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 181 records · Page 10Linked to original sources
PubMed1994

Latexin: a molecular marker for regional specification in the neocortex.

It largely remains to be elucidated how the mammalian neocortex is regionally specified during development. In an attempt to obtain molecular markers in the neocortex, we have generated a monoclonal antibody PC3.1 which recognizes a subset of neurons located in lateral, but not dorsal, neocortical areas. The antigen is a novel class of protein, named latexin, having a molecular weight of 29,000. Our in vitro studies have revealed that the neocortical regional specification for the production of latexin-positive neurons occurs very early prior to thalamocortical interactions and the completion of neurogenesis, indicating that elements intrinsic to the neocortex play important roles in the neocortical specification. Furthermore, our recent analyses have suggested that this regional specification is attributable, at least in part, to an early restriction of developmental potential in neocortical progenitor cells to become latexin-positive neurons.

Animals↗
PubMed1995

The development of neural visinin-like Ca(2+)-binding protein 2 immunoreactivity in the rat neocortex and hippocampus.

Neural visinin-like Ca(2+)-binding protein 2 (NVP2) immunoreactivity in the rat neocortex and hippocampus was barely detectable by immunoblot analysis on postnatal day 1 (P1), but increased during postnatal weeks 2-3, reaching a plateau on P28. Immunohistochemical analysis revealed moderate immunoreactivity firstly on P7 in some subsets of the hippocampal interneurons and in the hippocampal pyramidal cells and dentate granule cells. Immunoreactivity of the interneurons decreased during postnatal weeks 2-3 and disappeared by P28. In contrast, immunoreactivity of the cortical and hippocampal pyramidal cells and dentate granule cells abruptly increased during postnatal week 2. The distinctly immunoreactive cells were distributed throughout the neocortex, especially in the cortical plate, and the stratum pyramidale of Ammon's horn and granular layer of the dentate gyrus on P14. Immunoreactivity was homogeneously concentrated in the cell bodies and proximal dendrites at this stage, whereas thereafter immunoreactivity in the neuropil gradually increased, and underwent a relative decrease in the cell bodies. By P28, the higher and granular immunoreactivity in the neuropil covered whole layers of the neocortex, Ammon's horn and the dentate gyrus, the same as in adults. Differential expression of NVP2 in different neuron populations may reflect the differential functional consequences for neuronal development.

Animals↗
PubMed1992

Visualization of cholinoceptive neurons in the rat neocortex: colocalization of muscarinic and nicotinic acetylcholine receptors.

The present investigation analyzes the cellular distribution of muscarinic and nicotinic acetylcholine receptors in rat neocortex, by use of monoclonal antibodies raised against purified receptor proteins. The degree of colocalization of both types of receptors was determined by way of immunofluorescent double-labeling techniques. For both classes of receptors, pyramidal and nonpyramidal cells were found immunostained and an identical laminar distribution pattern of immunopositive neurons in the rat neocortex became apparent. A striking similarity in distribution of the two cholinergic receptor types was found in the frontal/motor and parietal cortex. Accordingly, we observed a high degree of colocalization of muscarinic and nicotinic acetylcholine receptors within immunopositive cortical neurons. Approximately 90% of the cholinoceptive neurons expressed both types of receptors. The current data demonstrate that (i) the distribution of muscarinic and nicotinic cholinoceptive neurons in the neocortex is present in identical laminar patterns and represent the same type of cells, (ii) both classes of cholinergic receptors are highly colocalized within cholinoceptive neurons, which points at individual neurons as a likely site of interaction between muscarinic and nicotinic acetylcholine receptor-mediated processes.

Animals↗
PubMed1982

Direct projections from the extrathalamic forebrain structures to the neocortex in the macaque monkey.

