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[Changes in the mRNA concentration of preprocholecystokinin in rat cerebral cortex and hippocampus after gastric distension].

Cholecyctokinin-octapeptide (CCK-8) is one of the brain-gut peptides widely distributed in neurons of the central nervous system, especially in cerebral cortex and hippocampus. This peptide is thought as a neurotransmitter or modulator. The role of central CCK in the integration of gastric motility and food intake is still unclear. The present investigation was undertaken to see whether the gastric distension exerts some effect on the expression of CCK mRNA in cerebral cortex and hippocampus by means of in situ hybridization and semi-quantitative RT-PCR techniques. The results are as follows. (1) Discrete positive hybridization cells were seen in cerebral cortex and hippocampus in control group. (2) Significant increases of CCK mRNA expression in cerebral cortex and hippocampus produced by gastric distention observed by increased of the volume, the number, the IOD and the SA of positive cells. (3) Amplified bands of the expected size of 158 base pairs were found in cerebral cortex and hippocampus, and signals of gastric distention group were higher than those of control group. The results from RT-PCR assay are in agreement with those based on in situ hybridization. These results imply that biosynthesis of CCK-containing neurons in cerebral cortex and hippocampus is accelerated by afferent signals from gastrointestinal system and may be involved in regulation of gastric motility and food intake.

Animals↗

The metabolic rate and vulnerability of dopaminergic neurons, and adenosine dynamics in the cerebral cortex, nucleus accumbens, caudate nucleus, and putamen of the common marmoset.

The pathophysiology of the striatum and cerebral cortex were studied from the pharmacological aspect. Investigation of the dopamine content in the cerebral cortex revealed that the premotor and motor area showed the highest level (61+/-6.2 ng/g). Intravenous injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at a dose of 10 mg/kg reduced the dopamine content in the caudate nucleus and putamen to 2-3% of the control level in common marmosets, while it fell to 60% in the nucleus accumbens. There was no alteration of the dopamine content in the cerebral cortex. Immunohistochemical staining for tyrosine hydroxylase in the midbrains of MPTP-treated marmosets showed almost complete disappearance of dopaminergic cells from the substantia nigra and good preservation of cells in the ventrotegmental area. Dopaminergic cells projecting to the caudate/putamen, nucleus accumbens, and cerebral cortex showed marked, moderate, and no vulnerability to MPTP, respectively. After systemic administration of MPTP, dopaminergic neurons projecting to the caudate nucleus and putamen were damaged equally. However, the compensatory increase of dopamine turnover was more prominent in the putamen than in the caudate nucleus. Thus, nigroputaminal dopaminergic neurons may have a higher level of activity than neurons in the caudate. The neural connections and functions of the caudate nucleus and putamen have already been differentiated anatomically or physiologically. This compensatory increase of the dopamine turnover rate is another aspect of functional differences between the caudate nucleus and putamen. Investigation of the dopamine content in the head, body, and tail of the caudate nucleus showed no differences in the concentration of dopamine. However, a study of the metabolic rate of dopamine using alpha-methyl-p-tyrosine, a tyrosine hydoxylase inhibitor, showed higher metabolism of dopamine in the head of the caudate nucleus in common marmosets. Thus, dopaminergic neurons projecting to the caudate nucleus may show topographical differences in their firing rates. A microdialysis study indicated an increase in the metabolism of adenosine in the striatum of MPTP-treated animals. Cholinergic neurons are interneurons and are one of the main sources of adenosine in the striatum. Dopaminergic input from the substantia nigra acting on cholinergic neurons was decreased following MPTP treatment. The increase of adenosine metabolism suggested that cholinergic neurons in the striatum receive inhibitory inputs from nigrostriatal dopaminergic neurons.

Adenosine↗

A binding site for [3H]glipizide in the rat cerebral cortex.

[3H]glipizide, a 2nd generation hypoglycemic sulfonylurea, binds specifically to rat cerebral cortex membranes in a time- and temperature-dependent way. The binding is saturable and reversible. The maximal binding capacity is 110 fmol/mg protein and the dissociation constant 1.5 nM. The binding site was destroyed by proteolytic and lipolytic enzymes suggesting a lipoprotein nature. Active analogs of sulfonylureas are characterized by IC50 values in the cerebral cortex which parallel their insulinotropic activity. In the cerebral cortex, adenylate cyclase was not stimulated by glipizide but sulfonylureas could inhibit, at high doses, the cAMP-dependent phosphodiesterase. This central binding site for glipizide displays the characteristics of the recognition moiety of a biological receptor.

