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Results for “Cerebral Cortex”

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At least 649 records · Page 36Linked to original sources

PubMed1995

Daily variations in GABA receptor function in Syrian hamster cerebral cortex.

The existence of diurnal changes in postsynaptic expression of gamma-aminobutyric acid (GABA) type A receptors was assessed in cerebral cortex of Syrian hamsters by measuring [3H]GABA binding and the influx of 36Cl- in synaptoneurosomes. A diurnal variation in dissociation constant of [3H]GABA binding to cerebral cortex membranes, and the absence of diurnal differences in maximal number of sites, were found. When the nycthemeral changes in muscimol-stimulated 36Cl- uptake by cortical synaptoneurosomes were assessed, a maximum occurred late at night (i.e. 0400 h). At 1600 h, micromolar concentrations of flunitrazepam potentiated significantly the influx of chloride induced by muscimol, while at 0400 h flunitrazepam did not exert any significant effect on 36Cl- uptake. The results indicate that postsynaptic type A GABAergic activity peaked at nocturnal hours in the cerebral cortex of Syrian hamsters.

Animals↗

PubMed1983

In vivo studies on the basal and evoked release of cholecystokinin and vasoactive intestinal polypeptide from cat cerebral cortex and periventricular structures.

In cat, radioimmunoassay revealed high concentrations of vasoactive intestinal polypeptide (VIP) and cholecystokinin (CCK) (approximately 10-90 ng/g wet weight tissue) in various regions of the cerebral cortex and in periventricular structures. Superfusion of cat cerebral cortex or perfusion from the lateral ventricle to the cisterna magna with artificial cerebrospinal fluid (CSF) was carried out in cats anesthetized with chloralose-urethane. The superfusate was assayed for VIP- and CCK-like immunoreactivity (VIP-LI and CCK-LI) simultaneously. Basal efflux of VIP-LI was 13.8 +/- 4.1 fmol/30 min/cm2 cortex and 31.6 +/- 5.0 fmol/30 min in ventriculo-cisternal superfusate. Basal efflux of CCK-LI, assayed in the same superfusate sample, was 10.7 +/- 2.5 fmol/30/min/cm2 cortex in cortical cup superfusate and 25.6 +/- 4.4 fmol/30 min in ventriculo-cisternal superfusate. The addition of potassium (50 mM) and veratridine (7.5 X 10(-5) M) to the superfusate produced significant increases in the levels of VIP-LI in both ventricular and cortical effluents. The potassium evoked release of VIP-LI and CCK-LI was inhibited by the substitution of cobalt (4 mM) for the calcium ion in the perfusion media; basal efflux was not affected. Separation of immunoreactivity by gel filtration chromatography demonstrated the CCK-LI in cat cortical tissue co-chromatographed with the COOH-terminal 4, 8, 33 and 39 amino acid peptide fragments of CCK and with a larger molecule. In contrast, the immunoreactivity in cortical and ventricular superfusate obtained during basal and evoked release co-migrated with authentic CCK octapeptide. For VIP, all immunoreactivity in tissue extract of cerebral cortex existed as a single peak which co-migrated with authentic VIP-28. The molecular pattern in cortical superfusate corresponded to that found in tissue extract.

Animals↗

PubMed1988

[Distribution of neurotensin-like immunoreactivity (NTLI) and neurotensin receptor in the rat brain and effects of various drugs on NTLI concentration and NT receptor in the rat cerebral cortex].

