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At least 415 records · Page 23Linked to original sources
PubMed1993

Synthesis of the foetal protein fetuin by early developing neurons in the immature neocortex.

The presence of the foetal protein fetuin has previously been demonstrated by immunocytochemistry to be specifically confined to the primordial plexiform layer, the early cortical plate and subplate zone cells in the developing neocortex of a number of species. In order to investigate its origin there, we have applied in situ hybridization in paraffin sections of Bouin's fixed foetal sheep brain, using a short anti-sense oligonucleotide probe. The distribution of fetuin mRNA has been compared with that of the protein by using anti-fetuin antibodies and immunocytochemistry. This allowed us to confirm that fetuin is synthesised initially in cells of the primordial plexiform layer and subsequently cortical plate and subplate cells. On the other hand, cells in the ventricular zone that are fetuin (protein) positive do not contain detectable fetuin mRNA. The time course of fetuin mRNA expression in the developing neocortex follows closely the previously described pattern of fetuin (protein) distribution in the sheep brain, apart from its absence from the ventricular zone where its origin is probably by uptake from cerebrospinal fluid.

Animals↗
PubMed1994

c-fos antisense reduces expression of Krox 24 in rat caudate and neocortex.

1. The aim of this study was to investigate the neurochemical effects and measure the anatomical spread of infusion of c-fos antisense (AS) DNA into the striatum. 2. Rats were anesthetized and infused in opposing striata with c-fos AS and c-fos sense (S) DNA. Ten hours later they were injected with apomorphine (2 mg/kg, i.p.) and 20 min later they were overdosed with sodium pentobarbital and their brains either perfused or frozen. Vibratome-cut sections were immunostained for the detection of c-fos, JunB, Krox 24, somatostatin, substance P, dynorphin, tyrosine hydroxylase, and enkephalin. Cryostat-cut sections from the caudate were immunostained for the detection of c-fos, JunB, and Krox 24, as well as in situ hybridization for proenkephalin mRNA. Sections from the globus pallidus were used for the autoradiographic localization of D2 dopamine and A2a adenosine receptors. Sections from the substantia nigra were used for the autoradiographic localization of D1 dopamine and cannabinoid receptors. A second group of rats were injected in opposing striata with biotin-labeled c-fos AS DNA and c-fos S DNA. Ten hours later they were challenged with apomorphine (2 mg/kg, i.p.) and 20 min later brains were either perfused or frozen. Sections from these brains were cut throughout the rostral-caudal extent of the forebrain and the biotin labeled AS DNA was localized. 3. Krox 24 was expressed at high levels on the sense side of the brain in the striatum and overlying neocortex. However, on the AS-injected side there was a reduction in Krox 24 expression in striatum and overlying cortex. The biotin-labeled AS studies confirmed that the striatal infusion spread throughout the dorsal striatum as well as the overlying neocortex. We did not detect any changes in neurotransmitter receptors, neuropeptides, or tyrosine hydroxylase in AS/S-injected rat brains. 4. These results demonstrate that c-fos AS reduces Krox 24 expression in striatal and neocortical neurons but does not change the expression of a number of other proteins involved in basal ganglia function. Whether this effect is due to nonspecific actions of c-fos AS or to its effects on a component of the transduction pathway responsible for basal Krox 24 expression (NMDA receptors?) is unknown.

Animals↗
PubMed1993

Phorbol ester-induced neuritic alterations in the rat neocortex. Structural and immunocytochemical studies.

