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PubMed2000

Colocalization of glutamate ionotropic receptor subunits in the human temporal neocortex.

alpha-Amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA), kainate and N-methyl-D-aspartate (NMDA) receptors represent major classes of glutamate receptors (GluR) which play fundamental roles in normal excitatory synaptic activity and, probably, in the etiology of several brain diseases. These receptors are composed of multiple receptor subunit proteins, and the differential expression of these subunits in cortical neurons is considered to be one of the substrates for the functional diversity of cortical excitatory circuitry. In the monkey neocortex, different subpopulations of neurons have been identified on the basis of immunocytochemical colocalization studies using subunit-specific antibodies, but no comparable investigations have been made in the human neocortex. The aim of the present study was to determine quantitatively GluR subunit combinations in the human temporal neocortex by double-labeling immunocyto- chemical experiments. We quantified the neuronal populations expressing different receptor subtypes with fluorescent tags visualizing them with confocal laser microscopy. We studied AMPA, kainate- and NMDA-receptor subunits, using antibodies against GluR1, GluR2, GluR2/3, GluR2/4, GluR5/6/7 and NMDAR1 subunits. A high degree of colocalization (93-100%) using combinations of antibodies against GluR2 with GluR2/3, GluR2/3 with GluR2/4, and GluR2 or GluR2/4 with NMDAR1 was found, whereas for other combinations the degree of colocalization varied between 38% and 88%. Some of the percentages reported here are similar to those found in the monkey cortex, whereas others differ considerably. These results emphasize the diversity of excitatory circuits in the human neocortex, and suggest species differences with regard to some of these GluR-mediated circuits.

Animals↗
PubMed1999

Interference with the development of early generated neocortex results in disruption of radial glia and abnormal formation of neocortical layers.

Early generated layers of neocortex are important factors in forming the subsequent architecture of the cerebral cortex. To further explore the role of early generated cortex, we disrupted formation of an early generated cohort of cells by intraperitoneal injections of the mitotic inhibitor methylazoxymethanol (MAM) into pregnant ferrets timed to coincide with generation of subplate neurons in the ventricular zone. Our studies demonstrate that if early development of the neocortex is interrupted by injection of MAM during embryogenesis (on embryonic day 24 or 28; E24 or E28), a distinct laminar pattern fails to form properly in the parietal cortex. A reduced number of MAP2-positive cells were observed in the region of the subplate when compared with the number of MAP2-positive cells found in normal animals. Interference with the superficial neocortical layers that form later during development (on embryonic day 33) by appropriately timed MAM injections does not result in a severely disrupted laminar pattern. The interrupted laminar pattern that arises after early MAM injections coincides with distorted radial glial cells (identified by immunoreactivity to the intermediate filament protein, vimentin), which occur after early, but not late, MAM injections. Further analysis suggests that interference with early development of neocortex leads to premature differentiation of radial glial cells into astrocytes, as demonstrated by the presence of glial fibrillary acidic protein (GFAP). Experiments involving injections of the thymidine analog, bromodeoxyuridine (BRDU), demonstrated that 4 days after E24 MAM injection cells are generated and migrate into the thin cortical plate. By E38, however, cells continue to be generated in animals treated with MAM on E24 but do not reach their normal positions in the cortical plate. In addition, immunoreactivity using the CR50 antibody, which identifies presumptive Cajal-Retzius cells present in layer 1, demonstrates that the CR50-positive cells, normally precisely located in the outer portion of layer 1, are distributed in disarray throughout the thickness of the neocortex and intermediate zone in early MAM-treated animals, but not in those treated with MAM injections later during gestation. These findings are consistent with the idea that early generated layers are important in providing factors that maintain the environment necessary for subsequent neuronal migration and formation of neocortical layers.

Animals↗
PubMed1997

Interneuron migration from basal forebrain to neocortex: dependence on Dlx genes.