A radioimmunoassay for neurotensin(NT) and binding assay for NT receptor have been developed to determine neurotensin-like immunoreactivity (NTLI) concentration and to characterize NT receptor in the rat brain. The effect of various drugs affecting the dopaminergic system in the brain were also investigated to clarify the relationship between NT and dopamine. NTLI was widely distributed in various regions of the rat brain: the highest level was 53.1 +/- 14.1 ng/g wet wt in the hypothalamus, 11.9 +/- 6.0 ng/g wet wt in the thalamus, 6.9 +/- 0.7 ng/g wet wt in the cerebral cortex and 0.7 +/- 0.2 ng/g wet wt in the cerebellar cortex. The Bmax of NT receptor was 20.2 +/- 4.6 fmol/mg protein in the cerebral cortex, 16.0 +/- 4.9 fmol/mg protein in the hypothalamus, 13.3 +/- 3.7 fmol/mg protein in the thalamus and no detectable level in the cerebellar cortex. The Kd of NT receptor was 2.7 +/- 0.7 nM in the cerebral cortex, 1.9 +/- 0.8 nM in the hypothalamus, 1.1 +/- 0.2 nM in the thalamus. Intraperitoneal(ip) bolus administration of L-DOPA caused the reduction in NTLI concentration from 9.2 +/- 1.0 ng/g wet wt to 5.3 +/- 2.1 ng/g wet wt and Bmax of NT receptor from 19.7 +/- 3.1 fmol/mg protein to 13.9 +/- 2.6 fmol/mg protein with no change in Kd. Intracerebroventricular administration of dopamine also induced a significant reduction of NTLI concentration and Bmax of NT receptor with no change in Kd. Inversely, ip bolus administration of alpha-methyldopa evoked an increase in NTLI concentration from 6.9 +/- 0.9 ng/g wet wt to 12.0 +/- 3.0 ng/g wet wt and that in Bmax of NT receptor from 15.9 +/- 2.9 fmol/mg protein to 24.2 +/- 4.6 fmol/mg protein. Serial administration of haloperidol evoked an increase in Bmax of NT receptor from 16.9 +/- 1.5 fmol/mg protein to 20.5 +/- 1.9 fmol/mg protein with no changes in Kd and NTLI concentration. These results suggest that dopamine may modulate the action of NT in the rat cerebral cortex.

Animals↗

PubMed1990

[Visual evoked potentials produced by monocular flash stimuli in the cerebral cortex of the rabbit. I. Typology].

Visually evoked potentials obtained from the cerebral cortex of pigmented rabbits in response to monocularly applied flashes were studied. In agreement with their morphology, the VEP of the cerebral cortex of the rabbit were classified in three fundamental types: the first one is characterized by the presence of a large positive wave, (P1), followed by a negative wave, (N1), and finally, another positive wave, (P2); these last two being of quite variable amplitudes. The second one is characterized by an initial large negative wave, (N1), followed by a usually large positive wave, (P2). Should a positive, (P1), appear previous to N1 there would be little amplitude. The third one is characterized by the presentation of an early negative wave, (N0), of variable amplitude. This is usually followed by a large wave, (P1). N1 and P2 are present but their amplitude is variable.

Animals↗

PubMed1982

Topographic organization of basal forebrain neurons projecting to the rat cerebral cortex.

The topographic organization of basal forebrain neurons projecting to the rat cerebral cortex was investigated using the retrograde transport of horseradish peroxidase (HRP). HRP injections in cingulate and occipital cortices labeled neurons in the nucleus of the diagonal band of Broca. In contrast, injections in the frontal cortex labeled mostly neurons in the substantia innominata, and injections in the temporal and parietal cortices labeled neurons in the medial and ventral boundaries of the globus pallidus. These results suggest that the basal forebrain projection to the cerebral cortex is topographically organized.

Animals↗

PubMed1990

The action of stress and anxiolytic and anxiogenic benzodiazepine receptors ligands on [35S] T-butylbicyclophosphorothionate binding in the rat cerebral cortex.

The effect of foot shock stress on [35S] t-butylbicyclophosphorothionate (TBPS) binding to fresh unwashed membrane preparations from rat cerebral cortex was studied and was compared to those of positive and negative modulators of the GABAergic transmission. 35S-TBPS binding was increased (30%) in cerebral cortex of rats exposed to foot shock compared to the non stressed rats. In contrast, the in vitro addition and the in vivo administration of anxiolytic and positive modulators of the GABAergic transmission inhibited the specific binding of 35S-TBPS. On the other hand, the anxiogenic beta-carbolines DMCM, beta CCM, FG 7142 and beta CCE mimicked in vivo and in vitro the effect of stress. The demonstration that stress, similar to anxiogenic beta-carbolines and opposite to benzodiazepines and anxiolytic beta-carbolines, increases 35S-TBPS binding in the rat cerebral cortex, suggests that some emotional state related to stress and anxiety may result from a diminished GABAergic transmission at the level of the GABA/benzodiazepine receptor/chloride ionophore complex.

