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At least 721 records · Page 40Linked to original sources

PubMed1998

Differential regulation of GABA(A) receptor gene expression by ethanol in the rat hippocampus versus cerebral cortex.

Previous research has shown that chronic ethanol consumption dramatically alters GABA(A) receptor alpha1 and alpha4 subunit gene expression in the cerebral cortex and GABA(A) receptor alpha1 and alpha6 subunit gene expression in the cerebellum. However, it is not yet known if chronic ethanol consumption produces similar alterations in GABA(A) receptor gene expression in other brain regions. One brain region of interest is the hippocampus because it has recently been shown that a subset of GABA(A) receptors in the hippocampus is responsive to pharmacologically relevant concentrations of ethanol. Therefore, we directly compared the effects of chronic ethanol consumption on GABA(A) receptor subunit gene expression in the hippocampus and cerebral cortex. Furthermore, we investigated whether the duration of ethanol consumption (14 or 40 days) would influence regulation of GABA(A) receptor gene expression in these two brain regions. Chronic ethanol consumption produced a significant increase in the level of GABA(A) receptor alpha4 subunit peptide in the hippocampus following 40 days but not 14 days. The relative expression of hippocampal GABA(A) receptor alpha1, alpha2, alpha3, beta(2/3), or gamma2 was not altered by either period of chronic ethanol exposure. In marked contrast, chronic ethanol consumption for 40 days significantly increased the relative expression of cerebral cortical GABA(A) receptor alpha4 subunits and significantly decreased the relative expression of cerebral cortical GABA(A) receptor alpha1 subunits. This finding is consistent with previous results following 14 days of chronic ethanol consumption. Hence, chronic ethanol consumption alters GABA(A) receptor gene expression in the hippocampus but in a different manner from that in either the cerebral cortex or the cerebellum. Furthermore, these alterations are dependent on the duration of ethanol exposure.

Animals↗

PubMed1984

Magnesium ions potentiate the formation of adenosine 3',5'-monophosphate induced by depolarizing agents in the rat cerebral cortex in vivo.

Pretreatment of the rat cerebral cortex by topical application of 1.5 mol X 1(-1) MgCl2 in order to prevent the induction of spreading depression by depolarizing agents did not inhibit but potentiated the ability of 1.0 mol X 1(-1) K+ (39 pmol cAMP/mg prot.) and 0.2 mol X 1(-1) veratridine [11 pmol cAMP/mg prot.] to produce the accumulation of cyclic adenosine monophosphate [cAMP] by 110% and 180% respectively. Hypertonic NaCl solutions [2.0 and 3.5 mol X 1(-1)] alone did not affect the normal cAMP levels in the cortex, neither was the effect of K+ modulated by pretreatment of the cortex by topical application of 3.5 mol X 1(-1) NaCl. Additive effects of K+ and veratridine were found on cAMP formation. The mechanism of potassium-stimulation of cAMP formation and the effect of Mg2+ is discussed.

Animals↗

PubMed1990

Differential regulation by dexamethasone of glucocorticoid receptor messenger RNA concentrations in neuronal cultures derived from fetal rat hypothalamus and cerebral cortex.

1. Differential regulation, by dexamethasone, of glucocorticoid receptor gene expression was studied in three different neuronal cultures derived from hypothalamus amygdala, and cerebral cortex. 2. Cellular glucocorticoid receptor (GR) mRNA concentration was measured by hybridization using a 32P-labeled RNA probe complementary to a 2.2-kb fragment of the glucocorticoid receptor mRNA. Changes in the amount of GR mRNA were evaluated in relation to the content of beta-actin mRNA. 3. In cells derived from either hypothalamus or cerebral cortex, we observed a complex pattern of GR mRNA concentrations which were characterized by cyclic variations of GR mRNA content during continuous treatment with dexamethasone for up to 72 hr. 4. In contrast to cells derived from the hypothalamus where a persistent 30-40% reduction in GR mRNA levels was seen for up to a least 72 hr, we observed, in cells derived from the cerebral cortex, a sustained increased (1.4-fold) of the GR mRNA at this same time interval.

Animals↗

PubMed1980

Two-dimensional maps of the cerebral cortex.