In order to explore the effect of aberrant sprouting in the CNS, phorbol 12-myristate 13-acetate (PMA) was administered into the neocortex of adult rats. PMA is a growth-promoting agent that activates and eventually downregulates protein kinase C (PKC), and induces in the rat the expression of several genes, including amyloid precursor protein (APP). We found that multiple injections of 100 nM PMA into the rat neocortex promote, in the first week postinjection, a widespread vacuolization of the neuropil with a subsequent disruption of the synapses in the injection site, followed, at d 15, by the formation of abnormally distended clusters of neurites that resembled aberrant, sprouting axons. At d 30, fewer aberrant sprouts were observed, and many degenerating neurites were found. At the ultrastructural level, the PMA-induced abnormal neurites at d 7-15 resembled growth cones, whereas the dystrophic neurites at d 30 contained abundant dense and laminated bodies. Immunohistochemical analysis indicated that the abnormal neurites in the areas of denervation and PMA administration were positive with antisynaptophysin and antigrowth-associated protein 43 (GAP-43), with an increased APP immunoreactivity surrounding them. APP immunoreactivity around the injection site was mostly associated with pyramidal neurons and glial cells. Control experiments, where saline alone or 4 alpha-phorbol 12, 13-didecanoate (PDD, an inactive phorbol derivative) was injected, failed to show aberrant sprouting neurites. Further immunohistochemical analysis showed that the PMA-treated animals presented increased amyloid beta immunoreactivity in the pyramidal cells at the site of injection, when compared with control injections. These findings suggest that aberrant sprouting induced by overstimulation could be followed by neurodegeneration. Alternatively, PKC downregulation could directly induce the neurodegeneration, with a secondary sprouting response.

Amyloid↗
PubMed1997

Altered synaptic circuitry in the human temporal neocortex removed from epileptic patients.

Quantitative electron microscopic methods were used to study possible alterations in presumptive excitatory and inhibitory synaptic circuits in human neocortex removed from patients with intractable temporal lobe epilepsy. Synaptic density was compared between normal and abnormal regions as identified by Nissl staining and immunocytochemistry for the Ca2+-binding protein parvalbumin (PV). The normal regions showed a normal cytoarchitecture and normal pattern of staining for PV, whereas the abnormal regions displayed focal neuronal cell loss and a decrease in immunostaining for PV. In the abnormal regions the overall synaptic density (per 100 microm2 and per mm3) was approximately 30% higher than in normal regions, which corresponded to an increase of approximately 300 million synapses per mm3. The number of excitatory and inhibitory synapses was significantly higher and lower, respectively, than in normal regions. We suggest that these changes are a result of a focal sprouting of excitatory axon terminals and loss of inhibitory terminals which leads to hyperexcitatory synaptic circuits. These circuits may represent a neural substrate for the initiation or propagation of seizure activity in human epileptogenic neocortex.

Adolescent↗
PubMed1975

Partial Klüver-Bucy syndrome produced by destroying temporal neocortex or amygdala.

The temporal neocortex was removed in 4 monkeys, and 5 received amygdala destruction. Four control animals received skin and muscle incisions. The monkeys were compared on a visual pattern discrimination task, a food-non-food discrimination, and a rating scale that measured agonistic and approach behavior. Only the cortical lesion disrupted retention of the visual pattern task and neither lesion disrupted performance of the food-non-food task. Both lesions produced oral behavior, increased reaction to stimuli and decreased emotionality. Thus, the major symptoms of the Klüver-Bucy syndrome are produced by destroying either the temporal neocortex or the amygdala.

Amygdala↗
PubMed1977

Electrophysiological concomitants of eating induced from neocortex and hippocampus by electrical stimulation and injection of KC1 or norepinephrine.

EEG and DC activity were recorded from the hippocampus and neocortex in freely moving rats during consummatory behavior elicited by electrical stimulation and application of KC1 or norepinephrine to these structures. Eating induced by KC1 application or electrical stimulation of the neocortex or hippocampus was accompanied by single or multiple waves of spreading depression (SD), i.e., by traveling slow potential change. An analysis of single vs. multiple cortical SD waves indicated that when multiple waves occurred, feeding was elicited by the first wave. Injection of norepinephrine into the hippocampus resulted in a significantly larger and qualitatively different feeding response compared to KC1 injections. No apparent changes in the EEG or DC activity occurred upon norepinephrine injections.

Action Potentials↗
PubMed1978

Noradrenaline neuron innervation of the neocortex in the rat.