Extrathalamic direct projections from the subcortical forebrain structures to the neocortex were examined in the macaque monkey by the horseradish peroxidase method. The enzyme, when injected into discrete regions in the neocortex, labeled cell bodies of extrathalamic forebrain neurons in the basal nucleus of Meynert, nucleus of the diagonal band, medial septal nucleus, hypothalamus, claustrum and dorsolateral part of the basal amygdaloid nucleus. Neurons in the basal nucleus of Meynert, lateral hypothalamus and claustrum appeared to send their axons widely, but not diffusely, to the neocortex.

Animals↗
PubMed1986

An immunocytochemical demonstration of alpha 2HS-glycoprotein in the developing neocortex of the rat.

The presence of the plasma protein alpha 2HS-glycoprotein (alpha 2HS) has been demonstrated in the developing rat neocortex, using biotin-streptavidin immunocytochemistry. alpha 2HS was observed in the neocortex on embryonic day 20 but not earlier. At this age it was present in cells of the subplate and of the intermediate layer and in layer I anteriorly. Between postnatal day 5 and day 10 alpha 2HS-positive cells were found in greater number in various cortical layers and in fibres in layer I. At postnatal day 28 no alpha 2HS-positive cells or fibres could be found in the neocortex. alpha 2HS has been reported to be very closely related to fetuin which is a fetal plasma protein found in cells of the developing cortex in the sheep and the pig. It is suggested that these glycoproteins may be important in some aspects of early neocortical differentiation.

Aging↗
PubMed1993

Injection of tetanus toxin into the neocortex elicits persistent epileptiform activity but only transient impairment of GABA release.

Focal injection of a minute quantity of tetanus toxin into the rat neocortex induces chronic epileptogenesis. Within a day, spontaneous and stimulus-evoked paroxysmal discharges appear in widespread regions of both hemispheres and this lasts for at least nine months. Tetanus toxin blocks transmitter release, apparently by catalysing the breakdown of synaptobrevin, a synaptic protein. It specifically binds to neuronal membranes but its potent epileptogenic properties have been ascribed to a higher affinity for inhibitory neurons. Following focal injection of tetanus toxin into the hippocampus a long-lasting epileptic syndrome also develops. During the early part of the syndrome GABA release is depressed in slices from the injected side, but not in slices from the contralateral, secondary focus. In the present experiments on neocortex, release of radiolabelled GABA was measured from primary and secondary epileptic foci induced by unilateral focal injection of tetanus toxin into the parietal cortex. By four weeks after the injection, no differences were detected in GABA release from any neocortical site in control or toxin-injected animals, despite the persistence of profound epileptic activity in slices from the latter. At earlier times (1.5 days) after the toxin injection, however, release was significantly depressed in both hemispheres. The results indicate that at first, the toxin induces focal neocortical epileptogenesis by directly impeding GABAergic synaptic transmission but that with time there is a recovery from this initial effect. We propose, as has also been suggested for other models, that the initial epileptogenesis leaves in its wake a long-lasting change in the local functional connectivity, such that the neocortex is rendered permanently epileptic.

Animals↗
PubMed1995

Low extracellular magnesium unmasks N-methyl-D-aspartate-mediated graft-host connections in rat neocortex slice preparation.

The main purpose of this study was to investigate the role of N-methyl-D-aspartate receptors in host-graft synaptic transmission in the neocortex. The effects of low extracellular magnesium, the glutamate agonist N-methyl-D-aspartate and N-methyl-D-aspartate antagonists on the synaptic activation of connections between embryonic neocortical graft tissue and the surrounding host tissue were studied in 17 perfused slices of rat neocortex. In standard artificial cerebrospinal fluid, stimulation of the host white matter evoked field potentials in four of 17 grafts. However, in Mg(2+)-free medium, the same stimulation evoked field potentials in an additional six grafts, with significant increases in the mean duration of the evoked responses in the 10 responsive grafts. In five of these slices stimulation of the graft also evoked field potentials in the host tissue, suggesting reciprocal interaction between graft and host. Simultaneous extracellular recordings from graft and host tissues in Mg(2+)-free medium showed that spontaneous epileptiform discharges developed in the graft and host tissue synchronously. In Mg(2+)-free medium, application of N-methyl-D-aspartate induced a shift of the baseline with superimposed epileptiform discharges in both graft and host. Application of the non-competitive N-methyl-D-aspartate antagonist ketamine and the competitive antagonist D,L-2-amino-5-phosphonovaleric acid attenuated or reversibly blocked both the spontaneous epileptiform discharges and the evoked field potentials. Our data provides evidence that N-methyl-D-aspartate receptors are present at synapses created between fetal graft and host neocortex, and that the N-methyl-D-aspartate-activated receptor-channel complex plays an active role in mediating excitatory synaptic transmission in host-graft circuitry.