A procedure is described for constructing two-dimensional, unfolded representations of the cerebral cortex. The technique is based on information contained in outlines of histological sections, and it allows an entire hemisphere to be represented on a single cortical map. Maps for different hemispheres from individuals of the same species are similar in size, shape, and organization, and their configuration is largely independent of the plane of sectioning used for reconstruction. Many types of information pertaining to the location and organization of different functional subdivisions can be displayed on cortical maps; representative applications of the technique to mapping cerebral cortex in the macaque and the cat are shown. Areal measurements on cortical maps correspond closely (generally within 20%) to actual surface areas in the intact hemisphere. Therefore, the maps can also be used to provide accurate determinations of the absolute and relative extent of various anatomical and functional subdivisions of the cortex.

Animals↗

PubMed2005

Ovariectomy enhances acetylcholinesterase activity but does not alter ganglioside content in cerebral cortex of female adult rats.

In the present work we investigated the effect of ovariectomy on acetylcholinesterase (AChE) activity and ganglioside content in cerebral cortex of female rats. We also studied the activity of butyrylcholinesterase (BuChE) in serum of these animals. Adult Wistar rats were divided into three groups: (1) naive females (control), (2) sham-operated females and (3) castrated females (ovariectomy). Thirty days after ovariectomy, rats were sacrificed by decapitation without anaesthesia. Blood was collected and the serum used for BuChE determination. Cerebral cortex was homogenized to determine AChE activity and extracted with chlorophorm:methanol for ganglioside evaluation. Results showed that rats subjected to ovariectomy presented a significant increase of AChE activity, but did not change the content and the profile of gangliosides in cerebral cortex when compared to sham or naive rats. BuChE activity was decreased in serum of rats ovariectomized. Our findings suggest that the alteration in the activity of brain AChE, as well as serum BuChE activity caused by ovariectomy may contribute to the impaired cognition and/or other neurological dysfunction found in post-menopausal women.

Acetylcholine↗

PubMed1991

Multiple representations of pain in human cerebral cortex.

The representation of pain in the cerebral cortex is less well understood than that of any other sensory system. However, with the use of magnetic resonance imaging and positron emission tomography in humans, it has now been demonstrated that painful heat causes significant activation of the contralateral anterior cingulate, secondary somatosensory, and primary somatosensory cortices. This contrasts with the predominant activation of primary somatosensory cortex caused by vibrotactile stimuli in similar experiments. Furthermore, the unilateral cingulate activation indicates that this forebrain area, thought to regulate emotions, contains an unexpectedly specific representation of pain.

Adult↗

PubMed1993

Expression of GAD (M(r) 67,000) and its messenger RNA in basal ganglia and cerebral cortex after ischemic cortical lesions in rats.

Glutamic acid decarboxylase (GAD) is present in most efferent neurons of the striatum and in interneurons both in the striatum and the cerebral cortex. We have examined the effects of unilateral lesions of the frontoparietal cortex by thermocoagulation of pial vessels in adult rats on GAD expression in the basal ganglia and in the contralateral cerebral cortex. Levels of GAD were measured in the striatum and its target areas (pallidum and substantia nigra) with radioimmunohistochemistry and an antibody specific for GAD (M(r) 67,000: GAD67); levels of the corresponding mRNA were measured at the single-cell level by in situ hybridization histochemistry with a [35S]RNA probe. Five days after surgery, GAD67 immunoreactivity was markedly increased in striatal target areas on the side of the lesion. In the striatum, increases in immunoreactivity were small at 5 days, larger at 3 weeks, and accompanied by an increase in mRNA levels lasting up to 3 months after surgery. In contrast, in the frontal cortex contralateral to the lesion, levels of labeling for GAD67 mRNA per neuron were decreased 3 weeks and 3 months after surgery. The results suggest that local ischemic lesions of cerebral cortex in adult rats lead to prolonged and opposite alterations in GAD67 synthesis in basal ganglia and contralateral cortex.

Animals↗

PubMed1989

Age-dependent modifications of mitochondrial proteins in cerebral cortex and striatum of rat brain.

The protein composition of free mitochondria purified from cerebral cortex and striatum during aging was analyzed by gel electrophoresis. Mitochondria were isolated from cerebral cortex and striatum of 4-, 12-, and 24-month-old rat brain. The percent amount of mitochondrial proteins after gel-electrophoretic separation was determined densitometrically. A significant decrease in the amount of two polypeptides (with molecular weights of 20 and 16 kDa, respectively) in both brain regions during aging was found. The decrease was higher in the striatum indicating a greater vulnerability of this brain area to the aging process. The age-dependent modifications of mitochondrial proteins observed may play an important role in several mitochondrial functions, such as energy transduction and transport processes as well as in structural changes occurring with age, causing altered membrane permeability and fluidity.