Animals↗

PubMed1985

Carbachol stimulation of phosphatidic acid synthesis: competitive inhibition by pirenzepine in synaptosomes from rat cerebral cortex.

Carbachol stimulated phosphatidic acid synthesis in cholinergically enriched synaptosomes from rat cerebral cortex. Increasing concentrations of pirenzepine (10-1000 nM) produced parallel concentration-response curves to carbachol which were shifted to the right. A pA2 value for pirenzepine of 8.4 +/- 0.3 was obtained from Schild analysis. We hypothesize that high affinity pirenzepine binding to M1 receptors is coupled to phosphatidic acid synthesis in the rat cerebral cortex.

Animals↗

PubMed2001

The expression of glutamate transporter GLT-1 in the rat cerebral cortex is down-regulated by the antipsychotic drug clozapine.

We show here that clozapine, a beneficial antipsychotic, down-regulates the expression of the glutamate transporter GLT-1 in the rat cerebral cortex, thereby reducing glutamate transport and raising extracellular glutamate levels. Clozapine treatment (25--35 mg kg(-1) day(-1) orally) reduced GLT-1 immunoreactivity in several brain regions after 3 weeks; this effect was most prominent after 9 weeks and most evident in the frontal cortex. GLT-1 protein levels were reduced in the cerebral cortex of treated rats compared with controls and were more severely affected in the anterior (71.9 +/- 4.5%) than in the posterior (53.2 +/- 15.4%) cortex. L-[(3)H]-glutamate uptake in Xenopus laevis oocytes injected with mRNA extracted from the anterior cerebral cortex of rats treated for 9 weeks was remarkably reduced (to 30.6 +/- 8.6%) as compared to controls. In addition, electrophysiological recordings from oocytes following application of glutamate revealed a strong reduction in glutamate uptake currents (46.3 +/- 10.2%) as compared to controls. Finally, clozapine treatment led to increases in both the mean basal (8.1 +/- 0.7 microM) and the KCl-evoked (28.7 +/- 7.7 microM) output of glutamate that were 3.1 and 3.5, respectively, higher than in control rats. These findings indicate that clozapine may potentiate glutamatergic synaptic transmission by regulating glutamate transport.

ATP-Binding Cassette Transporters↗

PubMed2004

Effect of thuringiensin on adenylate cyclase in rat cerebral cortex.

The purpose of this work is to evaluate the effect of thuringiensin on the adenylate cyclase activity in rat cerebral cortex. The cyclic adenosine 3'5'-monophosphate (cAMP) levels were shown to be dose-dependently elevated 17-450% or 54-377% by thuringiensin at concentrations of 10 microM-100 mM or 0.5-4 mM, due to the activation of basal adenylate cyclase activity of rat cerebral cortical membrane preparation. Thuringiensin also activated basal activity of a commercial adenylate cyclase from Escherichia coli. However, the forskolin-stimulated adenylate cyclase activity in rat cerebral cortex was inhibited by thuringiensin at concentrations of 1-100 microM, thus cAMP production decreased. Furthermore, thuringiensin or adenylate cyclase inhibitor (MDL-12330A) reduced the forskolin (10 microM)-stimulated adenylate cyclase activity at concentrations of 10 microM, 49% or 43% inhibition, respectively. In conclusion, this study demonstrated that thuringiensin could activate basal adenylate cyclase activity and increase cAMP concentrations in rat cerebral cortex or in a commercial adenylate cyclase. Comparing the dose-dependent effects of thuringiensin on the basal and forskolin-stimulated adenylate cyclase activity, thuringiensin can be regarded as a weak activator of adenylate cyclase or an inhibitor of forskolin-stimulated adenylate cyclase.

Adenosine↗

PubMed1980

Rapid thyroxine to 3,5,3'-triiodothyronine conversion and nuclear 3,5,3'-triiodothyronine binding in rat cerebral cortex and cerebellum.