Although previous analyses indicate that neocortical neurons originate from the cortical proliferative zone, evidence suggests that a subpopulation of neocortical interneurons originates within the subcortical telencephalon. For example, gamma-aminobutyric acid (GABA)-expressing cells migrate in vitro from the subcortical telencephalon into the neocortex. The number of GABA-expressing cells in neocortical slices is reduced by separating the neocortex from the subcortical telencephalon. Finally, mice lacking the homeodomain proteins DLX-1 and DLX-2 show no detectable cell migration from the subcortical telencephalon to the neocortex and also have few GABA-expressing cells in the neocortex.

Animals↗
PubMed2000

Arealization of the neocortex in mammals: genetic and epigenetic contributions to the phenotype.

The neocortex is composed of areas that are functionally, anatomically and histochemically distinct. In comparison to most other mammals, humans have an expanded neocortex, with a pronounced increase in the number of cortical areas. This expansion underlies many complex behaviors associated with human capabilities including perception, cognition, language and volitional motor responses. In the following review we consider data from comparative studies as well as from developmental studies to gain insight into the mechanisms involved in arealization, and discuss how these mechanisms may have been modified in different lineages over time to produce the remarkable degree of organizational variability observed in the neocortex of mammals. Because any phenotype is a result of the complex interactions between genotypic influences and environmental factors, we also consider environmental, or epigenetic, contributions to the organization of the neocortex.

Animals↗
PubMed2000

GABAergic inhibition suppresses paroxysmal network activity in the neonatal rodent hippocampus and neocortex.

In the adult cerebral cortex, the neurotransmitter GABA is strongly inhibitory, as it profoundly decreases neuronal excitability and suppresses the network propensity for synchronous activity. When fast, GABA(A) receptor (GABA(A)R)-mediated neurotransmission is blocked in the mature cortex, neuronal firing is synchronized via recurrent excitatory (glutamatergic) synaptic connections, generating population discharges manifested extracellularly as spontaneous paroxysmal field potentials (sPFPs). This epileptogenic effect of GABA(A)R antagonists has rarely been observed in the neonatal cortex, and indeed, GABA in the neonate has been proposed to have an excitatory, rather than inhibitory, action. In contrast, we show here that when fast GABAergic neurotransmission was blocked in slices of neonatal mouse and rat hippocampus and neocortex, sPFPs occurred in nearly half the slices from postnatal day 4 (P4) to P7 neocortex and in most slices from P2 to P7 hippocampus. In Mg(2+)-free solution, GABA(A)R antagonists elicited sPFPs in nearly all slices of P2 and older neocortex and P0 and older hippocampus. Mg(2+)-free solution alone induced spontaneous events in the majority of P2 and older slices from both regions; addition of GABA(A)R antagonists caused a dramatic increase in the mean amplitude, but not frequency, of these events in the hippocampus and in their mean frequency, but not amplitude, in the neocortex. In the hippocampus, GABA(A)R agonists suppressed amplitudes, but not frequency, of sPFPs, whereas glutamate antagonists suppressed frequency but not amplitudes. We conclude that neonatal rodent cerebral cortex possesses glutamatergic circuits capable of generating synchronous network activity and that, as in the adult, tonic GABA(A)R-mediated inhibition prevents this activity from becoming paroxysmal.

Action Potentials↗
PubMedDate not supplied

[Long-term changes in EEG spectra of the hippocampus and neocortex during pharmacological action on the cholinergic system].

Statistical analysis of EEG spectra averaged over 10-min periods showed that inhibitor of acetylcholinesterase physostigmine induced the long-term (tens of minutes) characteristic changes in the electric activity of the dorsal hippocampus (CA1 field) and somatosensory cortex of unrestrained rats. With increasing the physostigmine dose from 0.05 to 0.5 or 1 mg/kg the averaged power of the theta-rhythm did not rise in the range of 3.6-4.9 Hz and was suppressed in the range of 5.7-11.9 Hz both in the hippocampus and neocortex. The maximal frequency shifted to the left (from 3.6-6.4 to 3.6-4.9 Hz). In contrast to this, the averaged power in the delta (1-1.5 Hz)-I and beta-2 ranges (20.3-26.5 Hz) significantly nonlinearly increased and that of the beta-1 substantially decreased. Scopolamine eliminated all extrema of the hippocampal and neocortical EEG spectra induced by physostigmine, which is indicative of the role of M-cholinoreceptors in these effects. The increased dose of physostigmine (1 mg/kg) produced inversion of the ratio between the averaged power of beta-2 in neocortex and hippocampus: it became significantly higher than in the neocortex. All these data suggest that the mechanisms of cholinergic modulation of the theta- and beta-rhythms are essentially different. We think that significant enhancement of the content of endogenous acetylcholine content produce a long-term tonic decay of the functional activity of the hippocampus and neocortex and play an important role in the mechanisms of dissociated states of memory and consciousness, contextual learning and conditioned switching.

