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At least 703 records · Page 39Linked to original sources
PubMed1992

5-Hydroxytryptamine3 receptors sited on cholinergic axon terminals of human cerebral cortex mediate inhibition of acetylcholine release.

Synaptosomes prepared from freshly obtained human cerebral cortex and labeled with [3H]choline have been used to investigate the modulation of [3H]acetylcholine ([3H]ACh) release by 5-hydroxytryptamine (5-HT). The Ca(2+)-dependent release of [3H]-ACh occurring when synaptosomes were exposed in superfusion to 15 mM KCl was inhibited by 5-HT (0.01-1 microM) in a concentration-dependent manner. The effect of 5-HT was mimicked by 1-phenylbiguanide, a 5-HT3 receptor agonist, but not by 8-hydroxy-2-(di-n-propylamino)tetralin, a 5-HT1A receptor agonist. The 5-HT3 receptor antagonists tropisetron and ondansetron blocked the effect of 5-HT, whereas spiperone and ketanserin were ineffective. It is suggested that cholinergic axon terminals in the human cerebral cortex possess 5-HT receptors that mediate inhibition of ACh release and appear to belong to the 5-HT3 type.

Acetylcholine↗
PubMed1999

Two types of aggregate in the cerebral cortex of a seizure-sensitive strain of the Mongolian gerbil.

A 70-kDa protein, P70, found mostly in the pyramidal cells of the cerebral cortex of cobalt-induced epileptogenic rats, has been implicated in epileptogenesis. The presence of a P70-like substance was searched for immunohistochemically in the cerebral cortex of MGS/ldr, a seizure-sensitive strain of the Mongolian gerbil (Meriones unguiculatus) that we previously established. Immunoreactive aggregates were observed in the pyramidal neurons of the motor cortex and the primary somatosensory cortex. Analysis using confocal laser scanning microscopy revealed that the aggregates were often colocalized with a second type of aggregate with red autofluorescence at the marginal zone of the cell somata. Both aggregates appeared and increased before the appearance of generalized tonic-clonic convulsion. These may be involved in some change of physiological function of the cerebral cortex but their presence itself is not enough to determine the occurrence of epileptic seizure because the gerbils that showed no such seizure had both aggregates.

Animals↗
PubMed1988

Size and shape of the cerebral cortex in mammals. II. The cortical volume.

The geometry of the brain and cerebral cortex in mammals has been studied from an evolutionary perspective and is described in mathematical terms. The volume of the cerebral cortex, in contrast to the cortical surface area, scales to brain volume in a similar way, irrespective of the degree of cortical folding. Among mammals, Cetacea form a subgroup, in that their volumetric data fit an isometric model better than an allometric model. An index of corticalization is presented which contains information about both the mass of interconnective nerve fibers and the degree of intracortical processing. It is shown, furthermore, that a semilogarithmic equation appropriately describes the relationship between mean cortical thickness and brain volume. Finally, allometric equations between brain volume and cortical parameters, which can be used for predictive purposes, are presented.

Animals↗
PubMed2001

Dopamine transporter immunoreactivity in monkey cerebral cortex: regional, laminar, and ultrastructural localization.

Dopamine (DA) influences a number of cognitive and motor functions that are mediated by the primate cerebral cortex, and the DA membrane transporter (DAT) is known to be a critical regulator of DA neurotransmission in subcortical structures in rodents. To gain insight into the possible functional role of cortical DAT, we compared the regional, laminar, and ultrastructural distribution of DAT immunoreactivity to that of tyrosine hydroxylase (TH), the rate-limiting enzyme in DA synthesis, in the cerebral cortex of macaque monkeys. DAT-immunoreactive (DAT-IR) axons were present throughout the cortical mantle, with substantial differences in density and laminar distribution across cytoarchitectonic areas. In particular, high densities of DAT-IR axons were present in certain regions (e.g., posterior parietal cortex, dentate gyrus) not previously thought to receive a substantial DA input. The laminar distribution of DAT-IR axons ranged from a restricted localization of labeled axons to layer 1 in lightly innervated regions to the presence of axons in all six cortical layers, with a particularly dense plexus in deep layer 3, in highly innervated regions. These regional and laminar patterns paralleled those of TH-IR axons, but several differences in fiber morphology and ultrastructural localization of DAT were observed. For example, in contrast to TH, DAT immunoreactivity in the cortex was localized predominantly to small-diameter profiles, whereas, in the dorsolateral caudate nucleus, DAT and TH immunoreactivities were present in both large-diameter and small-diameter profiles, which may represent varicose and intervaricose axon segments, respectively. Overall, the distribution of DAT-IR axons confirms and extends the results of previous reports, using other markers of DA axons, that the DA innervation of the primate cerebral cortex is global but specialized on both a regional basis and a laminar basis. In particular, these observations reveal an anatomical substrate for a direct and potent influence of DA over neuronal activity in posterior parietal cortex and in certain regions of the temporal lobe. However, due to its predominant distribution to small-diameter profiles, immunoreactivity for DAT may not be an appropriate ultrastructural marker for larger DA varicosities in the primate cortex. Moreover, this distribution of DAT suggests that cortical DA fibers may permit greater neurotransmitter diffusion than subcortical DA axons.