Thyroxine (T(4)) to 3,5,3'-triiodothyronine (T(3)) conversion was evaluated in vivo in cerebral cortex, cerebellum, and anterior pituitary of male euthyroid Sprague-Dawley rats. Tracer quantities of (125)I-T(4) and (131)I-T(3) were injected into controls and iopanoic acid-pretreated rats 3 h before isolation of nuclei from these tissues. Specifically-bound nuclear (131)I-T(3), denoted T(3)(T(3)); (125)I-T(3), denoted T(3)(T(4)); and (125)I-T(4) were extracted and identified by chromatography. Plasma iodothyronines were similarly quantitated. In control rats, nuclear T(3)(T(3)) (percent dose per milligram DNA x 10(-4)) was 174+/-31 in cerebral cortex, 50+/-9 in cerebellum, and 932+/-158 in pituitary (all values, mean+/-SEM). Nuclear T(3)(T(4)) (percent dose per milligram DNA x 10(-4)) was 23.3+/-3.3 in cortex, 3.5+/-0.6 in cerebellum, and 39.4+/-6.9 in pituitary. Two-thirds of nuclear T(3)(T(4)) derived from local T(4) to T(3) conversion. Nuclear T(3)(T(4)) in all tissues was reduced to less than 15% of its control value by iopanoic acid treatment and all of the residual nuclear T(3)(T(4)) could be accounted for by plasma T(3)(T(4)). Nuclear T(3)(T(3)) binding was not inhibited by iopanoic acid. These results indicate there is rapid local T(4) to T(3) conversion in rat brain and nuclear binding of the T(3) produced. We have previously found that local T(3)(T(4)) production is the source of approximately 50% of the T(3) in rat anterior pituitary. The present observations that the ratio of locally derived nuclear T(3)(T(4)) to nuclear T(3)(T(3)) is much higher in cerebral cortex (0.1) and cerebellum (0.04) than in anterior pituitary (0.015) suggest that this locally produced T(3)(T(4)) is the predominant source of intracellular T(3) in these portions of rat brain.

Animals↗

PubMed2002

Maternal bilateral adrenalectomy alters nuclear composition in cerebral cortex of fetal rat.

The present study examined the effects of maternal bilateral adrenalectomy on cell nucleus composition of developing fetal rat cerebral cortex. Pregnant adult rats underwent adrenalectomy (ADX) on day 4 of gestation. Fetal brain tissues from sham and ADX groups were examined at each of 10 embryonal stages, E11-E20. From each fetus three slides of dorsal-central region of developing brain were taken and the diameter and long axis of nucleus of cells in these samples were measured. Maternal adrenalectomy generally produces increased nuclear diameter and number of ovoid nucleus in fetal cerebral cortex especially late prenatal stages. It is shown that ADX may change nuclear composition of developing cerebral cortex.

Adrenal Glands↗

PubMed1981

Patterns of vascular sprouting in the postnatal development of the cerebral cortex of the rat.

Light microscopic histochemistry for alkaline phosphatase was employed in a study of the development of vascular sprouting, with respect to time and distribution, inthe rat cerebral cortex. Sprouts were counted in the full thickness of the cerebral cortex at each day from birth to 21 days of age. Several distinct bursts of sprouting activity were observed at specific times and levels of cortex. From birth to 4 days of age, sprouting was intense in the superficial third of the cortex. At 7 to 8 days, a burst of sprouting was found which was greatest in the middle third. Additional bursts of sprouting appeared at 10 and 14 days. Developing vessels with characteristics of arteries, capillaries, or sprouts were alkaline-phosphatase positive, while veins were not. It is concluded that alkaline phosphatase is a useful marker for identification of both mature and immature vasculature, as it reveals patent and nonpatent vessels, and the sprouts which are precursors of the mature vascular bed. New vessels developing in the cortex arise mainly from blind sprouts of capillaries, evidently in response to the metabolic demands imposed by the maturational process. At birth, the majority of intracortical vessels are capillaries. By 10 days of age, most perforating vessels from the surface have taken on arterial or venous characteristics. The findings are discussed in connection with morphological and biochemical differentiation and the pattern of vascularization in the mature cerebral cortex.