Animals↗
PubMed1988

GABAergic basal forebrain neurons project to the neocortex: the localization of glutamic acid decarboxylase and choline acetyltransferase in feline corticopetal neurons.

Our objective was to determine whether GABAergic and cholinergic basal forebrain neurons project to the neocortex. The retrograde connectivity marker wheat germ agglutinin lectin-bound horseradish peroxidase was injected into the neocortex of adult cats. Histo- and immunohistochemical methods were combined to label sequentially connectivity and transmitter markers (glutamic acid decarboxylase; choline acetyltransferase) in forebrain neurons. The labels of each marker were identified by correlative light and electron microscopy. Two principal types of doubly labeled neurons were demonstrated. The connectivity marker was colocalized with glutamic acid decarboxylase or choline acetyltransferase. The neurons were located in the basal forebrain. Their ultrastructural, cellular, and regional organization supported 2 conclusions. (1) GABAergic basal forebrain neurons project to the neocortex. This is important new morphological evidence for the origin of inhibitory neocortical afferents from a subcortical brain site. (2) The GABAergic and cholinergic basal forebrain neurons projecting to the neocortex exhibit remarkable structural similarities. The transmitter diversity of these intertwined neocortical afferents may be significant for the pathology and treatment of human neurological disorders such as Alzheimer's disease.

Animals↗
PubMed1987

Asymmetrical involvement of the cerebral neocortex on the response to an immunopotentiator, sodium diethyldithiocarbamate.

We have previously shown that the neocortex in mice has a lateralized influence on the immune system. A partial left or bilateral neocortical lesion selectively decreases spleen T-cell numbers and function, natural killer and (NK) activity, but a right neocortical lesion do not affect NK activity, and increases T-cell numbers and T-cell-mediated events. Here we report that the immunopotentiating activity of sodium diethyldithiocarbamate (Imuthiol), a compound that selectively increases T-cell numbers and activities, is dependent on an intact neocortex. The effects of Imuthiol were examined in female C3H/HeJ mice 10 weeks after partial neocortical lesions. In animals with right or bilateral neocortical lesions, Imuthiol failed to increase the percentage of spleen T cells, did not influence the expression of class I MHC antigen on these cells, no longer induced the release in serum of specific T-cell-inducing factors, and failed to enhance T-cell-mediated events. In contrast, in animals with a left neocortical lesion, Imuthiol increased T-cell numbers and activities in a fashion that was comparable to that observed in unlesioned controls, but did not enhance NK activity. It is concluded that Imuthiol may affect immune responsiveness by acting directly on the neocortex and/or by interacting at subcortical levels with signals emitted by the neocortex. Moreover, this study reveals a major hemispheric asymmetry in the response to a drug.

Adjuvants, Immunologic↗
PubMed1992

Immunohistochemical localization of the proteinase inhibitor region of amyloid precursor proteins in the neocortex of Alzheimer's disease and aged controls.

The immunohistochemical localization of the proteinase inhibitor region of amyloid protein precursors (APPI) in the postmortem human neocortex was studied using a polyclonal antibody raised against a purified recombinant human APPI derivative produced by COS-1 cells. APPI-like immunoreactivity (APPI-LI) was found diffusely in the human neocortex. APPI-LI appeared as irregularly shaped granular structures. The size of the APPI-LI structures was 1-4 microns in diameter. APPI-LI usually formed a cluster of 10- to 20-microns diameter in the cortical gray matter and 20- to 40-microns diameter in the subcortical white matter. Double staining for APPI and glial fibrillary acidic protein indicated that APPI-LI in the white matter and molecular layer was localized exclusively in the fibrillary astrocytes. In contrast, APPI-LI was found in neurons as well as in the fibrillary astrocytes in layers II through to VI. Under fluorescence microscopy, APPI-LI in both neurons and fibrillary astrocytes were found in close association with lipofuscin. The present observations indicate that APPI is localized in neurons and astrocytes in the human neocortex and that APPI may be associated with lipofuscin or lysosome in the human neocortex.