Animals↗
PubMed1982

Effects of N-acetyl aspartate, aspartate, and glutamate on cAMP and cGMP levels in developing rat cerebral cortex.

N-Acetyl-aspartate (N-Ac-Asp) incubated with minced cerebral cortex caused a dose-dependent increase in the levels of cAMP and cGMP. This effect was followed during postnatal development. N-Ac-Asp elicits the greatest increase in cAMP in 5-day-old and in cGMP in 40-day-old rats. The levels of cyclic AMP were always higher than those of cGMP. We also studied the effects of L-aspartate (Asp) and L-glutamate (Glu) on the levels of cyclic nucleotides in the cerebral cortex minces of rats different ages, and observed that both amino acids produced the maximum increase in cAMP at 10 days, whereas in the case of cGMP the maximal effect of Asp occurs earlier than 20 days and of Glu after 40 days. In the adult rat, the N-Ac-Asp effect on cAMP was greater than that produced by either Asp or Glu, whereas the levels of cGMP were similarly affected by all three. The data show a peak response of cAMP and cGMP to N-Ac-Asp, Asp, and Glu during cortical maturation. Because this response varies with postnatal time, N-Ac-Asp, and Glu may act upon different receptor sites.

Adenylyl Cyclases↗
PubMed1987

Non-pyramidal neurons of layers I-III in the dog's cerebral cortex (parietal lobe). A Golgi survey.

In an attempt to classify neurons in the upper layers of the cerebral cortex according to modern nomenclature based on Golgi impregnations, non-pyramidal neurons in layers II and III of the dog's cerebral cortex have been categorized into thirteen types: large double-bouquet cells with long ascending and descending axons (type I double-bouquet cells); bipolar neurons; multipolar neurons with long tufted descending axons (type II double-bouquet cells); neurons with long ascending axons; neurons with superficial axon plexuses; elongated large multipolar neurons with extended generalized axonal arborizations; neurons with long descending axons; small bi-tufted neurons with short ascending, descending or local axons; small multipolar neurons with short ascending, descending or local axons; multipolar neurons with local or extended axonal arborizations usually forming arcades (some of them also with a long descending axon); basket cells; neurogliaform neurons, and chandelier cells. Neurons in the molecular layer were horizontal cells and multipolar neurons with short axons. These data have been compared with those described in other species to provide a provisional classification of non-pyramidal neurons located in the upper layers of the cerebral cortex.

Animals↗
PubMedDate not supplied

[The cerebral cortex modulates the cutaneous transmission through the dorsal column nuclei].

INTRODUCTION: The mechanisms used by the cerebral cortex to modulate the cutaneous information at prethalamic level have been scarcely studied. This article reviews experimental evidence leading to a better understanding of this issue at the level of the cuneate nucleus (Burdach nucleus). DEVELOPMENT: The primary afferents and the corticocuneate fibers make synaptic contact with cuneothalamic neurons and with inhibitory interneurons in the middle cuneate nucleus. By stimulating the skin at different places while recording the cuneothalamic intracellular activity in anaesthetized animals with the cortex intact, with the cortex pharmacologically inactivated, or in absence of a cerebral cortex it was possible to ascertain the functional role of the corticocuneate fibers. The primary afferents activated by stimulating a particular zone of the skin induce monosynaptic excitation on a group of cuneothalamic cells at the same time at which inhibit, through intranuclear interneurons, neighboring cuneothalamic cells with unmatched receptive fields. Similarly, the corticocuneate cells receiving information from the stimulated skin further increase the excitation of the cuneothalamic neurons with matched receptive fields while inhibiting others with unmatched fields. The cortex exaggerates an excited center surrounded by an inhibited periphery thus increasing the tactile discrimination both spatially and temporally which is essential for exploratory and manipulative purposes.

Cerebral Cortex↗
PubMed1978

Drug effect on cholinergic mechanisms in the cerebral cortex.

Investigations aimed to define the components of the cholinergic network in the cerebral cortex and their functional modifications under the effect of a number of psychotropic drugs are described. By measuring acetylcholine levels and acetylcholine output from the cerebral cortex in cats and rats with various subcortical lesions, at least two systems of cholinergic neurons ascending to the cortex were demonstrated. One of the systems originates from the septum and its activity is affected by drugs acting on dopaminergic receptors.

