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At least 847 records · Page 47Linked to original sources
PubMed1988

Exogenous GM1 gangliosides protect against retrograde degeneration following posterior neocortex lesions in developing hamsters.

Developing and adult hamsters received unilateral neocortex aspiration lesions and were then treated daily with exogenous ganglioside (GM1, 30 mg/kg, i.p.). When lesions were made at the age of two weeks, GM1-treated animals had less shrinkage of the dorsal lateral geniculate nucleus of the thalamus compared to controls. Although a similar observation was made in adults, the effect was not as striking. Thus, GM1-treatment reduces retrograde degeneration after neocortical lesions and this effect is most pronounced during early development.

Animals↗
PubMed1988

Microtubule-associated protein 2 (MAP 2) immunoreactivity in human fetal neocortex.

We used a monoclonal antibody to study the immunocytochemical distribution of microtubule-associated protein 2 (MAP 2) in human fetal neocortex between the ages of 16 and 22 weeks gestation. The staining pattern was lamina-specific. Neuronal somata and dendrites in all cortical layers and in the intermediate zone were labelled. Cajal-Retzius cells of layer I, large pyramidal neurons in the inner cortical plate and neurons in the subplate were most strongly immunoreactive. Separate from the underlying cortical plate a thin sheet of small neurons in the inner marginal zone was highlighted by MAP 2 immunoreactivity. The morphologic diversity, density and regional distribution of the interstitial neurons in the subplate was emphasized by MAP 2 staining. In general, the intensity of MAP 2 immunoreactivity in cell somata and dendrites correlated with the degree of neuronal differentiation but the pattern of intracellular staining also varied as a function of laminar position, and presumably cell type.

Cerebral Cortex↗
PubMed1989

Adrenergic mediated phosphatidylinositol metabolism is modulated by epileptic discharges in human neocortex.

Adrenergic mediated phosphatidylinositol (PI) hydrolysis was measured in tissues obtained from 21 patients immediately following surgery for focal epilepsy. Accumulation of [3H]inositol monophosphate (IP1) was significantly reduced (21%, P less than 0.01) in actively spiking neocortex (n = 15) versus samples from non-spiking regions (n = 9). Epileptic discharges may blunt alpha 1-adrenoceptor stimulated transmembrane signalling in human neocortical epileptic foci.

Action Potentials↗
PubMed1989

[125I]alpha-bungarotoxin binding marks primary sensory area developing rat neocortex.

The postnatal ontogeny of [125I]alpha-bungarotoxin (alpha-Btx) binding distribution in rat neocortex was described and quantified using autoradiography of in vitro labeled brain sections. During the first two weeks, distinctive transitory radial and laminar patterns emerged. Dense columnar bands of alpha-Btx binding extended through the depth of primary sensory cortex, including somatosensory, visual and auditory areas. An association of alpha-Btx binding with thalamic input zones was further demonstrated within developing somatosensory cortex, where discrete radial bands appeared over the whisker barrels around the time that ingrowing thalamocortical fibers segregate as they selectively innervate the barrels. The early laminar distribution of alpha-Btx binding also resembled that of developing thalamocortical afferents. From P12 to P20, alpha-Btx radial distinctions faded and the laminar pattern changed further to achieve the adult distribution. The spatiotemporal ontogeny of alpha-Btx binding suggests a role for alpha-Btx binding sites in the development of cortical connectivity.

Animals↗
PubMed1989

Preferential loss of GABAergic neurons in hypoxia-exposed neocortex slab cultures is attenuated by the NMDA receptor blocker D-2-amino-7-phosphonoheptanoate.

The preferential loss of GABAergic neurons in neocortex slab cultures after exposure to hypoxia was reinvestigated and confirmed using an improved morphometric analysis based on stereological principles. This preferential cell loss could be attenuated by treating the hypoxic slab cultures with the N-methyl-D-aspartate (NMDA) receptor blocker D-2-amino-7-phosphonoheptanoate (D-APH).

2-Amino-5-phosphonovalerate↗
PubMed1990

NMDA depolarizations and long-term potentiation are reduced in the aged rat neocortex.

N-Methyl-D-aspartate (NMDA) responses were recorded intracellularly in layer V neocortical neurons in in vitro slices taken from young (4-6 months) and aged (27-29 months) Fischer 344 rats. Increasing amounts of NMDA produced membrane depolarizations in both groups of cells. The regression analysis showed significantly reduced sensitivity to NMDA in old neurons compared to young. A significant long-term potentiation of the field potential evoked by subcortical white matter stimulation was present in young but not in old slices. These results suggest that aging results in a decreased sensitivity to NMDA and impaired synaptic plasticity in the neocortex.

Aging↗
PubMed1990

Release of acetylcholine, gamma-aminobutyrate, dopamine and glutamate, and activity of some related enzymes, in rat gustatory neocortex.