Animals↗
PubMed1994

Pharmacology and electrophysiology of a synchronous GABA-mediated potential in the human neocortex.

Spontaneous synchronous field potentials of negative polarity (duration = 200-700 ms, inter-event interval = 9.1 +/- 2.9 s; n = 27 slices) were recorded, during application of 4-aminopyridine (50 microM), from the superficial/middle layers of slices of human neocortex obtained in the course of neurosurgery for the relief of intractable seizures. The negative-going field potential corresponded to an intracellular long-lasting (duration = 200-1600 ms) depolarization that could be preceded by preceded by an excitatory postsynaptic potential-hyperpolarizing inhibitory postsynaptic potential sequence and followed by a long-lasting hyperpolarization. This synchronous activity continued to occur following blockade of excitatory synaptic transmission by excitatory amino acid receptor antagonists, but was greatly reduced and eventually disappeared during application of the GABAA receptor antagonist bicuculline methiodide. Simultaneous extracellular recordings from three sites in the slice located along an axis parallel to the pia showed that successive synchronous field potentials could originate from any of the three areas. They invaded the other two sites in c. 35.5% of the cases, while propagation to another site only or no propagation at all was observed, respectively, in 44.4% and 20% of instances. The velocity of lateral propagation of the synchronous field potential was 7.9 +/- 2.5 mm/s (range = 4.5-11.8 mm/s, n = 6). The modalities of origin and propagation remained the same after blockade of excitatory amino acid receptors. Under these conditions, however, there was a higher incidence of non-propagation and the velocity was significantly lower than in control (5.6 +/- 1.9 mm/s; range = 2.8-7.7 mm/s, n = 6). These data indicate that, in the human neocortex, 4-aminopyridine can reveal a synchronous field potential that correlates with an intracellular long-lasting depolarization and is mainly due to the activation of postsynaptic GABAA receptors. The action of excitatory amino acid receptors is not necessary for the generation and propagation of these GABA-mediated potentials. We propose that this potential represents a novel mechanism for synchronization and spread of neuronal activity, including seizure-like discharges in the human neocortex.

2-Amino-5-phosphonovalerate↗
PubMed1989

Thermogenetic changes following frontal neocortex stimulation.

Heat production changes were recorded in anesthetized female Sprague-Dawley rats after stimulation of orbital frontal neocortex. The results obtained show that orbital frontal neocortex stimulation significantly increases oxygen consumption, and core and brown adipose tissue temperature. The increase was more substantial after stimulation of left than right cortex. Administration of the beta-blocker propranolol abolished the increase in O2 consumption, core and brown adipose tissue temperature following cortical stimulation. These results are in agreement with our previous research showing that functional ablation of cerebral cortex blocked the increase in thermogenesis following lateral hypothalamic lesion. These findings also show that the orbital frontal neocortex in rats is specifically involved in the control of thermogenesis.

Adipose Tissue↗
PubMed1990

Ultrastructure of synapses and golgi analysis of neurons in neocortex of the lateral gyrus (visual cortex) of the dolphin and pilot whale.