3',5'-Cyclic-AMP Phosphodiesterases↗

Advances in cytoarchitectonic mapping of the human cerebral cortex.

The classic cytoarchitectonic maps of the human cerebral cortex (e.g., that of Brodmann [1909]) considerably influenced the concept of localization of function. Although they suffer from drawbacks such as the highly observer-dependent definition of areal borders and the lack of information on intersubject variability of location and size of a cortical area in a spatial reference system, these maps often serve as anatomic references in functional imaging studies. Recent methodologic progress in computerized image analysis of histologic specimens and the development of warping techniques to compensate for intersubject variability of brain structure in the three-dimensional (3-D) space made it possible to overcome these drawbacks. The authors propose a new concept of cytoarchitectonic mapping, which is based on (1) a definition of areal borders using multivariate statistical analysis, (2) a quantitative analysis of similarity and dissimilarity in architecture between cortical areas, and (3) a probabilistic mapping of cytoarchitectonic areas in a 3-D reference system. The combined analysis of architectonic maps and functional imaging data in an identical reference space offers exciting perspectives in the analysis of structural-functional correlations in the living human brain and provides new insights into the architecture of the cerebral cortex.

Animals↗

Regulation of phosphoinositide turnover in neonatal rat cerebral cortex by group I- and II- selective metabotropic glutamate receptor agonists.

1. The interactive effects of different metabotropic glutamate (mGlu) receptor subtypes to regulate phosphoinositide turnover have been studied in neonatal rat cerebral cortex and hippocampus by use of agonists and antagonists selective between group I and II mGlu receptors. 2, The group II-selective agonist 2R,4R-4-aminopyrrolidine-2,4-dicarboxylate (2R,4R-APDC; 100 microM) had no effect on basal total inositol phosphate ([3H]-InsPx) accumulation (in the presence of Li+) in myo-[3H]-inositol pre-labelled slices, but enhanced the maximal [3H]-InsPx response to the group I-selective agonist (S)-3,5-dihydroxyphenylglycine (DHPG) by about 100% in both hippocampus and cerebral cortex. In cerebral cortex the enhancing effect of 2R,4R-APDC occurred with respect to the maximal responsiveness and had no effect on EC50 values for DHPG (-log EC50 (M): control, 5.56+/-0.05; +2R,4R-APDC, 5.51+/-0.08). 2R,4R-APDC also caused a significant enhancement of the DHPG-stimulated inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) mass response over an initial 0-300 s time-course. 3. The enhancing effects of 2R,4R-APDC on DHPG-stimulated [3H]-InsPx accumulation were observed in both the presence and nominal absence of extracellular Ca2+, and irrespective of whether 2R,4R-APDC was added before, simultaneous with, or subsequent to DHPG. Furthermore, increasing the tissue cyclic AMP concentration up to 100 fold had no effect on DHPG-stimulated Ins(l,4,5)P3 accumulation in the absence or presence of 2R,4R-APDC. 4. 2R,4R-APDC and (2S, 1'R, 2'R, 3'R)-2-(2,3-dicarboxylcyclopropyl)glycine (DCG-IV), the latter agent in the presence of MK-801 to prevent activation of NMDA-receptors, each inhibited forskolin-stimulated cyclic AMP accumulation by about 50%, with respective EC50 values of 1.3 and 0.04 microM (-log EC 50 (M): 2R,4R-APDC, 5.87+/-0.09; DCG-IV, 7.38+/-0.05). In the presence of DHPG (30 microM), 2R,4R-APDC and DCG-IV also concentration-dependently increased [3H]-InsPx accumulation with respective EC50 values of 4.7 and 0.28 microM (-log EC50 (M): 2R,4R-APDC, 5.33+/-0.04; DCG-IV, 6.55+/-0.09) which were 3-7 fold rightward-shifted relative to the adenylyl cyclase inhibitory responses. 5. The group II-selective mGlu receptor antagonist LY307452 (30 microM) caused parallel rightward shifts in the concentration-effect curves for inhibition of forskolin-stimulated adenylyl cyclase, and enhancement of DHPG-stimulated [3H]-InsPx accumulation, by 2R,4R-APDC yielding similar equilibrium dissociation constants (KdS, 3.7+/-1.1 and 4.1+/-0.4 microM respectively) for each response. 6. The ability of 2R,4R-APDC to enhance receptor-mediated [3H]-InsPx accumulation appeared to be agonist-specific; thus although DHPG (100 microM) and the muscarinic cholinoceptor agonist carbachol (10 microM) stimulated similar [3H]-InsPx accumulations, only the response to the former agonist was enhanced by co-activation of group II mGlu receptors. 7. These data demonstrate that second messenger-generating phosphoinositide responses stimulated by group I mGlu receptors are positively modulated by co-activation of group II mGlu receptors in cerebral cortex and hippocampus. The data presented here are discussed with respect to the possible mechanisms which might mediate the modulatory activity, and the physiological and pathophysiological significance of such crosstalk between mGlu receptors.