Acetylcholine↗
PubMed1984

Thyrotropin-releasing hormone (TRH) and its analog (DN-1417): interaction with pentobarbital in oxygen consumption and cyclic AMP formation of rat cerebral cortex slices.

Effects of TRH or its analog DN-1417 (gamma-butyrolactone-gamma-carbonyl-L-histidyl-L- prolinamide ) and pentobarbital, alone or in combination, on oxygen consumption and cyclic AMP formation in rat cerebral cortex slices were investigated. The oxygen consumption of rat cerebral cortex slices as measured with a Warburg apparatus, increased linearly over time (0 to 60-min incubation at 37C). Addition of pentobarbital (1 to 7 x 10-4M) inhibited oxygen consumption, in a concentration-dependent manner, up to 45% of control. A concomitant application of DN-1417 (10-5M) or TRH (10-4M) and pentobarbital (5 x 10-4M) led to a partial recovery of the pentobarbital effect. The similar anti-pentobarbital effects were observed with the addition of carbachol (10-4M) or dibutyryl cyclic AMP (10-3M), but not norepinephrine (10-4M) or dopamine (10-4M). DN-1417, TRH, carbachol, norepinephrine or dopamine at 10-4M stimulated cyclic AMP formation in the cerebral cortex slices. Addition of pentobarbital (1 to 7 x 10-4M) inhibited the cyclic AMP formation, in a concentration-dependent manner. DN-1417, TRH or carbachol at 10-4M but not norepinephrine or dopamine at 10-4M significantly reversed the reduction of cyclic AMP formation induced by pentobarbital (5 x 10-4M). Atropine (10-4M) almost completely abolished DN-1417-, TRH- and carbachol-induced cyclic AMP formation in the presence and absence of pentobarbital.

Animals↗
PubMed2001

Automated manifold surgery: constructing geometrically accurate and topologically correct models of the human cerebral cortex.

Highly accurate surface models of the cerebral cortex are becoming increasingly important as tools in the investigation of the functional organization of the human brain. The construction of such models is difficult using current neuroimaging technology due to the high degree of cortical folding. Even single voxel misclassifications can result in erroneous connections being created between adjacent banks of a sulcus, resulting in a topologically inaccurate model. These topological defects cause the cortical model to no longer be homeomorphic to a sheet, preventing the accurate inflation, flattening, or spherical morphing of the reconstructed cortex. Surface deformation techniques can guarantee the topological correctness of a model, but are time-consuming and may result in geometrically inaccurate models. In order to address this need we have developed a technique for taking a model of the cortex, detecting and fixing the topological defects while leaving that majority of the model intact, resulting in a surface that is both geometrically accurate and topologically correct.

Cerebral Cortex↗
PubMed1995

Comparative study of the affinities of the 5-HT3 receptor antagonists, YM060, YM114 (KAE-393), granisetron and ondansetron in rat vagus nerve and cerebral cortex.

The 5-HT3 receptor blocking properties of YM060, YM114 (KAE-393), granisetron and ondansetron were examined in the vagus nerve and cerebral cortex of rats. 5-HT and 2-methyl-5-HT induced dose-dependent depolarizations of rat isolated vagus nerve with EC50 values of 2.53 (1.93-3.33) x 10(-6) and 4.03 (2.87-5.66) x 10(-6) M, respectively. YM060, YM114 and granisetron dose-dependently antagonized the depolarization of the rat vagus nerve induced by 5-HT, with decreases in the slope and maximal response at higher concentrations. Apparent pA2 values for these antagonists were 10.27 +/- 0.09, 10.12 +/- 0.16 and 9.44 +/- 0.40, respectively. Ondansetron produced a clear rightward shift of the concentration-response curve to 5-HT. The pA2 value was 8.63 (8.23-9.68). YM060 and YM114 at up to 10(-5) M produced no significant depression of the depolarizing responses to DMPP and GABA. YM060, YM114, granisetron and ondansetron displaced specific binding of [3H]GR65630 to rat cortical membranes with pKi values of 10.48 (10.41-10.57), 10.24 (10.18-10.28), 9.15 (9.02-9.28) and 8.70 (8.64-8.77), respectively. An excellent correlation (r = 0.97) was obtained between pA2 values in the vagus nerve and pKi values in the cerebral cortex. YM060, YM114, granisetron and ondansetron showed low affinities for 5-HT1A, 5-HT2 receptor, adrenergic alpha 1, alpha 2, dopamine D2, muscarinic M2, mu-opioid, benzodiazepine and histamine H1 receptors. These results support the possibility that the same type of 5-HT3 receptor occurs in rat vagus nerve and cerebral cortex.