Aging↗

PubMed1986

Measurement of endogenous noradrenaline release in the rat cerebral cortex in vivo by transcortical dialysis: effects of drugs affecting noradrenergic transmission.

The release of endogenous noradrenaline was measured in the cerebral cortex of the halothane-anesthetized rat by using the technique of brain dialysis coupled to a radioenzymatic assay. A thin dialysis tube was inserted transversally in the cerebral cortex (transcortical dialysis) and perfused with Ringer medium (2 microliter min-1). Under basal conditions, the cortical output of noradrenaline was stable over a period of at least 6 h and amounted to 8.7 pg/20 min (not corrected for recovery). Histological control of the perfused area revealed very little damage and normal morphology in the vicinity of the dialysis tube. Omission of calcium from the perfusion medium caused a marked drop in cortical noradrenaline output. Bilateral electrical stimulation (for 10 min) of the ascending noradrenergic pathways in the medial forebrain bundle caused a frequency-dependent increase in cortical noradrenaline output over the range 5-20 Hz. Stimulation at a higher frequency (50 Hz) resulted in a levelling off of the increase in cortical noradrenaline release. Systemic administration of the dopamine-beta-hydroxylase inhibitor bis-(4-methyl-1-homopiperazinylthiocarbonyl) disulfide (FLA 63) (25 mg/kg i.p.) markedly reduced, whereas injection of the monoamine oxidase inhibitor pargyline (75 mg/kg i.p.) resulted in a progressive increase in, cortical noradrenaline output. d-Amphetamine (2 mg/kg i.p.) provoked a sharp increase in cortical noradrenaline release (+450% over basal values within 40 min). Desmethylimipramine (10 mg/kg i.p.) produced a twofold increase of cortical noradrenaline release. Finally, idazoxan (20 mg/kg i.p.) and clonidine (0.3 mg/kg i.p.), respectively, increased and decreased the release of noradrenaline from the cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

PubMed1977

The nature of adrenoceptors in the guinea pig cerebral cortex: a microiontophoretic study.

1. Noradrenaline, isoprenaline, and phenylephrine have been applied my microiontophoresis to neurones in the guinea pig cerebral cortex. All three compounds produced depression of neuronal firing, and all could be antagonized to some extent by phentolamine or propranolol. 2. The responses to isoprenaline were substantially reduced in size after a few applications. Noradrenaline and phenylephrine responses were partially reduced at the time of isoprenaline insensitivity, and the responses could now be blocked completely by phentolamine. 3. The results suggest that two kinds of receptors are present in the guinea pig cerebral cortex, with properties similar to alpha and beta receptors in the periphery. A single receptor with intermediate properties would not readily explain the present results. 4. The results are not consistent with the proposal that alpha receptors mediate neuronal excitation, and beta receptors inhibition in the cerebral cortex. 5. It is also suggested that the failure of some previous studies on guinea pig cortex in vitro to demonstrate the presence of beta receptors may be due to the particularly rapid desensitization of these receptors.

Animals↗

PubMed2006

The role of cerebrospinal fluid on neural cell survival in the developing chick cerebral cortex: an in vivo study.

Cerebrospinal fluid (CSF) is secreted by the choroid plexuses located in the lateral, third and fourth ventricles. The fluid flows through the ventricular system, passing over all the regions of germinal activity. CSF contains growth factors and other neurotrophic factors, which are important for cell survival and proliferation. It has been shown that nerve growth factor deprivation induces apoptosis in the developing cerebral cortex. In this study, disruption of normal CSF flow on neural cell survival in the developing cortex has been investigated. Draining CSF from the ventricles of the brain during development increases the number of neural cell deaths and thinning of the cerebral cortex compared with normal ones. These data from our study indicate that normal CSF circulation is important for the survival of cells in the developing cerebral cortex and thus of CSF in the normal chick cerebral cortex development.

Animals↗

PubMed1979

Anomeric preferences of D-glucose uptake and utilization by cerebral cortex slices of rats.