Adenylyl Cyclase Inhibitors↗

The inner ring (5-) monodeiodination of thyroxine (T4) in cerebral cortex during fetal, neonatal, and adult life.

Inner ring (-5) monodeiodination of T4 was studied by incubating T4 (approximately 0.26 mumol/L) with rat cerebral cortical homogenate (approximately 4 mg protein) in the presence of dithiothreitol (up to 400 mmol/L) and quantifying the amount of the product, rT3, by a specific radioimmunoassay. The production of rT3 was dependent on duration of incubation (up to 2 hours), amount of tissue protein (up to 8 mg), temperature (optimal at 37 degrees C) and pH (optimal, 7.0) of the incubation mixture and the concentration of DTT (maximally stimulated at 400 mmol/L). The apparent Km and Vmax of the T4-inner ring monodeiodinating activity were 36 nmol/L and 1.75 pmol/mg protein/h, respectively. The activity was inhibited by T3 and 3,5-T2, but not by 3'5'-T2, PTU, methimazole, sodium salicylate, or 8-anilino-I-naphthalene sulfonic acid. Ipodate weakly inhibited T4-to-rT3 monodeiodination. Hyperthyroidism induced by T4 (100 micrograms/d IP X 3 days), T3 (80 micrograms/d IP X 3 days) or DIMIT (45 micrograms/d IP X 3 days) significantly stimulated T4-to-rT3 conversion; DIMIT was the most potent agent. Hypothyroidism inhibited T4-to-rT3 converting activity in cerebral cortex. Fasting for three days had no appreciable effect on T4-to-rT3 conversion in cerebral cortex. Cerebral cortical T4 5-deiodinase activity in the pregnant rat at term was about 50% of that in the adult nonpregnant rat, whereas that in the fetus was about three-fold higher than that in the nonpregnant adult.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Evidence that histamine homologues discriminate between H3-receptors in guinea-pig cerebral cortex and ileum longitudinal muscle myenteric plexus.

1. The binding of the selective histamine H3-receptor agonist ([3H]-R-alpha-methylhistamine) to sites in guinea-pig cerebral cortex and ileum longitudinal muscle myenteric plexus has been characterized and a comparison made of the apparent affinities of a series of H3-receptor ligands. 2. Saturation analysis suggested that [3H]-R-alpha-methylhistamine labelled a homogeneous population of histamine H3-receptors in guinea-pig cerebral cortex (pKD=9.91+/-0. 07; nH=1.07+/-0.03; n=5) and ileum longitudinal muscle myenteric plexus (pKD=9.75+/-0.21; nH=0.97+/-0.02; n=5). There was no significant difference in the estimated affinity of [3H]-R-alpha-methylhistamine in the two tissues. The cerebral cortex had a significantly higher receptor density (3.91+/-0.37 fmol mg-1 tissue) than the ileum longitudinal muscle myenteric plexus (0. 39+/-0.11 fmol mg-1). 3. Overall, the apparent affinities of compounds, classified as H3-receptor ligands, in cerebral cortex and ileum longitudinal muscle myenteric plexus were well correlated (r=0. 91, P<0.0001) and consistent with the cerebral cortex and ileum longitudinal muscle myenteric plexus expressing histamine H3-receptor population(s) that are pharmacologically indistinguishable by the majority of histamine H3-receptor ligands. However, it was evident that the homologues of histamine within this group of compounds could discriminate between the receptor populations in the two tissues. Thus, the estimated affinity of five imidazole unbranched alkylamines (histamine, homohistamine, VUF4701, VUF4732 and impentamine) were significantly higher in the guinea-pig cerebral cortex than in the ileum longitudinal muscle myenteric plexus assay.

