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At least 1,675 records · Page 93Linked to original sources
PubMed1995

Acidic FGF induces NGF and its mRNA in the injured neocortex of adult animals.

Recently we reported that human recombinant acidic fibroblast growth factor (aFGF) is capable of preventing degeneration of nucleus basalis magnocellularis neurons in vivo and inducing growth of astrocytes in vitro. In the present study, the effects of aFGF on the concentration of nerve growth factor (NGF) and its messenger RNA were investigated in the rat cerebral cortex following unilateral cortical infarction. Lesioned animals exhibited a significant increase of NGF in the remaining cortex ipsilateral to the lesion. After combining cortical lesion with intracerebroventricular application of aFGF (12 micrograms/day for 7 days), we observed an 8-fold increase in the NGF concentration and a marked increase in the level of steady state NGF mRNA relative to controls ipsilaterally, and a less pronounced aFGF effect in the contralateral cerebral cortex. These results support the hypothesis that the neurotrophic effects previously shown for aFGF and basic FGF (bFGF) in neurotrophin-sensitive neurons is mediated by inducing increased production of NGF within the injured central nervous system (CNS) of adult animals.

Animals↗
PubMed1983

Lack of cholinergic deficit in the neocortex in Pick's disease.

Choline acetyltransferase activity was decreased in the frontal cortex in Alzheimer's and Gerstmann-Straussler dementias but not in Pick's disease. Cortical somatostatin was only decreased in Alzheimer's dementia. Postsynaptic muscarinic binding sites appeared to be decreased in a subpopulation of Alzheimer's patients. Our data indicate that a loss of cholinergic innervation of the cortex is not common to all dementias.

Choline O-Acetyltransferase↗
PubMed1981

Unit activity changes elicited in amygdala and neocortex of anaesthetized rats by intraperitoneal injection of lithium chloride.

Intraperitoneal injection of 0.15 M LiCl (2% body weight) to anaesthetized rats elicited, after a 6 min latency, discharge of about 50% units i basolateral amygdala (n = 27). The activation lasted for 15 min on the average. Cortical neurones were not affected by the LiCl injection. It is suggested that the amygdalar reaction to LiCl administration may account for the association of the gustatory trace with the visceral signals of poisoning which mediates acquisition of conditioned taste aversion under anaesthesia.

Amygdala↗
PubMed1981

Neuronal and glial cells in the superficial layers of early postnatal mouse neocortex: immunofluorescence observations.

Sections of immature (postnatal day 5) mouse cerebral cortex was examined for several cell-type specific immunological markers. Glial fibrillary acidic (GFA) protein or vimentin were detected in astrocytic cell processes and--more rarely--cell bodies located in the superficial layers, but not within putative Cajal-Retzius cells (CRs). These cells did, however, react with cholera toxin, tetanus toxin and NS-4 antibodies. In agreement with previous ultrastructural observations, we conclude that CRs are neurons, or at least cells which display the basic characteristics of neurons.

Animals↗
PubMed1987

Bursting in human epileptogenic neocortex is depressed by an N-methyl-D-aspartate antagonist.

Intracellular recordings were performed in human neocortical neurons in 'in vitro' slices of brain samples excised during surgical treatment of epilepsy. In 14 of 38 neurons obtained from cortex exhibiting interictal spiking, bursts of action potentials arising from a synaptic depolarizing potential could be elicited by extracellular focal stimulation of adequate strength. The N-methyl-D-aspartate (NMDA) antagonist 2-amino-5-phosphonovalerate (APV) was capable of reducing and eventually blocking these bursts without affecting the repetitive firing evoked by depolarizing intracellular pulses or the membrane input resistance. These data suggest a role played by NMDA receptors in the bursting activity displayed by human neurons from spiking cortical areas and demonstrate a potential use of NMDA antagonists as antiepileptic drugs.

2-Amino-5-phosphonovalerate↗
PubMed1990

Differential activation of glutamate receptors by spontaneously released transmitter in slices of neocortex.

Whole-cell recordings were made from neurons in neocortical brain slices in order to characterize excitatory synaptic currents mediated by glutamate receptors. Glutamate receptor antagonists, D-aminophosphonovalerate (D-APV) and CNQX, selectively attenuated distinct components in evoked synaptic currents, and were used to differentiate spontaneous synaptic currents mediated by N-methyl-D-aspartate (NMDA) and non-NMDA receptors. Spontaneous excitatory synaptic currents were independent of action potentials, varied linearly with voltage, and were blocked by the non-NMDA receptor antagonist CNQX. An NMDA receptor-mediated component was not apparent in these spontaneous synaptic currents, however, when magnesium was omitted from the recording medium, fluctuations in current and sustained inward current became apparent, and these were blocked by the NMDA receptor antagonist D-APV. Based on these findings, we conclude that NMDA and non-NMDA receptors are activated differentially by transmitter released independently of action potentials.