Qualitative and computerized quantitative analyses of ultrastructural features of synapses in different layers of the primary visual cortex in the dolphin (Stenella coeruleoalba) and the pilot whale (Globicephala melaena) were carried out. Also, Golgi and cytoarchitectonic analyses were performed in the same species of cetaceans and, additionally, in Tursiops truncatus and Phocaena phocaena. It was found that on a synaptic level, as well as in cytoarchitectonic and Golgi features, the neocortex of cetaceans combines evolutionary progressive features and conservative features with a marked prevalence of the latter. Thus, the total number of synapses in visual neocortex in cetaceans is closer to this value in higher Primates. On the other hand, the laminar density of synapses per mm3 is generally the same in all layers in cetacean visual cortex and numerically is close to values found in small lissencephalic brains. Also, the synapse/neuron ratio in the dolphin visual cortex is of the same order as in cortices of rodents and lagomorphs and much higher than in cortices of advanced terrestrial mammals. Layers I and II contain approximately 70% of the total synapses in the cortical slab through visual cortex. Layer I also contains the extraverted dendrites of neurons of layer II and thus these two layers resemble a paleoarchicortical type of organization superimposed on a more typical neocortical organization of the lower cortical layers. In this respect the convexity neocortex of cetaceans is generally similar to the neocortices of phylogenetically ancient extant mammals such as basal Insectivora and Chiroptera.

Animals↗
PubMed2001

Corticocortical and thalamocortical projections to layer I of the frontal neocortex in rats.

Layer I of the neocortex is a dense synaptic zone consisting of horizontal corticocortical and widespread layer VII projections, in addition to thalamic inputs. In order to determine the origin and extent of corticocortical and thalamocortical projections to layer I of the frontal/premotor area M2 of the rat neocortex, we have used fluorescent anatomical tracing methods to determine the precise sources of cortical and thalamic input to the rostral and caudal aspects of layer I of M2. Retrograde tracer diamidino yellow (DY), applied directly to the pial surface on rostral or caudal areas of rat M2 (RM2 and CM2, respectively) labeled cells ipsilaterally throughout layers II/III, V, and VII of the adjacent primary motor area and the parietal areas (SI and SII). In addition, retrograde transport labeled contralateral CM2 or RM2 in layers II/III and V at sites homotopic to either CM2 or RM2 application sites. Contralateral layer VII was retrogradely labeled by the application to layer I of CM2, but not by the RM2 application. Retrograde DY transport from layer I of RM2 or CM2 of was seen in the ventral medial (VM), ventral lateral (VL), and posterior (Po) thalamic nuclei. However layer I transport from CM2 additionally labeled the thalamic central medial (CM) nucleus, while the RM2 labeled the mediodorsal (MD) thalamic nucleus. Upon determination that thalamic nuclei VM and VL were of primary interest in this study, due to their dense retrograde labeling, injections of anterograde tracer rhodamine dextranamine (RDA) into VM or VL were performed in order to study the projection patterns of these nuclei to layer I of the frontal cortex. RDA injections into VM labeled fibers extending through layer I of both RM2 and CM2 and throughout the cingulate cortex. Injections of RDA into VL consistently labeled dense fibers in layer I of both CM2 and RM2, although labeling was sharply decreased anterior to CM2. This study adds to a growing body of evidence that projections to layer I from all sources of cortical input make a significant contribution to integration throughout the neocortex.

Amidines↗
PubMed1997

Predominant expression of Brn-2 in the postmitotic neurons of the developing mouse neocortex.

The expression of Brn-2, a central nervous systems (CNS)-specific POU domain transcription factor, in the developing mouse neocortex was examined with an anti-Brn-2 antibody. Brn-2 protein was first detected in CNS on embryonic day (E) 11.5, and remained strong until E15.5. From E11.5 to postnatal day (P) 0, a high level of Brn-2 expression was observed in the subventricular zone, the intermediate zone, and the outer layer of the neocortex, but not in the ventricular zone. In the double-staining experiments, most of the Brn-2 positive cells were also positive for NCAM-H, an adhesion molecule specific to post-mitotic neurons. Furthermore, BrdU-labeling experiments demonstrated the presence of Brn-2 protein exclusively in postmitotic cells. These results indicated that, in the developing neocortex, Brn-2 expression is up-regulated after the final cell division. Therefore, this transcription factor may be involved in the migration and/or maturation process of the immature neuronal cells.