Animals↗

The resolution of dopamine and beta 1- and beta 2-adrenergic-sensitive adenylate cyclase activities in homogenates of cat cerebellum, hippocampus and cerebral cortex.

The stimulation of adenylate cyclase by dopamine and various beta-adrenergic agonists has been investigated in homogenates from 3 areas of cat brain: the cerebral cortex, cerebellum and hippocampus. The purpose of the study was to determine whether the beta-arenergic receptors coupled to adenylate cyclase could be classified as either beta 1 and beta 2 subtypes in the different regions studied. The stimulation of adenylate cyclase by the beta-adrenergic agonist, (-)isoproterenol (5 X 10(-6) M), was completely blocked by the specific beta-adrenergic antagonist, (p)alprenolol (1-(-5) M), but not by the dopaminergic antagonist, fluphenazine (10(-5) M), whereas the stimulation of adenylate cyclase by (-)epinephrine (10(-4) M) was blocked to varying extents by these two drugs in each of the 3 regions studied. The (-)epinephrine effect was always blocked in the combined presence of (p)alprenolol and fluphenazine. The adenylate cyclase stimulation by (p)epinephrine which is not blocked by (p)alprenolol was due to interaction of (p)epinephrine with a dopaminergic-sensitive adenylate cyclase which has been characterized in cerebral cortex, hippocampus and cerebellum. Regional differences in the affinity of beta-adrenergic-sensitive adenylate cyclase for various agonists were investigated in the presence of fluphenazine (10(-5) M). In the cerebellum the potency order was (+/-)protokylol greater than (+/-)hydroxybenzylisoproterenol greater than (+/-)isoproterenol greater than (-)epinephrine greater than (+/-)salbutamol greater than (-)norepinephrine, indicating the presence of a beta 2-adrenergic receptor. In the cerebral cortex the potency order was (-)isoproterenol greater than +/-)protokylol greater than (+/-)hydroxybenzylisoproterenol greater than (-)epinephrine = (-)norepinephrine ((+/-)salbutamol being inactive). A similar pattern was found in the hippocampus indicating the presence of a beta 1-adrenergic receptor in these two regions. (+/-)Salbutamol was a partial agonist in the cerebellum and a competitive antagonist in the cerebral cortex. The ratio of the antagonist potencies of (+/-)practolol and (+/-)butoxamine preferential beta 1- and beta 2-adrenergic antagonists respectively, to block the stimulation of adenylate cyclase was 25 in the cerebellum, compared to 0.5 in the cerebral cortex and 1.6 in the hippocampus. These results confirm the presence of a beta 2 subtype of receptor coupled to adenylate cyclase in the former and beta 1 subtypes in the latter two regions. The comparison between the affinities of a series of beta-adrenergic agonists and antagonists for the beta-adrenergic receptors coupled with an adenylate cyclase in cerebral cortex and cerebellum with their affinities for well characterized beta 2-adrenergic receptors in lung and beta 1-adrenergic receptor in heart substantiated this conclusion.

Adenylyl Cyclases↗

Effect of chronic haloperidol treatment on peripheral benzodiazepine binding sites in cerebral cortex of rats.

The effects of 21 days of haloperidol treatment on central benzodiazepine (BZ) receptors in the cerebral cortex of rats and on peripheral-type BZ binding sites (PBS) in the cerebral cortex and heart of rats were studied. Neuroleptic treatment did not affect the maximal binding capacity or the affinity of the central BZ receptor to 3H-flunitrazepam. Chronic haloperidol treatment resulted in a significant increase of 38% in PBS density in the cerebral cortex, with no alteration in PBS density in the heart. No alteration in PBS affinity for its ligand 3H-PK 11195 was observed, either in the cerebral cortex or in the heart. The modulatory effect of chronic haloperidol administration on PBS density in the brain may be related to some of the neurobehavioral or hormonal effects of the drug.

Animals↗

Retina accumulates more glucose than does the embryologically similar cerebral cortex in diabetic rats.