Noradrenaline innervation of the rat neocortex is studied by glyoxylic acid histochemistry and radioisotopic biochemical analysis. The data indicate that all neocortical areas receive a noradrenergic innervation which is identical in organization but varies in density from area to area. Radioisotopic analysis of catecholamines in the cortical areas studied reveals only the presence of significant levels of noradrenaline. Unilateral locus coerulus ablation greatly diminishes ipsilateral noradrenaline content and fiber innervation in all neocortical areas studied. Detailed histochemical analysis reveals a diffuse plexus-like arrangement of noradrenaline fibers, with each cortical layer having a distinctive pattern of innervation. Single noradrenergic fibers enter layer VI of cortex and branch at all levels to undergo extensive collateralization. Terminal horizontal branching in the molecular layer results in the most dense fiber plexus of all cortical layers. This pattern of noradrenaline innervation is similar to that of other non-specific afferent systems innervating neocortex.

Animals↗
PubMed1983

Cholinergic enzymes in neocortex, hippocampus and basal forebrain of non-neurological and senile dementia of Alzheimer-type patients.

Choline acetyltransferase (ChAT) activity and acetylcholinesterase (AChE) staining were examined in different cortical regions, hippocampal formation and basal forebrain of non-neurological controls and of patients afflicted with senile dementia of Alzheimer type (SDAT). Both enzymes showed a clear topographical distribution in the various regions studied. In SDAT cases, ChAT activity was reduced by 0-60% in the neocortex and by up to 97% in the hippocampus depending on the area and layer examined. In the nucleus of the diagonal band of Broca (NDB) and the medial septal nucleus (MSN), the activity was decreased by 65% and 55%, respectively; no significant change was found in the lateral septal nucleus (LSN), nucleus basalis of Meynert (NBM), substantia innominata (SI) and globus pallidus (GP). Comparable changes were seen in AChE staining. The results indicate that degeneration or dysfunction of cholinergic neurons in the medial septal area and possibly neocortex is an important characteristic of SDAT.

Acetylcholinesterase↗
PubMed1983

Axon collaterals of pontine taste area neurons project to the posterior ventromedial thalamic nucleus and to the gustatory neocortex.

Retrograde axonal transport of fluorescent dyes was used to demonstrate collateral projections from neurons of the pontine taste area (PTA) to gustatory-responsive areas of the posterior ventromedial thalamic nucleus (VPM), and to the gustatory neocortex (GN) of the rat. Dual-labeled PTA neurons were reliably observed following application of two different fluorescent dyes to the GN and to VPM thalamus. Dye injections into the GN and into thalamic regions surrounding the VPM nucleus, the bed nucleus of stria terminalis or the infralimbic neocortex, did not result in dual-labeled cells within the PTA. This finding suggests that gustatory information may be relayed simultaneously and specifically to VPM thalamus and to the GN via collateral axons of PTA neurons.

Animals↗
PubMed1986

Somatostatin- and neuropeptide Y-immunoreactive neurons in the neocortex in senile dementia of Alzheimer's type.

Morphological changes in neocortical somatostatin- and neuropeptide-Y-immunoreactive cells in senile dementia of the Alzheimer type (SDAT) were studied using light-microscopic immunohistochemical methods. The density of somatostatin-immunoreactive cells in the neocortex did not decrease in cases of SDAT compared with aged normal subjects. However, many somatostatin-positive fibers were abnormally swollen and bulbous in shape and they were often observed within senile plaques. The morphology of these swollen and bulbous fibers was similar to that of the swollen neurites present in senile plaques demonstrated by the silver-impregnation method. Similar fiber abnormalities were observed in sections stained with antibodies to neuropeptide Y. Somatostatin-positive cells in aged normal subjects were distributed from layer II through to the subcortical white matter. These cells were multipolar, bitufted, or pyramidal in shape, with the majority of cells being of the multipolar type. Neuropeptide Y-positive cells also were distributed from layer II through to the subcortical white matter. Most of these cells were multipolar, but a few bipolar cells were also observed. We suggest that a primary degenerative process might begin at the fiber terminals of the somatostatin neuronal system in the neocortex in SDAT.