Animals↗
PubMed1996

Evidence for the Hebbian hypothesis in experience-dependent physiological plasticity of neocortex: a critical review.

Over the past decade, the number of experimental papers reporting physiological plasticity in primary neocortical regions, following certain types of controlled sensory experience, have increased greatly. These reports have been characterized by specific changes in receptive fields of individual neurons and/or the distributions of receptive fields across cortical maps. There is a widespread belief these types of plasticities have underlying Hebbian/covariance induction mechanisms. This belief appears to be based mainly on: (a) indirect evidence, largely from experiments on the kitten visual cortex, indicating that Hebbian induction mechanisms could be involved in neocortical plasticity; (b) the observation that some types of plasticity in systems other than neocortex follow Hebbian rules of induction; and (c) the adaptability of Hebbian induction mechanisms to models of neural plasticity. In addition, some experiments have directly tested the role of Hebbian induction mechanisms in experience-dependent neocortical plasticity. The present review critically analyzes these (and related) experiments, in order to evaluate the evidence for the Hebbian Hypothesis in experience-dependent physiological plasticity of neocortex. First, we present a set of criteria to show the involvement of a Hebbian process in any form of plasticity. Next, we compare evidence from each primary neocortical region to these criteria. Finally, we examine unresolved issues. While selected developmental studies are included, emphasis is placed on plasticity in the adult neocortex. It is concluded that there is some evidence meeting the criteria for the Hebbian hypothesis in neocortical plasticity. However, this evidence is quite limited considering the popular belief in the validity of the Hebbian hypothesis.

Animals↗
PubMed1997

Empirical assessment of synapse numbers in primate neocortex.

Reliable methods are needed to assess the impact of synaptic loss on brain function. In this empirical study we demonstrate a novel and efficient method using immunocytochemistry (ICC) and modern stereological techniques to quantify synapses in neocortex of adult primates (Macaca fascicularis). Systematic-uniform-random sections through forebrain from two 10-year-old monkeys were immunostained for estimation of synaptophysin-immunoreactive (synaptophysin-IR) presynaptic boutons (synapses). Adjacent sections were stained with cresyl violet for estimation of total number of neuronal cell bodies. The unbiased Cavalieri method was used to estimate total forebrain and neocortical volumes to a high level of precision (coefficient of error (CE) < or = 0.10)). Synapse-to-neuron ratios varied from 860 in frontal cortex to 2300 in parietal-temporal cortex. The combination of Cavalieri and optical disector methods provided a direct means of estimating approximately 1.25 trillion (x 10(12)) total synaptophysin-immunopositive boutons and approximately 1.01 billion (x 10(9)) cell bodies in neocortex, with low CEs (0.12). Time required to make precise estimates of total neocortical and forebrain volumes and total numbers of synapses and neurons in neocortex was approximately 2-3 h per case from stained sections. The approach is a direct and efficient technique to quantify total synapse and neuron numbers within a defined brain structure.

Animals↗
PubMed1989

Tongue protrusion mediated by spared anterior ventrolateral neocortex in neonatally decorticate rats: behavioral support for the neurogenetic hypothesis.