AIMS/HYPOTHESIS: The retina is embryologically similar to cerebral cortex and the tissues of both are exposed to similar blood glucose concentrations. Nevertheless, in diabetes the retina develops metabolic abnormalities and microvascular lesions from which cerebrum seems relatively protected. We directly compared glucose concentrations and expression of GLUT-1 (the major carrier transporting glucose from blood into the neural retina and cerebrum) in the two tissues from normal and diabetic rats. METHODS: Tissue and intracellular glucose were measured using two methods: direct assay of glucose and assay of Amadori products on intracellular proteins. The expression of GLUT-1 was measured using western blots in tissue and in the isolated endothelial luminal membrane of the two vascular beds. RESULTS: Both methods assessing intracellular glucose indicate that intracellular concentrations of glucose in diabetes increased significantly in the retina but not in cerebral cortex. Concentrations of free glucose and Amadori product in retinas of diabetic animals were increased above normal by 334% and 122%, respectively, whereas there was no statistically significant increase in either parameter in the cerebral cortex of diabetic animals. In contrast to the observed increase in glucose in the retina in diabetes, expression of GLUT-1 on the luminal plasmalemma of the retinal vascular endothelium and in homogenates of whole retina decreased to a statistically significant extent (55% and 36%, respectively compared to normal). In the luminal cell membrane of the cerebral vasculature, diabetes did not decrease expression of GLUT-1 but tended to increase it slightly. CONCLUSIONS/INTERPRETATION: Even among tissues that do not require insulin for glucose uptake, tissue glucose concentration varies in diabetes. The greater increase in glucose concentration in retina than in cerebrum in diabetes probably contributes to the tissue differences in biochemical and histopathologic sequelae of the disease. The expression of GLUT-1 in the microvasculature is unlikely to account for the differences in tissue glucose between retina and cerebrum.

Animals↗

Androgen receptors in the cerebral cortex of fetal female rhesus monkeys.

The present study characterizes putative androgen receptor activity in the cerebral cortex cytosol of the female fetal monkey (Macaca mulatta) on days 125-135 postconception. Binding activities were compared using tritiated 5 alpha-dihydrotestosterone (DHT) and methyltrienolone (R1881) as ligands. Receptor concentration and association constants (Ka) were estimated from bound/total vs. total ligand binding curves. For R1881 and DHT, Ka values were 4.3 X 10(9) and 7.0 X 10(9) M-1, respectively. Receptor concentrations using the two ligands were estimated to be 5.5 X 10(-15) mol/mg protein (R1881; n = 2) and 1.7 X 10(-15) mol/mg protein (DHT). Analysis of receptor binding on DEAE-cellulose columns (KCl gradient) revealed multiple binding peaks (0.05-0.3 M KCl); similar elution profiles were obtained for the two ligands. Competition with either R1881 or DHT significantly reduced [3H]DHT binding throughout the KCl gradient, while triamcinolone acetonide had no effect. In contrast, [3H]R1881 binding was reduced by all three competitors. Cytosol from fetal male seminal vesicles had [3H]ligand-binding activity that was chromatographically similar to that of cerebral cortex. In contrast, binding in fetal male serum was negligible. Competition of cerebral cortex binding with a variety of hormones, including SCH-16423, progesterone, and cortisol, and analysis of the results on DEAE-cellulose suggested that there may be additional species of ligand-binding molecules. In summary, the findings verify the existence of a specific androgen receptor(s) in the cerebral cortex of fetal female rhesus monkeys. Its presence may be important for understanding both the influence of androgens on central nervous system development and the potential for teratogenic agents to disrupt normal patterns of central nervous system development.

Animals↗

Cocaine exposure decreases GABA neuron migration from the ganglionic eminence to the cerebral cortex in embryonic mice.

Recurrent exposure of the developing fetus to cocaine produces persistent alterations in structure and function of the cerebral cortex. Neurons of the cerebral cortex are derived from two sources: projection neurons from the neuroepithelium of the dorsal pallium and interneurons from the ganglionic eminence of the basal telencephalon. The interneurons are GABAergic and reach the cerebral cortex via a tangential migratory pathway. We found that recurrent, transplacental exposure of mouse embryos to cocaine from embryonic day 8 to 15 decreases tangential neuronal migration and results in deficits in GABAergic neuronal populations in the embryonic cerebral wall. GABAergic neurons of the olfactory bulb, which are derived from the ganglionic eminence via the rostral migratory pathway, are not affected by the cocaine exposure suggesting a degree of specificity in the effects of cocaine on neuronal migration. Thus, one mechanism by which prenatal cocaine exposure exerts deleterious effects on cerebral cortical development may be by decreasing GABAergic neuronal migration from the ganglionic eminence to the cerebral wall. The decreased GABA neuron migration may contribute to persistent structural and functional deficits observed in the exposed offspring.