Aged↗
PubMed1986

Influence of subcortical neurons on the functional development of cerebral neocortex in tissue culture.

The role of subcortical input and/or output pathways in the development of cortical networks was examined in organotypic tissue cultures derived from neonatal mouse brain. Comparisons were made between cultures of cerebral neocortex grown with large amounts of subcortical tissue and those that were completely isolated or included small amounts of subcortical tissue. Extracellular electrophysiological recordings showed differences in excitability and spatial distribution of responses elicited by electrical stimulation of the dorsal edge of cerebral neocortex. Cultures with proportionately greater amounts of subcortical tissue showed enhanced cortical excitability and also displayed a sharper columnar arrangement than was evident in explants that were completely isolated from subcortical influences. The data suggest that subcortical inputs and/or target fields may provide signals that influence the progressive functional development of cerebral neocortical circuitry.

Animals↗
PubMed1989

Fetal brain grafts induce recovery of learning deficits and connectivity in rats with gustatory neocortex lesion.

Three groups of rats showing disrupted taste aversion due to gustatory neocortex lesions, were studied. One group received a transplant of homotopic cortical tissue, another of heterotopic tectal tissue, obtained from 17-day-old fetuses. The third group remained without transplant as a lesioned control group. Comparisons of the taste aversion scores before and after graft, revealed that cortical grafted animals significantly improved the taste aversion, whereas those which received tectal grafts, and the cortical-lesioned controls did not. Moreover, results with horseradish peroxidase (HRP) histochemistry revealed that the homotopic, but not the heterotopic, brain transplants were able to re-establish connections with amygdala and with the ventromedial nucleus of the thalamus areas who normally kept connectivity with the gustatory neocortex. These results support the hypothesis that fetal brain transplants can reestablish cognitive functions, as well as connectivity with its host tissue.

Amygdala↗
PubMed1990

Patterns of immune rejection of mouse neocortex transplanted into neonatal rat brain, and effects of host immunosuppression.

We studied the histological and immunological characteristics of graft rejection in the rodent central nervous system (CNS) using embryonic mouse neocortex transplanted into the CNS of neonatal rats. Grafts from animals aged 8-145 days (n = 210) were examined using standard histological techniques for demonstrating cell morphology and fiber projections. Immunohistochemical techniques were used to identify graft projections into the host CNS. The incidence of graft rejection was 18% for animals between 18 and 30 days of age, but increased abruptly to 73% for animals older than 30 days. No graft rejection was seen in animals younger than 18 days. In a smaller group of xenograft recipient rats sacrificed at specific time points before and after one month of age, detailed immunohistochemical studies were performed to correlate the histological appearance of the graft with the level of major histocompatibility complex (MHC) class I and II immunoreactivity, and microglial, astrocytic and lymphocytic staining within the graft and host brain. Evidence of mild rejection as manifested by the appearance of scattered lymphocytes within the graft coincided with the development of Class I and II immunoreactivity within the graft and at the graft-host interface, which was demonstrated in some animals as early as 24 days. At 29 days of age, rejecting grafts showed diffuse MHC expression within the graft and at the graft-host interface; in contrast, unrejected grafts failed to show MHC immunoreactivity. Thirty-four day-old grafts often showed severe rejection with perivascular lymphocytic cuffing within the graft and in host parenchyma remote from the graft associated with increased MHC immunoreactivity within the host brain. In grafts older than 34 days there was frequently a violent rejection reaction with disruption of the cytoarchitecture of the graft and surrounding host tissues, and widespread MHC antigen expression. Immunosuppression with cyclosporin A was effective in avoiding rejection. The high incidence of rejection with neocortical xenografts is in striking contrast to the much lower incidence seen with retinal xenografts. This suggests that there are immunological features unique to neocortex which incite host recognition and rejection.

Animals↗
PubMed1990

Antibody to a soluble protein purified from brain selectively labels layer V corticofugal projection neurons in rat neocortex.