Many changes in anatomical organization and behavior follow circumscribed, neonatal cortical ablations. These include functional sparing and compensatory anatomical changes. An objective of this study was to examine the generality of such changes by reversing the usual experimental procedure, removing all cortex but a circumscribed area and examining whether the remnant made new anatomical connections, adopted new functions and whether it continued to subserve the typical functions of that area. All neocortex and cingulate cortex, except a small portion of anterior-lateral neocortex, which is normally involved in tongue and mouth use, was removed from one-day-old or adult rats. Fluorescent labelling and behavioral tests were used to evaluate its function. The results showed: (1) The remnant cortical tissue maintained similar connections in neonatal and adult groups and similar connections to those found in rats that had received no lesions. (2) The rats still displayed behaviors normally supported by this cortex, including tongue protrusion to obtain food and picking up and eating hard food efficiently. (3) Impairments were obtained on tests normally mediated by the ablated cortex, including skilled reaching and grooming. (4) When the cortical remnant was removed, tongue protrusion and efficiency of food consumption were similarly impaired in both neonate and adult groups. An additional serendipitous finding was a dissociation between two types of tongue movement: licking from a ventrally-located surface survived cortical removal but tongue protrusion did not. The results show that bilaterally spared small remnants of neocortex maintain normal functions and do not assume new functions or make new connections despite neonatal decortication. The results provide behavioral support for the neurogenetic hypothesis, which postulates that cortical circuitry is specified during early embryonic development. This suggests that there are constraints on neural remodelling and behavioral recovery following neonatal lesions. The implications of these results are discussed with respect to the documented remodelling and sparing that occur following partial or unilateral lesions within functional systems.

Animals↗
PubMed1976

Preservation of cross-modal transfer of a rate discrimination in the bushbaby (Galago senegalensis) with lesions of posterior neocortex.

The effect of lesions of posterior neocortex was assessed, using a test method that permits the demonstration of cross-modal transfer in intact bushbabies. Eight bushbabies were trained to discriminate light flashes of 18/sec and 3/sec in a go-no-go shock-avoidance task. On completion of training, four bushbabies received lesions of posterior neocortex by aspiration. After 6 wk both lesion and intact animals were returned to training in the visual discrimination. On the day following criterion performance on the visual tests, auditory clicks off the same rate and contingencies were substituted and maintained to criterion. All eight bushbabies demonstrated rapid transfer and the lesion animals were not retarded as compared with intact subjects. The cross-modal transfer of a specific rate discrimination was thus preserved in the absence of posterior intersensory neocortex. The results are discussed in terms of a hypothetical subcortical system capable of the amodal coding of simple stimulus dimensions.

Animals↗
PubMed1978

Behavior of the rat after removal of the neocortex and hippocampal formation.

After surgical removal of the neocortex and hippocampal formation, rats retained most of the movement patterns of locomotion, climbing, grooming, feeding, and fighting. However, forepaw immobility during swimming was abolished. Feeding behavior was suppressed temporarily but recovered partially. The distinctive postures of sleep and walking and a circadian rhythm of motor activity were retained. However, behaviors were often not performed at the appropriate time and place. The normal sequence of grooming behavior was disrupted; food hoarding and social behavior were essentially abolished. Removal of the neocortex alone had much the same effect as removal of neocortex and hippocampus together. Removal of hippocampus alone produced only a mild disruption of behavior. It is suggested that ascending nonspecific projections to the cerebral cortex play an important role in the moment-to-moment control of behavior but are not essential for the sleep-waking cycle.

Aggression↗
PubMed2000

Cellular and network mechanisms of rhythmic recurrent activity in neocortex.

The neocortex generates periods of recurrent activity, such as the slow (0.1-0.5 Hz) oscillation during slow-wave sleep. Here we demonstrate that slices of ferret neocortex maintained in vitro generate this slow (< 1 Hz) rhythm when placed in a bathing medium that mimics the extracellular ionic composition in situ. This slow oscillation seems to be initiated in layer 5 as an excitatory interaction between pyramidal neurons and propagates through the neocortex. Our results demonstrate that the cerebral cortex generates an 'up' or depolarized state through recurrent excitation that is regulated by inhibitory networks, thereby allowing local cortical circuits to enter into temporarily activated and self-maintained excitatory states. The spontaneous generation and failure of this self-excited state may account for the generation of a subset of cortical rhythms during sleep.

Action Potentials↗