adult-lesioned cats (by 56.7%) and it was the smallest for the P30 group (43.4%), with a tendency towards a greater atrophy as the age at lesion increased. A similar pattern of atrophy was seen for the contralateral thalamus but the volume reduction was much less pronounced such that it was significant only for the four older age-at-lesion groups (ranging from 18.2% to 11.2% for the P120 and P90 groups respectively). Once again, the shrinkage was the smallest for the P30 group (5.3%). The remaining neocortex also shrunk in these animals, but the volume decrease was significant only for the adult-lesioned (17.8%) and the P120 group (15.4%), while the P30 group had practically no shrinkage (2.4%). The frontal cortex had no atrophy or it was minimal but the shrinkage gradually increased caudally such that all lesioned groups had some size reduction of the occipital cortex. The present results, together with the main conclusion of the preceding paper, indicate that there is a critical maturation period (CMP) of reduced forebrain vulnerability to neocortical injury which, in cats, tends to end between 30 to 60 days postnatally. The implications for developmental brain damage in other higher mammal species as well as the possible morphological ontogenetical underpinnings of this period are discussed.

Aging↗

PubMed1997

Expression of group one metabotropic glutamate receptor subunit mRNAs in neurochemically identified neurons in the rat neostriatum, neocortex, and hippocampus.

Metabotropic glutamate receptors (mGluRs) can be divided into three groups based on sequence homology and pharmacology. We studied expression of group I mGluRs (mGluR1 and mGluR5) in identified neurons of the rat neostriatum, neocortex, and hippocampus using in situ hybridization. Tissue sections were hybridized with radiolabeled RNA probes for mGluR1 or mGluR5 and digoxygenin labeled RNA probes detecting somatostatin (SOM), preproenkephalin (ENK), preprotachykinin (SP), glutamic acid decarboxylase 67 (GAD67), parvalbumin (PARV), or choline acetyltransferase (ChAT) mRNA. In the striatum, mGluR1 hybridization signal was observed in all six neuronal populations. The strongest signal was found in SP-positive neurons, with a lower signal in ENK-positive neurons. All striatal interneurons were labeled less intensely than ENK- and SP-positive projection neurons. For striatal mGluR5 mRNA, both SP- and ENK-positive projection neurons were intensely labeled, but only GAD67-positive interneurons exhibited a significant signal. In the neocortex and hippocampus, mGluR1 and mGluR5 hybridization signals were studied in SOM-, GAD67-, and PARV-positive neurons. Hybridization signal for mGluR1 mRNA was intense in SOM-positive neurons of the cortex, CA1, CA3, and dentate gyrus, and weaker in GAD67-positive neurons of CA3 and dentate gyrus. MGluR5 signals were intensely labeled in SOM-, GAD67- and PARV-positive neuronal populations of the cortex and hippocampus. SOM-positive neurons were more intensely labeled in the hippocampus than cortex.

Animals↗