Aging↗

PubMed1993

5'-Monodeiodinase activity in developing human cerebral cortex.

Iodine status of aborted fetuses (11-25 wk gestation) was determined on the basis of maternal thyroid status and urinary iodine excretion. Fetal cerebral cortex thyroxin and 3,5,3'-triiodothyronine (T3) contents peaked at 15-18 wk gestation and then fell in iodine sufficiency. In mild iodine deficiency T3 concentration was maintained at a higher level until week 22, although it were still significantly less than in the iodine-sufficient group. Reverse T3 (rT3) rose from 11 to 22 wk gestation without any effect of iodine status. The activity of 5' and 5-monodeiodinase also increased from 11 to 22 wk gestation, with 5' monodeiodinase activity significantly increased by mild and moderate iodine deficiency. In contrast, cerebral cortex 5-monodeiodinase activity was significantly lower in moderate iodine deficiency at 15-18 wk gestation. The observations indicate that cerebral cortex 5' and 5 monodeiodinase activities are modulated in iodine deficiency to enhance T3 production from thyroxin (T4) during the period that coincides with neuroblastogenesis.

Cerebral Cortex↗

PubMed1982

Noradrenergic neurotransmission in the brain of a convulsive mutant mouse, differences between the cerebral cortex and the brain stem.

The Quaking mouse is a genetically determined model of convulsive disorders. We investigated the modulation of noradrenergic neurotransmission through alpha 2-adrenoceptors in the occipital cortex and the brain stem of this mutant. The endogenous levels of noradrenaline were similar in the cerebral cortex of the Quaking mice and their corresponding controls, while a significant increase of endogenous noradrenaline was found in the brain stem of the mutants. The rate of disappearance of noradrenaline in the cerebral cortex and the brain stem after injection of FLA 63 was identical in control and Quaking mice. The calcium-dependent electrically evoked overflow of 3H-noradrenaline from slices of occipital cortex was inhibited by clonidine and enhanced by yohimbine in Quaking as well as in normal mice. The negative feed-back mechanism mediated by presynaptic alpha 2-adrenoceptors operates to a similar extent in both strains of mice. In contrast to the occipital cortex, in the brain stem, the amount of neurotransmitter released by electrical stimulation was significantly increased in Quaking mice when compared with controls. However, in the brain stem, the negative feed-back regulation of noradrenaline release operates to a similar extent in both strains of mice. When the endogenous levels of MOPEG were determined in the brain stem, they were found to be significantly higher in the Quaking mice when compared to the controls. The results suggest that an increase in noradrenergic neurotransmission in the brain stem, rather than in the cerebral cortex, could contribute to the behavioural abnormalities exhibited by the Quaking mice.

Animals↗

PubMed1992

Detection of thymosin beta 4 in situ in a guinea pig cerebral cortex preparation using 1H NMR spectroscopy.

In the present work we have investigated the macromolecules that contribute to the brain 1H NMR spectrum. The cerebral cortex showed distinct resonances at the uncrowded methyl- and methylene chemical shift scale of the spin-echo 1H NMR spectrum. The peaks at 1.22 and 1.40 ppm (relative to the methyl protons of N-acetyl aspartate at 2.02 ppm) arise from cerebral macromolecules without evidence for co-resonances from low molecular weight metabolites as shown by the spin-spin relaxation decays of these resonances. In addition to these NMR signals, peaks at 0.9 and 1.7 ppm from macromolecules were detected. These resonances are from proteins, and we have identified the polypeptides that contributed to the 1H NMR peaks. Two proteins that were present at concentrations of 250 and 350 micrograms/g of dryed tissue showed 1H NMR spectra that resembled the macromolecular pattern in the cerebral 1H NMR spectrum. They were identified as thymosin beta 4 and histone H1, respectively. Thymosin beta 4 was present in soluble high speed cytoplasmic fraction and in P2 pellet, whereas histone H1 was detected in nuclear enriched fraction. A chemical shift-correlated two-dimensional 1H NMR spectrum of thymosin beta 4 in vitro revealed a coupling pattern that matched the macromolecule in the cerebral cortex which we have previously noted (Kauppinen R. A., Kokko, H., and Williams, S. R. (1992) J. Neurochem. 58, 967-974). On the basis of both one- and two-dimensional NMR evidence, subcellular distribution and high concentration, we assign the 1H NMR signals at 0.9, 1.22, 1.40, and 1.7 ppm in the cerebral cortex to thymosin beta 4.