Aged↗
PubMed1988

The early development of subcortical projections to presumptive somatic sensory-motor areas of neocortex in the North American opossum.

We have studied the early development of subcortical projections to presumptive somatic sensory-motor areas of neocortex in the North American opossum Didelphis virginiana. The opossum is born in a very immature state, 12-13 days after conception, and climbs into an external pouch where it is available for experimental manipulation. Using the retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase, we have obtained evidence that axons from the dorsal raphe and superior central nuclei, the substantia nigra, the locus coeruleus and the parabrachial nuclei reach presumptive somatic sensory-motor areas of neocortex by at least postnatal day (PND) 10. Axons showing serotonin-like immunoreactivity, presumably from the dorsal raphe and/or superior central nuclei, and axons containing tyrosine hydroxylase immunoreactivity, presumably from the substantia nigra and/or locus coeruleus, are present in the same areas at birth or shortly thereafter. Thalamic axons do not grow into comparable areas of neocortex until after PND 10. Such axons reach the subplate region of ventrolateral neocortex first and then proceed dorsomedially; by estimated PD (EPND) 21, they are present in presumptive layers I, V and VI, but they do not innervate an identified layer IV until EPND 48. The developmental sequences suggested by our study are compared with those reported for other species and are discussed in light of their importance in the formation of major sensory and motor circuits.

Animals↗
PubMedDate not supplied

Preferential ipsilateral influence of the posterior hypothalamus on the neocortex.

On the 10th--20th day after precollicular transection of the brain stem weak low-frequency electrical stimulation of the posterior hypothalamus preferentially activates the ipsilateral neocortex. After unilateral injury to the posterior hypothalamus, synchronous activity predominates in the ipsilateral neocortex. In premesencephalic animals weak single electrical stimulation of the posterior hypothalamus evokes the appearance of spindles in ipsilateral zones of the frontal cortex, whereas stronger single stimulation causes the diffuse generation of spindles in various parts of the neocortex. Besides this preferential unilateral effect, the influence of the posterior hypothalamus is found to be more strongly expressed in the frontal than in the occipital cortex. It is postulated that the posterior hypothalamus exerts its influence on the neocortex through the thalamic nuclei.

Animals↗
PubMed1976

Quantitative data on serotonin nerve terminals in adult rat neocortex.

Serotonin (5-HT) nerve terminals, specifically labeled with [3H]5-HT have been counted in light microscope radioautographs from the fronto-parietal neocortex of adult rats, following prolonged superfusions with relatively high concentrations of tracer (10(-5) M or 10(-4) M), and after 15 or 30 days of radioautographic exposure. Comparative analysis of the results indicated that all 5-HT varicosities did not possess the same capacity to accumulate the exogenous amine. Nevertheless, superfusions with 10(-4) M[3H]5-HT provided a sufficient loading of 5-HT boutons to allow their complete detection within any given layer of the neocortex. The labeled varicosities were found to be present within all cortical layers, except layer VI. Their total number was extrapolated to be approximately 1 X 10(6)/cu.mm of cortex. This figure represented a mean incidence of one 5-HT nerve terminal/850-1400 cortical synapses (0.07-0.12%). The intralaminar density of 5-HT innervation increased progressively from layer V to layer I, in a distribution pattern suggestive of unspecific afferents. Based on endogenous 5-HT levels of 346 +/- 32 ng/g for the fronto-parietal neocortex, the mean 5-HT content per varicosity could be estimated to be 0.35 X 10(-3) pg, and the concentration 1900 ng/g wet weight of terminal or 0.2%. In view of their particular ultrastructural features7, ubiquitous repartition and endogenous amine content, 5-HT nerve endings may be considered as capable of exerting a rather widespread influence in the neocortex.

Animals↗
PubMed1979

Development of the noradrenergic innervation of neocortex.