Animals↗

The mode of projections of single locus coeruleus neurons to the cerebral cortex in rats.

Axonal distributions of single locus coeruleus neurons within the cerebral cortex were examined with antidromic stimulation technique combined with cortical lesions (frontal lobotomy and lobectomy). In urethan-anesthetized rats, stimulating electrodes were implanted in 10 points extending over nearly the entire cerebral cortex, and antidromic responses of single locus coeruleus neurons to stimulation of these stimulus sites were analysed. Fifty percent of locus coeruleus neurons examined were activated antidromically from at least one cortical point in the cerebral cortex. The pattern and extent of axonal distributions of single locus coeruleus neurons in the cortex appeared to vary from cell to cell. From the results obtained in rats with the cortical lesions, it is concluded that in addition to locus coeruleus neurons with intracortical axons running from rostral to caudal, there are the neurons projecting to the occipital cortex without innervating the frontal cortex and those projecting simultaneously to the frontal and occipital cortex with two axonal branches. There was no topographic order between the recording sites within the locus coeruleus and the projection sites in the cortex.

Afferent Pathways↗

The relationship between age and the fatty acid composition of cerebral cortex and erythrocytes in human subjects.

The important role that neural tissue fatty acid composition plays in neurodevelopment and various pathological states is increasingly recognized. However, there are limited data regarding the fatty acid composition of normal human brain at various ages. The purpose of this study was to describe human cerebral cortex fatty acid composition from ages 2 to 88 years. The relationship between cerebral cortex and erythrocyte fatty acid composition was also investigated. Samples of frontal cerebral cortex and of erythrocytes were obtained from 58 human subjects on whom autopsies were performed. The mean age of subjects was 40 +/- 29 years, with a range of 2 to 88 years. The fatty acid composition of tissues was determined, and linear regression models were used to describe the relationship between age and the fatty acid composition of cerebral cortex and erythrocytes. The data were bilinear, with changes occurring after the approximate age of 18 years. Therefore, the cohort was divided into subjects with ages < or =18 and >18 years. In the younger group, the polyunsaturated fatty acids generally decreased with age, with the exception of 22:6n3, which demonstrated a significant increase. The level of mono-unsaturated fatty acids, in contrast, generally increased to the age of 18 years. Several of the polyunsaturated fatty acids also decreased with age in the older cohort, particularly 20:4n6. The levels of 18:2n6, however, increased significantly with age in the older cohort. Among subjects < or =18 years of age, there was no significant relationship between cerebral cortex and erythrocyte fatty acid levels. In the older cohort, there was a significant relationship between brain and erythrocyte levels for several fatty acids, particularly 16:0. These data demonstrate that levels of cerebral cortex fatty acids change from early childhood through late adulthood, and indicate that the levels of several erythrocyte fatty acids may be useful in predicting brain fatty acid levels in adults.

Adolescent↗

Postnatal changes in dolichol-pathway enzyme activities in cerebral cortex neurons.

Neuronal perikarya were isolated from rat cerebral cortex at different stages of postnatal development. Membranes sedimenting at 100000 g were obtained from these neurons to study several glycosyltransferases of the dolichol pathway. Enzyme activities from stages before and during synapse formation were compared (days 5 and 15 respectively). Dolichyl diphosphate (Dol-P-P) N-acetylglucosamine, dolichyl phosphate mannose and dolichyl phosphate glucose synthases and the enzymes catalysing Dol-P-P-GlcNAc2Man9Glc3 formation were higher at day 15 of postnatal development. The glycosyl transfer of the latter compound to endogenous protein(s) as well as to a dinitrophenyl-heptapeptide was also measured. The activity was higher at day 15. Furthermore, the activity of dolichyl phosphate mannose synthase was also measured during the time when the number of synapses ceased to increase (day 36) and in the adult stage. The activity of dolichyl phosphate mannose synthase was higher at day 36 than at day 15, and declined in the adult stage. From these results it may be concluded that there is an increase in the glycosylation of asparagine-type glycoproteins during synapse formation in the neurons of the cerebral cortex.