On aerobic incubation of rat cerebral cortex slices with anomers of D-glucose and with 2-deoxy-D-glucose (2DG) for 5 min, the disappearance of beta-D-glucose from the incubation mixture was greater than that of alpha-D-glucose and both anomers had a greater rate of disappearance than that of 2DG. In addition, there were significantly greater consumption of oxygen and production of lactate with the beta-anomer than with the alpha-anomer. In similar experiments with 3H-labeled D-glucose anomers and [1-3H]-3-O-methyl-D-glucose (3MG), the accumulation of [1-3H]-beta-D-glucose (up to 5 min) by rat cerebral cortex slices was greater than that of [1-3H]-alpha-D-glucose. Although initially lower than that of the anomers, the accumulation of [1-3H]-3MG increased at a greater rate and, by 5 min of incubation, was greater than that of both glucose anomers. This preferential accumulation was seen to disappear when the slices were preincubated with 2DG (hexokinase inhibitor) or when the temperature of incubation was reduced to 20 degrees C. Under those conditions the data with the glucose anomers were similar to those obtained with 3MG. Our data then suggested that the greater accumulation of beta-D-glucose than of alpha-D-glucose by the slices was probably not due to differences in transport through brain cell membranes but rather to the preferential metabolism of the beta-D-glucose.

Animals↗

PubMed2005

Antioxidant defenses and lipid peroxidation in the cerebral cortex and hippocampus following acute exposure to malathion and/or zinc chloride.

This study investigates the effects of acute exposure to organophosphate insecticide malathion (250 mg/kg, i.p.) and/or ZnCl2 (5 mg/kg, i.p.), with the following parameters: lipid peroxidation and the activity of acetylcholinesterase (AChE), glutathione reductase (GR), glutathione S-transferase (GST), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PDH), and the levels of total glutathione (GSH-t) in the hippocampus and cerebral cortex of female rats. Malathion exposure elicited lipid peroxidation and reduced AChE activity in the cerebral cortex and hippocampus. It also reduced the activity of GR and GST, and increased G6PDH activity in the cerebral cortex, without changing the levels of GSH-t and GPx activity. ZnCl2 exposure reduced AChE activity and caused a mild pro-oxidative effect, since lipid peroxidation was increased in the hippocampus. ZnCl2, individually or in combination with malathion, caused a reduction in GR and GST activity in the cerebral cortex. Malathion and/or ZnCl2 did not change the GSH-t levels. Moreover, ZnCl2 prevented the increase in G6PDH activity caused by malathion. It showed that ZnCl2 had little effect against the changes induced by malathion. In fact, zinc itself produced pro-oxidant action, such as the reduction in the activity of the antioxidant enzymes GR and GST.

Acetylcholinesterase↗

PubMed1997

Associations between neuropeptide Y nerve terminals and intraparenchymal microvessels in rat and human cerebral cortex.

Neuropeptide Y (NPY) can influence local brain perfusion, possibly via direct relationships with the microvascular bed. To evaluate this possibility, the authors quantitatively analyzed by light and electron microscopy the morphological associations between immunostained NPY neuronal elements and intraparenchymal microvessels in the rat and human cerebral cortex. At the light microscopic level in the rat frontoparietal cortex, about 16% of NPY neurons and large proximal processes as well as a subset of nerve terminals not affected by double sympathectomy were associated with penetrating arterioles and local microvessels. In human temporal cortex, a dense network of NPY nerve fibers was observed, many of which approached and/or contacted intracortical vessels. At the ultrastructural level, 14% of NPY axonal varicosities in the rat cerebral cortex were considered perivascular and associated with capillaries (approximately 70%) or microarterioles (approximately 30%). They were particularly enriched in the immediate vicinity (< 0.25 micron) of the microvessels, where the perivascular astrocytic leaflets represented a frequent target. In human cerebral cortex, NPY varicosities were observed in proximity to microvessels corresponding primarily to capillaries. Perivascular NPY varicosities never established synaptic junctions with vascular or astroglial elements. The results show that central NPY nerve terminals associate with microvessels and perivascular astroglial cells in the rat and human cerebral cortex. Thus, NPY released from these nerves could possibly influence (via a parasynaptic mode of action) vascular and/or astrocytic functions depending on the distribution of NPY receptors in these cellular compartments. These results provide morphological support for the effects of NPY on brain perfusion and homeostasis.

Adult↗