The gustatory neocortex (GN), final relay along the gustatory pathway, is a region of the brain involved in the neural integration of feeding behavior. Since information on the neurotransmitters in this nucleus is scarce, the aim of the present work was to establish whether acetylcholine (ACh), gamma-aminobutyric acid (GABA), dopamine and glutamate may act as transmitters within this structure. It was found that GN slices are able to release labeled GABA, ACh and glutamate but not dopamine. Additionally, it was possible to detect significant glutamic acid decarboxylase, choline acetyltransferase and acetylcholinesterase activities in GN homogenates. The activity of the two enzymes involved in acetylcholine metabolism was higher than that observed in other cortical regions. These findings suggest that GABA, ACh and glutamate probably are neurotransmitters in the GN, whereas dopamine is not.

Acetylcholine↗
PubMed1990

Correlation between acetylcholine release and recovery of conditioned taste aversion induced by fetal neocortex grafts.

Rats with lesions of the gustatory neocortex (GN) show deficits in the acquisition of taste aversion. Fetal GN grafts to a lesioned animal restore taste aversion learning and establish connections with the host brain. In this work, we examined whether the grafts are biochemically functional and whether this fact can be related to behavioral recovery. Gustatory or occipital cortices from rat fetuses were transplanted to GN-lesioned rats. Two months later, taste aversion recovery was tested and the release of labeled gamma-aminobutyric acid (GABA), acetylcholine (ACh), dopamine and glutamate from the grafted tissue was assayed. Fetal GN grafts promoted recovery of learning and released GABA, ACh and glutamate in response to K+ depolarization. Occipital cortex grafts did not induce behavioral recovery, although they were capable of releasing GABA. In contrast, these grafts did not release ACh. Moreover, GN-grafted rats in which behavioral recovery was not seen also failed to release ACh. These results are in agreement with previous findings that cholinergic transmission is important in the GN and suggest that ACh may play a role in the graft-mediated behavioral recovery observed in this model.

Acetylcholine↗
PubMed1991

The electrophysiological basis of epileptiform magnetic fields in neocortex: spontaneous ictal phenomena.

In a previous report (Barth, D.S. and Di, S., Brain Research, 530 (1990) 35-39), electrical measurements of epileptiform cellular currents produced by physiologically evoked interictal penicillin spikes in rat somatosensory cortex were directly compared to the extracranial magnetic fields these currents generate. The present study uses the same methodology to extend these observations to spontaneous interictal and ictal phenomena in rat auditory cortex, and provides a more realistic empirical foundation for physical models with which to interpret non-invasive neuromagnetic recordings of human focal seizures. These data indicate that seizure foci under 1 x 1 cm2 in cortical surface area are capable of producing magnetic fields that may be recorded at extracranial distances similar to those used in humans. Furthermore, physical models based on the dipole approximation appear to be appropriate for the interpretation of ictal magnetic field phenomena in neocortex.

Animals↗
PubMed1991

Autoradiographic distribution of sigma receptors in human neocortex, hippocampus, basal ganglia, cerebellum, pineal and pituitary glands.

Autoradiographic distributions of [3H]1,3-di-O-tolylguanidine, [3H]DTG, binding to sigma (sigma) receptors were studied in key human brain regions. High densities occurred in the substantia nigra pars compacta and cerebellum. Pineal and pituitary levels were moderate. In neocortex, binding was high in laminae II-IVA and much lower in the midzone. Moderate binding occurred over hippocampal dentate granular cells and in the striatum. These results differ from those reported for the rodent.

Adult↗
PubMed1991

Influence of substantia innominata neuronal activity on neocortex neuronal reactions during conditioned reflex.

Impulse activity of substantia innominata (SI) and motor cortex neurons was studied in cats during conditioned placing with food reinforcement. It was shown that SI neurons have been activated first directly by sound stimuli and later by food reward. Stimulation of SI did not change the background activity of neocortex neurons but promoted the modulation of impulse response to conditioned stimuli. The modulating effect of the SI has a mainly excitatory character, that manifested itself either in a change and increase of the impulse responses of cortical neurons which responded initially to sound stimuli, or in the appearance of impulse responses in those neurons which showed no initial reaction to conditioned sound stimuli.

Acoustic Stimulation↗
PubMed1992

Calbindin immunoreactivity in normal human temporal neocortex.