The development of the noradrenaline (NA)-neuron innervation of rat neocortex was studied by fluorescence histochemistry, high affinity uptake of [3H-]NA, and biochemical assay of regional NA content. Fluorescence histochemistry indicates that NA axons enter areas of developing neocortex prenatally and the innervation matures rapidly during early postnatal life. Frontal and lateral neocortical areas are the first to be innervated followed by occipital and parietal areas. All cortical layers receive innervation. The distribution and density of neocortical NA innervation achieves the adult pattern by the end of the first postnatal week. High affinity uptake studies confirm the observations from fluorescence histochemistry and show a very rapid maturation of the NA axon innervation with adult levels of uptake occurring by postnatal day 9. Following birth, there is a brief rise in NA content from PO to P2 in all neocortical areas. NA content then drops to low levels in all areas by P4. This is followed by a gradual increase in NA content in all areas occuring over several months. This pattern of development of NA axon innervation of neocortex demonstrates that the density and distribution of NA axons in developing neocortex matures much earlier than shown in previous studies whereas the NA content of the developing axonal plexus achieves adult levels later in postnatal life.

Adrenergic Fibers↗
PubMed1995

Immunocytochemical localization of non-NMDA ionotropic excitatory amino acid receptor subunits in human neocortex.

The distribution of immunocytochemically localized subunits that comprise ionotropic non-NMDA excitatory amino acid receptors was examined in human frontal, parietal and temporal association neocortex. AMPA/kainate receptor subunits were identified using a monoclonal antibody (3A11) that recognizes an epitope common to GluR2 and GluR4 [GluR2(4)], as well as polyclonal antisera that recognize GluR2 and GluR3 (GluR2/3). Kainate receptor subunits were identified using a monoclonal antibody (4F5) that recognizes an epitope common to GluR5/6/7. For all three antibodies used, labeling was observed in a large number of neurons throughout the human association neocortex with the highest immunoreactivity present in pyramidal-like neurons, a cellular pattern largely similar to that observed in the monkey neocortex. These data demonstrate the cellular localization patterns for some non-NMDA receptor subunits in human neocortex, details upon which further studies on the roles of these subunits in human neurological diseases can be based.

Adolescent↗
PubMed1991

Integration of neocortical embryonal grafts with the neocortex of host rats examined by Leao's spreading cortical depression.

Cortical spreading depression (SD) was used to assess the density and organization of neural elements in neocortical transplants and their connectivity with the host brain. Embryonal neocortex (E14) was transplanted into cavities in the frontoparietal cortex of 3-month-old rats. SD elicited in the cortex of anesthetized host rats (n = 12) 3 to 8 months after transplantation did not penetrate into the grafts. SD could be elicited in large transplants but did not propagate to the surrounding host neocortex. Spontaneous unit activity in the transplants was affected by SD elicited in the neocortex of the host rats anesthetized with urethane. Most units (n = 49) displayed excitatory-inhibitory (52%) or inhibitory (29%) reactions, whereas purely excitatory reactions were less frequent (8%). The results suggest that the packing density of neurons in the transplant can support SD but that the conditions at the graft-host boundary (glial scar, scarcity of neurons) stop SD propagation. High reactivity of the graft neurons to SD in the host neocortex indicates that afferentation from the host brain represents an important, predominantly excitatory contribution to the spontaneous activity of the transplant.

Animals↗
PubMed1992

Differential distribution of parvalbumin-immunoreactive pericellular clusters of terminal boutons in developing and adult monkey neocortex.