Animals↗

[Ultrastructural changes in the cerebral cortex following transcranial micropolarization].

Electron microscopy of the cerebral cortex in cats and monkeys following transcranial micropolarization (TCMP) demonstrated ultrastructural changes whose degree was dependent on the electric current intensity and the stimulation period. In the focus of stimulation the current affected the brain tissue directly, different elements of the cerebral cortex showing unegual sensitivity to various TCMP regimens. The glia was the first to respond, then the neuronal bodies, and the last -- the synaptic structures. In the areas distant from the TCMP focus synaptic components altered first. The ultrastructural changes revealed were not of pathological character.

Animals↗

Decreased signal intensity of cerebral cortex on T2-weighted MR images.

To define the frequency of decreased signal intensity (DSI) in cerebral cortex on T2-weighted images relative to aging and to the incidence of identifying white matter pathology, T2-weighted MR brain images of 906 patients consecutively examined between July 1989 and June 1991 were reviewed. MR images of cerebral cortex were divided into five areas: frontal lobe (F), pre- and postcentral gyri (C), parietal lobe (P), occipital lobe (O) and temporal lobe (T). Each area was separately and independently evaluated for the presence or absence of DSI. The frequency of DSI in each area was plotted against patients' ages. The severity of leukoaraiosis was evaluated in relation with DSI in each cortical area. Patients with DSI in area F numbered 61 (5.7%), in area C 236 (26.0%), in area P 174 (15.9%), in area O 428 (47.2%), and in area T 10 (1.1%). The number of patients with DSI in each area increased with age. The greater the severity of leukoaraiosis, the greater the chance of finding DSI of the cerebral cortex. The incidence of DSI in the cerebral cortex increased with the patient's age as well as with the severity of co-existent white matter pathology.

Adolescent↗

The earliest-generated neurons of the cat cerebral cortex: characterization by MAP2 and neurotransmitter immunohistochemistry during fetal life.

The earliest-generated neurons of the cat cerebral cortex have been studied here during development using a combination of 3H-thymidine birthdating with immunohistochemistry for the neuron-specific protein MAP2 or for several neuropeptides/transmitters. These neurons are the first postmitotic cells of the cortex, with birthdates during the 1-week period preceding the genesis of cells of the adult cerebral cortex (Luskin and Shatz, 1985a; Chun et al., 1987). However, they are transient and the majority disappear by adulthood (Luskin and Shatz, 1985a; Chun and Shatz, 1989). When autoradiographic birthdating is combined with MAP2 immunostaining during fetal life, the entire population of these early-generated neurons appears to be stained, resulting in labeled bands above and below the cortical plate. The band above the cortical plate (in the marginal zone) contains early-generated neurons with horizontal morphologies, while the thicker band beneath the cortical plate (within the intermediate zone) contains the somata of early-generated neurons and their elaborate processes that are frequently directed towards the ventricular surface. In view of the correspondence between the location of the early-generated neurons and the MAP2-immunostained band beneath the cortical plate, we suggest that this combined approach can be used to define accurately the subdivision of the intermediate zone known as the subplate. The early-generated neurons are also immunoreactive for GABA, neuropeptide Y (NPY), somatostatin (SRIF), and cholecystokinin (CCK) during fetal life. While GABA, NPY, and SRIF immunostaining could be detected by embryonic day 50 (E50), that for CCK was not found until E60. Moreover, there is a relationship between neuropeptide immunoreactivity and location within the cerebral wall. The marginal-zone neurons are immunoreactive only for CCK. The subplate neurons are immunoreactive for CCK, SRIF, and NPY. Most of those immunoreactive for SRIF tend to be clustered within the upper part of the subplate, while those immunoreactive for NPY tend to be located more deeply. Cells immunoreactive for GABA are more uniformly distributed throughout the cerebral wall. These observations demonstrate directly that the marginal zone and subplate contain peptide- and GABA-immunoreactive neurons that belong to the earliest-generated cell population of the cerebral cortex. The presence of these early-generated neurons, which achieve a remarkable degree of maturity during fetal life, suggests that they perform an essential, yet transient, role in the development of the cerebral cortex.

Animals↗