Animals↗
PubMed1991

Depolarizing effects of anoxia on pyramidal cells of rat neocortex.

The response of rat neocortical pyramidal neurons (layers II III) in vitro to brief periods of anoxia is a reversible depolarization of 3.8 +/- 1.01 mV (mean +/- S.E.M.; n = 114), which is accompanied by a moderate decrease in input resistance and significant depression of evoked synaptic activity. This effect is mimicked by ouabain, and is partially attenuated by the excitatory amino acid (EAA) antagonist, kynurenic acid. The estimated reversal potential (Vrev) for the anoxic depolarization (AD) is between -35 and -40 mV; in the presence of TTX a Vrev of -65 mV is obtained. Although a partial failure of Na(+)-K(+) pump activity and release of EAAs may contribute the generation of the AD, other processes are likely to be involved.

Animals↗
PubMed1991

Frequency of occurrence of perforated synapses in developing rat neocortex.

The frequency of occurrence of perforated synapses in the molecular layer of rat parietal cortex has been determined using the disector method. Perforated and non-perforated synapses were examined in electron micrographs, all quantitative procedures being carried out on adjacent sections, as required by the disector procedure. The numerical densities of perforated, non-perforated and all synapses were determined at nine ages, ranging from 0.5 to 22 months of age. The frequencies of perforated synapses were subsequently calculated. These ranged from 18.1% at 0.5 months to a peak of 37.2% at 10 months of age, and remained at around 34% up to 19 months. A frequency of 26.7% was found at 22 months of age. The mean projected height of the total perforation increased from 66 nm at 0.5 months to 133 nm at 22 months of age. These results suggest that perforated synapses are present throughout the life-span of the animal, and increase in complexity with increasing age.

Aging↗
PubMed1991

Acetylcholine and norepinephrine mediate slow synaptic potentials in normal and epileptic neocortex.

Slow excitatory postsynaptic potentials (EPSPs) were identified in rat neocortical slices. Such potentials, resistant to blockade of glutamate and gamma-aminobutyric acid-A (GABAA) receptors, were partially antagonized by muscarinic or beta-adrenergic antagonists separately, and completely blocked when these agents were added in combination. Slow EPSPs were enhanced by a cholinesterase inhibitor or catecholamine reuptake blockers. Spontaneous epileptic discharges induced by picrotoxin also triggered slow EPSPs. Such potentials were pharmacologically identical to those induced by electrical stimulation under normal conditions. A non-conventional mechanism for synaptic transmission is postulated to account for triggering of slow EPSPs by epileptic discharges.

Acetylcholine↗
PubMed1994

Colocalization of binding sites for somatostatin, muscarine and nicotine on cultured neurones of rat neocortex, cerebellum, brain stem and spinal cord: combined autoradiographic and immunohistochemical studies.

The cellular localization of binding sites for [125I]1-tyramine somatostatin ([125I]SS) was studied in explant cultures of rat CNS by autoradiography. In cultures from cortex, brain stem and spinal cord many neurones revealed binding sites for the peptide whereas in cerebellar cultures only little binding of [125I]SS was observed. In addition to neurones, astrocytes were also labelled by the peptide. By combined immunohistochemical and autoradiographic techniques, it was demonstrated that the majority of neurones which expressed binding sites for [125I]SS were also immunostained by the monoclonal cholinergic muscarinic or nicotinic receptor antibodies (M 35 and W 6, respectively), providing evidence for a colocalization of cholinergic and somatostatin receptors on the neuronal membrane.

Animals↗
PubMed1994

Pituitary adenylate cyclase activating peptide (PACAP) mRNA in the rat neocortex.

In agreement with previous studies, Northern blots revealed expression of pituitary adenylate cyclase-activating peptide (PACAP) mRNA in the rat cerebral cortex. In order to identify the cells expressing PACAP mRNA, semiquantitative in situ hybridization histochemistry was applied. A moderate concentration of PACAP mRNA transcripts was determined in the cingulate and frontal cortices, whereas lower concentrations were found in other cortical areas. In emulsion dipped sections, grains were detected over cell bodies in cortical layers II, III and IV. Grains were diffusely distributed over cells in the outer granular layer of the anterior cingulate and the retrosplenial areas. In the outer pyramidal cell layer a few neurons contained a large number of grains. These data show that PACAP mRNA is present in cells outside the hypothalamus and implies that PACAP could play a broader transmitter role in the CNS than earlier anticipated.