Amino Acid Sequence↗

PubMed1987

Regional and laminar density of the dopamine innervation in adult rat cerebral cortex.

The topographic distribution and density of the dopamine innervation in adult rat cerebral cortex were investigated by means of a recently improved radioautographic procedure for the light microscopic visualization and counting of monoamine axonal varicosities. Dopamine terminals were specifically labeled by high-affinity uptake in whole cerebral hemisphere slices incubated for 15 min at 35 degrees C with 10(-6) M tritiated dopamine in the presence of 10(-4) M pargyline and 5 X 10(-6) M desipramine. The slices were subsequently fixed, embedded in Epon and processed for light microscope radioautography as large 4-micron-thick (whole hemisphere) or smaller, semi-thin sections (selected areas). In radioautographs of serial semi-thin sections exposed for various periods of time, the number of labeled axonal varicosities reached a plateau after 12-14 days of exposure. Counts on such sections of increasing thickness allowed to calculate a correcting factor to transform numbers obtained from 4-micron-thick sections into their equivalent for a tissue thickness of 0.5 micron from which all varicosities were detected. The number of labeled varicosities could then be expressed per mm3 of tissue after measuring their mean caliper diameter in electron microscope radioautographs. As visualized at 3 transverse levels representing most of the major cytoarchitectonic divisions of cerebral cortex, two novel aspects were recognized in the topographic distribution of dopamine terminal: (1) the presence of a dopamine innervation in layer VIb of the frontal, parietal, temporal and occipital neocortex, and (2) a significant contingent of dopamine varicosities within the deep and not only upper layers of supragenual cingulate cortex. A fair number of dopamine varicosities were also detected in the upper layers of the dorsomedial frontal area, in the retrosplenial and adjacent occipital cortex as well as in the ventral subiculum and field CAl of the hippocampus. As measured in 10 sectors representing different cortical regions, the highest density of dopamine innervation was found in the supragenual cingulate cortex (1.7 X 10(6] and particularly in its layers II and III (3.1 X 10(6)). A slightly lower density was measured in the anteromedian "prefrontal" cortex (1.0 X 10(6)). The rostrorhinal and the perirhinal cortex showed moderate dopamine innervation (3.0 and 5.5 X 10(5)) with varicosities in every layer. The piriform and the posterior entorhinal cortex were also moderately and ubiquitously innervated (2.5 and 3.0 X 10(5)).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1982

Kinetics of resolution of transient increases in extracellular potassium activity: relationships to regional blood flow in primate cerebral cortex.

Previous studies have established that in cerebral cortex subjected to progressive reduction in blood flow, two distinct thresholds of flow may be identified below which cellular function is impaired: the cortical evoked response loses amplitude when local flow falls below 18ml/100gm/min, and below 11ml/100gm/min a major increase in extracellular K+ activity (Ke) occurs. However, further evidence suggests that even at higher flows the capacity of the tissue to handle induced ionic changes may be impaired. To investigate this point, we studied the kinetics of resolution of Ke following a transient increase produced by local electrical stimulation, in relation to the local pre-stimulus flow (reduced by acute middle cerebral artery occlusion) in baboons. Flow was measured by the hydrogen clearance method and Ke by ion-exchanger micro-electrodes, in the same cortical regions. In primary induced transients (those increases in Ke elicited by cortical stimulation, and reported previously,) Ke attained a maximum value of 8-10 mM and then decayed towards the 4-mM baseline. The half-time of this decay was significantly increased from normal in the flow range 20-40 ml/100 gm/min, and increased further at lower flows until, below 11ml/100gm/min, Ke clearance was undetectable. Thus, cortical ion homeostasis appeared impaired at flows substantially closer to normal than those thresholds mentioned above, a result discussed in terms of impairment of active Ke clearance mechanisms. Secondary induced transients arose during a primary induced transient, reaching considerably higher peak values (8-30 mM) of Ke (indicating temporary clearance loss) and with slower decay rate than the primary. Spontaneous transients, not associated with any stimulus, were also observed; like secondary transients, they occurred only at flows below 20ml/100gm/min and showed a reduction in clearance rate with progressive ischemia. They resemble spreading depression and their generation is discussed in terms of the ionic and metabolic conditions at their time of origin.

Animals↗

PubMed1992

Diverse migratory pathways in the developing cerebral cortex.