An antibody to a soluble protein (protein 36) isolated and purified from rat brain labels the cell bodies and processes of pyramidal cells within layer V of the rat neocortex. We have used the fluorescent retrograde axonal tracer, Fast blue, in combination with FITC immunocytochemistry to determine the projection sites of the cortical neurons detected by this antibody. Retrogradely labeled pyramidal tract neurons and corticotectal neurons are labeled with the protein 36 antibody, but the callosally projecting neurons within layer V are not. Thus within the neocortex the antibody to protein 36 may selectively detect a particular class of neuron, the corticofugal projection neurons of layer V.

Animals↗
PubMed1991

Protein kinase C activity and intracellular distribution in surgically excised human epileptic neocortex.

Protein kinase C (PKC) activity assayed by phosphorylation of exogenous histone, was measured in neocortex obtained from 32 patients following surgery for focal epilepsy and from 6 non-epileptic patients. PKC activity was not significantly different in either the particulate or cytosolic fraction from epileptic foci (n = 17) versus samples from non-spiking regions (n = 22) or neocortex from non-epileptic patients (n = 6). From 67% to 70% of total PKC activity was present in the cytosolic fraction. Phosphorylation of endogenous cytosolic substrate proteins was also not significantly different in epileptic foci.

Biopsy↗
PubMed1992

The autoinhibitory feedback control of acetylcholine release in human neocortex tissue.

Slices of human neocortex prelabelled with [3H]choline were superfused and stimulated electrically (3 Hz, 2 ms, 24 mA) in order to investigate the autoreceptor-mediated modulation of acetylcholine (ACh) release. The concentration-response curve of the muscarinic agonist oxotremorine (pKd = 6.76 +/- 0.06), which was equipotent to ACh, was shifted to the right in a parallel manner by atropine (pA2 = 8.56 +/- 0.11), as evaluated by non-linear regression analysis. Calculation of the biophase concentration of ACh showed that no ACh could be assumed to be present under these conditions, whereas following inhibition of the acetylcholinesterase by physostigmine (0.1 microM) a biophase concentration of 10(-6.89 +/- 0.11) M was estimated. The depression of ACh release due to physostigmine and tacrine, another anticholinesterase, was antagonized by atropine. When the autoinhibition was operative atropine and the M2 subtype specific muscarinic antagonists, AF-DX 116 and methoctramine, significantly increased the release of ACh whereas the 'facilitatory' effects of the M1 and M3-specific drugs, pirenzepine and hexahydrosiladifenidol, were not significant. Although different disinhibitory effects of the subtype-specific antagonists were found, they did, however, not show a pattern which would allow a clear characterisation of the subtype of muscarinic receptor associated with the autoreceptor. The release of ACh from neocortex tissue of the (non-demented) neurosurgical patients decreased with their age. This finding is consistent with the hypothesis that the normal aging process resembles a delayed and attenuated disease process of senile dementia of Alzheimer's type.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Low levels of somatostatin-like immunoreactivity in neocortex resected from presumed seizure foci in epileptic patients.

The concentration of somatostatin-like immunoreactivity (SS-LI) was determined by radioimmunoassay in neocortical tissue resected from 20 patients with pharmacologically intractable complex partial seizures. Most resections included either the anterior temporal pole neocortex (15 cases) or cingulate gyrus neocortex (3 cases). The concentration of SS-LI was lowest in cortical tissue immediately adjacent to cortical tumors. Preoperative electrical recordings suggested that this tissue was the seizure focus. In vitro recordings showed that this tissue also exhibited abnormal hyperexcitable synaptic responses. Higher levels of SS-LI, similar to normal values previously reported in human cortex, were present in non-focal temporal neocortical tissue (resected from patients in whom the seizure focus was in the ipsilateral hippocampus) in which no hyperexcitable synaptic activity was present in vitro. The functional loss of inhibitory transmitters suggested by the low SS-LI levels might provide a theoretical basis for the hyperexcitability observed in vivo and in vitro.

Cerebral Cortex↗