Calbindin immunoreactivity in the temporal neocortex was examined in 4 subjects with no neurological, metabolic or malignant disease. The brains were obtained between 1 and 4 h after death and rapidly fixed by perfusion with 4% paraformaldehyde through the carotid arteries, cut into slabs, cryoprotected and stored at -80 degrees C. Sections of the whole left temporal lobe obtained with a freezing microtome were processed free-floating with a well known monoclonal antibody against calbindin according to the peroxidase-antiperoxidase (PAP) method. Calbindin-immunoreactive (CaBP-ir) neurons were found to be local-circuit neurons (interneurons) mainly distributed in the upper cortical layers (layers I, II and III), and were categorized as small multipolar neurons with ascending dendrites ramifying in the molecular layer, small bitufted cells, pyramid-like cells in layer II, horizontal neurons in the molecular layer, multipolar neurons with long descending dendrites, and large double-bouquet cells, some of them exhibiting a very long dendrite with claw-shaped terminals in layer V. Less than 10% of all CaBP-ir neurons were localized in the remaining cortical layers. Pyramidal cells were only very weakly or not stained at all. In addition, CaBP-ir fibres formed a dense plexus in the molecular layer, and vertical bundles 8-10 microns thick and 500-600 microns long, separated by blank spaces 20-40 microns wide were distributed in layers III and V/VI.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Location of nicotinic and muscarinic cholinergic and mu-opiate receptors in rat cerebral neocortex: evidence from thalamic and cortical lesions.

In vitro receptor binding techniques were used to identify the cellular location of nicotinic and muscarinic cholinergic and mu-opiate receptors in the fronto-parietal region of rat cerebral neocortex. Changes in the normal pattern of receptor binding of ligands for these 3 receptors were examined in a series of adjacent sections after unilateral thalamic fiber or cortical cell lesions. Thalamocortical fibers were destroyed by making either electrolytic lesions or kainic acid injections centered in the region of the thalamic ventrobasal complex. These lesions reduced cortical labeling of nicotinic ([3H]nicotine) and mu-opiate ([3H]DAGO) receptors while they did not affect cortical muscarinic ([3H]quinuclidinyl benzilate ([3H]QNB)) labeling. Intracortical injections of quinolinic acid (QA) were used to destroy cortical neurons and spare extrinsic fibers. Cortical QA lesions markedly reduced muscarinic and mu-opiate labeling, but had no significant effect on nicotinic binding at short survivals. Our results suggest that a subset of nicotinic receptors is located presynaptically on the specific thalamo-cortical fibers, while muscarinic receptors are located primarily on cortical neurons. Receptors of the mu-opiate type appear to be located both presynaptically on thalamo-cortical terminals and on intrinsic cortical neurons. The differences in the location of these receptor types suggest that each one modulates discrete aspects of cortical processing.

Animals↗
PubMed1993

Microdialysis of interstitial amino acids during spreading depression and anoxic depolarization in rat neocortex.

We have examined the effect of cortical spreading depression (SD) and anoxic depolarization (AD) on the interstitial concentration changes of amino acids (AA) in the neocortex of anesthetized rats using microdialysis and HPLC. Accompanying SD alanine increased to 126 +/- 11%, arginine to 116 +/- 3%, aspartate to 160 +/- 17%, glutamate to 163 +/- 9%, glycine to 158 +/- 21%, serine to 125 +/- 9%, and taurine to 172 +/- 15% (mean +/- 1 S.E.M.). The increases lasted for about 1 min. Histidine decreased to 74% +/- 4% at 1 min following SD, and returned to normal 4 min later. Cardiac arrest triggered AD after approximately 2 min, immediately followed by changes of interstitial AAs. At 5 min after AD alanine had increased to 183 +/- 13%, aspartate to 3,458 +/- 656%, GABA to 338 +/- 35%, glutamate to 1,696 +/- 546%, glycine to 297 +/- 37%, serine to 153 +/- 12%, and taurine to 1721 +/- 98% as compared to control values (mean +/- 1 S.E.M.). Histidine decreased to 78 +/- 2% at 3 min following AD while arginine exhibited insignificant variations around the baseline. The increase of glutamate during SD is consistent with activation of NMDA-receptors as an essential requirement for this reaction. The increase of AAs may also contribute to the sequence of events leading to AD, though the exact mechanism remains unknown. SD is an important pathophysiological mechanism of the ischemic penumbra associated with focal cerebral ischemia, while AD reflects the electrophysiological status of the infarct core.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1995

Changes of extracellular calcium concentration induced by application of excitatory amino acids in the human neocortex in vitro.

The influence of the glutamate subreceptor agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) on cortical field potentials and on changes in extracellular free calcium concentration ([Ca2+]o) was tested on human neocortical slices (eleven from nine different patients). The tissue used was a small portion of that which is normally removed for the treatment of a brain tumor. [Ca2+]o and field potentials were measured by Ca(2+)-selective microelectrodes. Local pressure-microejection of NMDA (100 mumol/l)- and AMPA (1 mmol/l)-induced negative field potentials with maximal amplitudes of 0.9 +/- 0.1 mV (11 slices, mean +/- S.E.M.) and 1.0 +/- 0.1 mV (nine slices), respectively. The negative field potentials induced by NMDA were accompanied by monophasic decreases of [Ca2+]o (0.8 +/- 0.1 mmol/l, nine slices). AMPA elicited no (three slices) or only minor decreases of [Ca2+]o (0.2 +/- 0.1 mmol/l, five slices). The responses to the glutamate subreceptor agonists NMDA and AMPA were reversibly depressed by adding their specific antagonists DL-2-amino-5-phosphonovalerate (APV, 100 mumol/l, six slices) and 6-cyano-7-nitroquinoxalin-2,3-dion (CNQX, 5 mumol/l, four slices), respectively. The results correspond to findings in animal experiments and are consistent with the interpretation that in the human neocortex the Ca2+ permeability of channels gated by NMDA is higher than those gated by AMPA.