Animals↗
PubMed1990

Influence of the pituitary-adrenal axis on benzodiazepine receptor binding to rat cerebral cortex.

The role of the pituitary-adrenal axis on receptor binding and diurnal rhythmicity of benzodiazepines (BNZ) was assessed in the rat cerebral cortex. Groups of intact, adrenalectomized (ADx) and/or hypophysectomized (HPx) rats were killed at six different time intervals during the 24-hour cycle. BNZ binding was estimated by Scatchard analysis of 3H-flunitrazepam high-affinity binding to rat cerebral cortex. Intact and sham ADx animals show a similar pattern in diurnal thythm of BNZ binding, with a maximal concentration at midnight. Bilateral ADx induced a significant increase in Bmax at all time intervals studied, the largest rise appearing at midnight. HPx alone led to a slightly smaller rise in Bmax than in ADx rats, while HPx performed in ADx rats did not modify the response to ADx alone. Bmax of BNZ binding in ADx rats reached maximal values at 3-7 days after surgery, and decreased somewhat at 15 days post-ADx. Corticosterone administration at a single dose of 5 mg i.p. 24 h before sacrifice returned Bmax to normal values in ADx as well as in ADx plus HPx rats. The corticosterone effect is not exerted on the BNZ binding sites themselves, as revealed by the lack of effect of this glucocorticoid in vitro. These findings indicate that BNZ receptors in rat cerebral cortex can be modified by the adrenal gland, with corticosterone as a primary effector.

Adrenalectomy↗
PubMed1984

Similarities and differences between high-affinity binding sites for cocaine and imipramine in mouse cerebral cortex.

Previously we found close similarities between high-affinity binding sites for [3H]cocaine and those for [3H]imipramine in the mouse cerebral cortex in regard to their association with neuronal uptake of serotonin. In the present study we investigated whether the two ligands bind to the same site. The two ligands had the following high-affinity binding properties in common: localization in both synaptosomal and microsomal fractions; vulnerability to treatment with N-ethylmaleimide, trypsin, and phospholipase A2; and resistance to exposure to dithiothreitol. In contrast, cocaine binding in the cerebral cortex was more sensitive to heat inactivation than imipramine binding. In addition, the mechanism by which cocaine inhibited [3H]imipramine binding differed from that by which imipramine inhibited [3H]cocaine binding. These data suggest that the high-affinity binding sites for [3H]cocaine and [3H]imipramine in the cerebral cortex are distinct entities.

Animals↗
PubMed2004

Thinning of the cerebral cortex in aging.

The thickness of the cerebral cortex was measured in 106 non-demented participants ranging in age from 18 to 93 years. For each participant, multiple acquisitions of structural T1-weighted magnetic resonance imaging (MRI) scans were averaged to yield high-resolution, high-contrast data sets. Cortical thickness was estimated as the distance between the gray/white boundary and the outer cortical surface, resulting in a continuous estimate across the cortical mantle. Global thinning was apparent by middle age. Men and women showed a similar degree of global thinning, and did not differ in mean thickness in the younger or older groups. Age-associated differences were widespread but demonstrated a patchwork of regional atrophy and sparing. Examination of subsets of the data from independent samples produced highly similar age-associated patterns of atrophy, suggesting that the specific anatomic patterns within the maps were reliable. Certain results, including prominent atrophy of prefrontal cortex and relative sparing of temporal and parahippocampal cortex, converged with previous findings. Other results were unexpected, such as the finding of prominent atrophy in frontal cortex near primary motor cortex and calcarine cortex near primary visual cortex. These findings demonstrate that cortical thinning occurs by middle age and spans widespread cortical regions that include primary as well as association cortex.

Adolescent↗
PubMed2003

Restricted expression of Slap-1 in the rodent cerebral cortex.

The deep layers of the mammalian cerebral cortex contain pyramidal neurons that project predominantly to subcortical targets. To understand the mechanisms that determine the identity of deeper layer neurons, a PCR based subtractive hybridisation was performed to isolate genes that are specifically expressed during the specification of these neurons. One of the genes we isolated was the rat homologue of the mouse Slap-1. SLAP-1 is an adaptor protein containing SH2-SH3 domains and it participates in the signalling of Receptor Tyrosine Kinases. In situ hybridisation studies have shown that Slap-1 is not substantially expressed before E17. At later stages, it is specifically and selectively expressed by deeper layer neurons and by neurons of layers II/III in the developing cortex. The specific timing and location of its expression, suggests that this gene may play a role in the differentiation of these neurons.

Adaptor Proteins, Signal Transducing↗