Animals↗
PubMed1994

The plasma membrane Ca(2+)-ATPase mRNA isoform PMCA 4 is expressed at high levels in neurons of rat piriform cortex and neocortex.

Ca2+ transport mediated by the plasma membrane Ca(2+)-ATPase (PMCA) serves an important role in regulation of cytosolic-free Ca2+ in a variety of cells. Isoform PMCA4 mRNA distribution in rat brain was studied by in situ hybridization using 33P-labeled antisense oligodeoxynucleotide probes. Very high levels of hybridization were found in piriform cortex with high levels in amygdaloid nucleus and laminae 2 and 6 of cerebral cortex. Significantly lower levels were found in hypothalamic nuclei and very low or undetectable levels were found in cerebellum, habenula, olfactory bulb, thalamus, choroid plexus of the third and fourth ventricles and in CA1 and CA3 cells of the hippocampus. These results suggest that PMCA4 is not a housekeeping form of the Ca(2+)-ATPase.

Animals↗
PubMed1995

Preservation of acetylcholine muscarinic M2 receptor G-protein interactions in the neocortex of patients with Alzheimer's disease.

The efficacy of acetylcholine muscarinic M2 receptor-G protein coupling was investigated in Alzheimer's disease and control neocortical membranes by measuring the effects of MgCl2 and 5'-guanylylimidodiphosphate (Gpp[NH]p) on high-affinity [3H]oxotremorine-M ([3H]OXO-M) binding. MgCl2 gave similar enhancements of [3H]OXO-M binding in Alzheimer's disease and control occipital cortex. In contrast, MgCl2 enhanced [3H]OXO-M binding was significantly higher in Alzheimer's disease superior temporal cortex, compared to controls. MgCl2 enhanced [3H]OXO-M binding in both the occipital and temporal cortices of the Alzheimer's disease cases was reversed to control levels by Gpp[NH]p. It is concluded that the number of high-affinity muscarinic M2 sites is increased in Alzheimer's disease superior temporal, but not occipital, cortex and that M2 sites in both regions maintain an efficient G-protein coupling.

Aged↗
PubMed1995

Unilateral grafting of fetal neocortex into a cortical cavity improves healing of a symmetric lesion in the contralateral cortex of adult rats.

Fetal neocortical tissue (ED 14) was grafted unilaterally into a cortical cavity made bilaterally in the sensorimotor cortex of adult rats. Transplantation was done immediately after the lesion (group TR0, n = 8) or with 14-day delay (group TR14, n = 8). Six rats served as lesion only controls (group LES). After long-term survival (up to 15 months) the brains were photographed and surface areas of transplant and contralateral cavities were measured by means of a graphic tablet. The results show that (a) the presence of a transplant in one lesion cavity in the cortex decrease the size of a similar cavity in the contralateral cortex and that (b) the better host transplant integration there is, the greater the effect on the contralateral lesion. No correlation between the size of the transplant and the size of the symmetric traumatic lesion was found. The ameliorating effect of the transplant on the contralateral cortical lesion size is most likely related the long-term influence of growth of trophic factors released by transplanted cells which lead to the healing of the symmetric lesion.

Animals↗
PubMed1995

Cellular distribution of the mRNA for the kappa-opioid receptor in the human neocortex: a non-isotopic in situ hybridization study.

Opioid receptors (OR) provide primary interaction sites of the human brain with opiates. Presently kappa-OR mRNA expression was studied in different cortical areas (A4, A10, A17) by in situ hybridization using digoxigenin-labeled oligonucleotides and an alkaline phosphatase-mediated color reaction. kappa-OR mRNA was expressed mainly in layers II/III and V pyramidal and layer VI multiform neurons. A4 giant pyramidal and A17 giant stellate neurons stood out labeled. These findings fit in with our data on kappa-OR protein distribution. Combined cellular assessment of protein and mRNA will enable the study kappa-OR expression under physiological and pathological conditions.

Adult↗
PubMed1996

Distribution of parvalbumin immunoreactivity in the neocortex of hypothyroid adult rats.

Early hypothyroidism produces a generalized damage in the brain and in particular, changes in the connectivity of neocortical sensory areas. In this paper, the potential alterations in local neocortical circuits have been explored using immunocytochemistry for parvalbumin (PV) in normal and hypothyroid adult rats. The number and radial distribution of PV-positive cells were similar in both groups, but in hypothyroid rats, the density of PV-positive terminal-like puncta and processes was dramatically reduced, especially in layers II-III and the lower part of layers IV-V and VI. These results suggest that thyroid hormones are necessary for normal development of cortical circuits in which PV-positive cells are involved.

Animals↗