During early development of the mammalian cerebral cortex, young neurons migrate outward from the site of their final mitosis in the ventricular zone into the cortical plate, where they form the adult cortex. Time-lapse confocal microscopy was used to observe directly the dynamic behaviors of migrating cells in living slices of developing cortex. The majority of cells migrated along a radial pathway, consistent with the view that cortical neurons migrate along radial glial fibers. A fraction of cells, however, turned within the intermediate zone and migrated orthogonal to the radial fibers. This orthogonal migration may contribute to the tangential dispersion of clonally related cortical neurons.

Animals↗

PubMed1989

Dopamine synaptic complex with pyramidal neurons in primate cerebral cortex.

Dopamine (DA)-containing projections to the cerebral cortex are considered to play an important role in cognitive processes. Using a recently developed monoclonal antiserum directed against DA and an antibody directed against tyrosine hydroxylase in combination with Golgi impregnation and electron microscopy, we have observed that DA and tyrosine hydroxylase afferents establish symmetric membrane specializations with the soma, dendritic shafts, and spines of identified pyramidal cells in the prefrontal, cingulate, and motor cortex of primates. The axospinous contacts invariably formed part of a synaptic complex in which the dendritic spine of a pyramidal neuron was the target of both a DA-positive symmetric and an unlabeled asymmetric bouton. This arrangement allows direct DA modulation of the overall excitability of cortical projection neurons by altering local spine responses to excitatory inputs.

Animals↗

PubMed1996

In vitro effect of lead on Ca(2+)-ATPase in synaptic plasma membranes and microsomes of rat cerebral cortex and cerebellum.

Earlier investigations from this laboratory suggest that lead interferes with the calcium homeostasis of rat brain through modulation of an inositol polyphosphate second-messenger system. The present investigation was initiated to study the comparative effects of lead chloride and lead acetate on synaptosomal and microsomal Ca(2+)-ATPase of rat cerebral cortex and cerebellum in vitro. The synaptic plasma membranes and microsomes were prepared by using sucrose gradient (1.2-0.8 M). The assay of Ca(2+)-ATPase was done by hydrolysis of ATP and the liberated inorganic phosphate was estimated. Both lead chloride and lead acetate at micromolar concentrations significantly inhibited the Ca(2+)-ATPase of synaptic plasma membranes and microsomes of cerebral cortex and cerebellum in a concentration-dependent manner. The IC50 values of Ca(2+)-ATPase for both lead salts in synaptosomes were significantly lower (P < 0.05) than that of microsomes, indicating more sensitivity. Significantly (P < 0.05) lower IC50 values for both synaptosomal and microsomal Ca(2+)-ATPase were obtained for lead acetate than for lead chloride. The results suggest that lead acetate is more potent than lead chloride in inhibiting the Ca(2+)-ATPase. The microsomal Ca2+ uptake was also studied in cerebellum and cerebral cortex in the presence of different concentrations of both the lead salts. However, these lead salts in vitro did not reveal a significant (P < 0.05) change in the microsomal Ca2+ uptake of cerebellum and cerebral cortex. But earlier investigations indicated that in vitro lead (0.25-2 microM) inhibits inositol 1,4,5-triphosphate-mediated Ca2+ uptake and release in microsomes of rat cerebellum.

Adenosine Triphosphate↗

PubMed1992

The effect of cycloheximide on natural and X-ray-induced cell death in the developing cerebral cortex.

Naturally occurring cell death in the cerebral cortex and subcortical white matter is increased after X-irradiation, and this process is curbed with cycloheximide, an inhibitor of protein synthesis. However, cycloheximide alone increases cell death during development, and this effect is dose-dependent. This suggests that, in both normal and experimentally-induced cortical cell death during development, different proteins are activated or inhibited, depending on the agent, the time of its application, and the previous metabolic or functional state of the cell.

Animals↗

PubMed1987

Choline acetyltransferase-immunoreactive neurons in fetal monkey cerebral cortex.

Two monoclonal antibodies to choline acetyltransferase (ChAT) were used to stain the cerebral cortex of fetal monkeys at 110-150 days post-conception. In addition to a small number of immunostained fibers, cells resembling typical non-pyramidal neurons were immunostained in developing layers V and VI and in the subjacent white matter of each area examined (sensory-motor and visual areas). ChAT-immunoreactive neurons have not been described in the cerebral cortex of adult primates, but the present observations indicate such neurons exist in the developing primate cortex.

Animals↗