2-Amino-5-phosphonovalerate↗
PubMed1994

Calcium-activated proteolysis in rat neocortex induced by transient focal ischemia.

Ischemia-induced elevation of intracellular calcium triggers a cascade of events which is considered to play a major role in neuronal death. One candidate to participate in this process is the calcium-sensitive protease, calpain. This protease is activated by calcium, and is capable of degrading critical cytoskeletal and regulatory proteins. In order to further elucidate the role of calpain in focal ischemic damage, the present study investigated the proteolysis of spectrin, a preferred substrate for calpain, in response to transient focal ischemia. Ischemia was induced by occluding reversibly both carotid arteries and the left middle cerebral artery for three hours in Sprague-Dawley rats. Western blotting techniques were used to identify and quantify the amounts of spectrin breakdown products (BDPs) in neocortical samples from the area destined for infarction, the peri-infarct area, and the contralateral hemisphere. Substantial increases in spectrin proteolysis were observed within the first few hours of ischemia in the areas that will undergo infarction. The increase in spectrin BDPs in these areas reached a plateau around the end of the 3 h ischemic period. In the peri-infarct zone, the levels of spectrin BDPs increased in a biphasic manner. A small to moderate increase was observed by the second hour of ischemia, followed by a larger increase between the 6th and 24th hours post-ischemia. The contralateral neocortex showed a significant increase in BDPs at 2 h after the initiation of ischemia. A smaller increase in BDPs was observed thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Post-activation potentiation in the neocortex: I. Acute preparations.

Long-term potentiation is widely studied as a memory model, and has been demonstrated in a number of subcortical sites in both acute and chronic preparations. In the neocortex, however, most of the demonstrations of LTP have been in neocortical slice or acute preparations, and even these have often required a drug-induced attenuation of inhibition before the LTP could be reliably expressed. In this paper we show that LTP can be reliably expressed in adult rats in a number of neocortical sites, both ipsilateral and contralateral to the site of callosal stimulation. We also show that, when recording field potentials, LTP is expressed roughly equally at all cortical depths. In a third experiment, we monitored input/output (I/O), paired-pulse inhibition and short-term potentiation effects over the course of LTP induction. The ipsilateral responses were, as expected, of shorter latency and larger amplitude than contralateral responses. They also showed small spike-like components that correlated with cell discharge. Nevertheless, the contralateral responses tended to show the largest LTP effects. The paired pulse effect was mainly depression, lasting for up to 3000 ms, at both ipsilateral and control sites. The short-term potentiation components were best fit by two summed exponentials with time constants of about 70 s and 12 min. The LTP effect lasted at least two h which was the longest period monitored in these experiments.

Animals↗
PubMed1994

Post-activation potentiation and depression in the neocortex of the rat: II. Chronic preparations.

Although long-term potentiation (LTP) has been demonstrated in a number of subcortical sites in chronic preparations, there have been no demonstrations of LTP in the neocortex of chronic preparations. Even neocortical slice and acute preparations often require a drug-induced suppression of inhibition before LTP effects can be reliably induced. We have attempted to induce LTP in neocortical sites in 7 different experiments using chronically prepared adult rats. We were unable to obtain any evidence, even a trend, for the induction of LTP. The following manipulations were tested: (1) standard stimulation train parameters that have been shown to be highly effective in subcortical and hippocampal sites; (2) a 10-fold increase in the intra-train pulse durations; (3) variations in train pulse frequency (1 Hz to 300 Hz) and train duration (100 ms to 15 min); (4) co-activation of multiple inputs by stimulation of combinations of cortical sites or cortical and thalamic sites; (5) reduction of inhibition by administration of picrotoxin; 5) Housing of animals in an enriched environment; (6) utilization of the neocortical stimulation trains as a cue in a learning task; (7) application of pilocarpine to co-activate cholinergic systems. Although none of these manipulations produced LTP, the application of pilocarpine did facilitate the induction of a long-lasting depression effect. These findings contrast with the results obtained from anesthetized rats and from studies using brain slices, where LTP can be reliably induced. These results are discussed in light of other recent findings with respect to LTP and LTD effects.

Animals↗