Basket cells are GABAergic inhibitory interneurons and known regulators of pyramidal cells, the major class of excitatory neurons in neocortex. Parvalbumin (PV), a calcium binding protein, has been colocalized with GABA in cortical neurons (Celio, 1986. Science 231: 995-998) and has been reported to be present in the terminal boutons of basket neurons forming pericellular clusters in monkey neocortex (Hendry et al. 1989. Exp. Brain Res. 76: 467-472). In this study, we used immunohistochemical methods to evaluate the regional and laminar distributions of PV-immunoreactive (PV-IR) pericellular clusters of terminal boutons in the neocortex of neonatal, infant, adolescent, and adult rhesus monkeys. PV-IR pericellular clusters were composed of labeled terminal boutons that outlined the somata and proximal dendrites of large pyramidal neurons in layers III and V of primary motor cortex, layers V and VI of primary visual cortex, and layer V of visual association cortex (area 18). This laminar pattern was present in neonatal animals and did not change with age in motor cortex. However, in the visual regions of adolescent and adult animals, such PV-IR structures were not detected. PV-positive pericellular clusters were not observed in the prefrontal cortex at any age. The pattern of distribution of PV-containing pericellular clusters paralleled that of a subpopulation of pyramidal neurons containing nonphosphorylated neurofilament proteins (NFP); double labeling studies confirmed that a subgroup of NFP-positive pyramidal neurons were the targets of PV-IR pericellular clusters. The distribution of PV-IR pericellular clusters was compared to that of PV-IR terminal boutons of another class of interneurons, the chandelier cells. Terminal boutons of chandelier neuron axons align in vertical rod-like structures known as cartridges. Subpopulations of chandelier axon cartridges have been previously shown to be PV-IR and their distribution in visual and prefrontal cortices has been described (DeFelipe et al. 1989. Brain Res. 503: 49-54; Lewis and Lund. 1990. J. Comp. Neurol. 293: 599-615). These two types of structures composed of PV-IR terminal boutons tended to be present in different laminae in all regions and ages examined, except in layer III of primary motor cortex where both PV-IR pericellular clusters and chandelier cartridges were found. These findings indicate that in monkey neocortex PV immunoreactivity is present in pericellular clusters of terminal boutons that are likely to arise from basket cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1993

Induction of antidepressive activity by monoaminergic transplants in rat neocortex.

To assess the ability of monoaminergic transplants to reduce immobility in the forced swimming test (FST), either adrenal medullary tissue, pineal gland tissue, or equal volumes of sciatic nerve were transplanted into the rat frontal neocortex. In the FST the duration of immobility is thought to indicate the level of antidepressant activity, as immobility times are reliably reduced by antidepressant therapies. Immobility times were reduced in rats with adrenal medullary grafts and pineal grafts to the rat frontal neocortex. In contrast, immobility times were not reduced in control sciatic nerve tissue grafts. Biochemical analysis using HPLC revealed that pineal-grafted neocortex contained higher levels of serotonin (5-HT) and adrenal medullary-grafted neocortex contained higher levels of norepinephrine (NE) than sciatic nerve-grafted or nongrafted controls. Immunocytochemical studies showed that the monoaminergic grafts survived well and continue to produce high levels of monoamines. These results support an important role for neocortical 5-HT and NE transmission in antidepressant activity and suggest that transplants of monoaminergic-containing tissue can reduce biochemical deficits in depression.

Adrenal Medulla↗
PubMed1991

Time-dependent recovery of taste aversion learning by fetal brain transplants in gustatory neocortex-lesioned rats.

We recently showed that fetal brain transplants produced a significant recovery in the ability of gustatory neocortex-lesioned rats to learn a conditioned taste aversion. In this report we assessed the capability of gustatory neocortex fetal brain transplants to produce behavioral recovery at different times. Four groups of male Wistar rats showing disrupted taste aversions due to gustatory neocortex lesions were studied. The lesioned animals received fetal cortical grafts, obtained from 16-day-old fetuses, and were retrained in the behavioral procedure after 15, 30, 45, or 60 days postgraft. Behavioral results showed a very good functional recuperation at 60 days, slight recovery at 45 and 30 days, and a poor recovery at 15 days postgraft. Results with HRP histochemistry revealed that at 30, 45, and 60 days postgrafting there were increased connections with the ventromedial nucleus of the thalamus and with the amygdala. At 15 days postgrafting there was an absence of HRP-labeled cells. In addition, behavioral recovery was correlated with increased acetylcholinesterase activity, detected histochemically, and with morphological neuronal maturation, revealed by Golgi staining. These results suggest that morphological maturity and reconnectivity between grafts and host tissue are important for behavioral recovery in gustatory neocortex-lesioned rats.

Acetylcholinesterase↗