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PubMed1990

On the involvement of multiple muscarinic receptor subtypes in the activation of phosphoinositide metabolism in rat cerebral cortex.

We have examined the activation of phosphoinositide metabolism by muscarinic agonists in rat cerebral cortex, in an attempt to delineate the mechanisms by means of which some selective antagonists inhibit this response in a manner that deviates from simple mass action law. The accumulation of [3H]inositol phosphates induced by the full agonist carbamylcholine in cell aggregates preparations was inhibited by muscarinic antagonists with the following order of potency: telenzepine greater than atropine greater than 4-diphenylacetoxy-N-methyl-piperidine methbromide greater than pirenzepine greater than hexahydro-sila-difenidol greater than AF-DX 116. The same order of potency was found for the competition of these antagonists with [3H]telenzepine binding to M1 muscarinic receptors. The inhibition of the formation of [3H]inositol phosphates activated by acetylcholine, carbamylcholine, and oxotremorine-M by pirenzepine and telenzepine showed biphasic curves, with 62-73% of the response being inhibited with high affinity. Atropine, AF-DX 116, and pirenzepine shifted the concentration-response curves of oxotremorine-M to the right in a parallel manner. However, pirenzepine at micromolar concentrations showed deviation from linearity of the Schild regression. The blockade by high concentrations of pirenzepine and telenzepine showed less than additive dose ratios when assayed in the presence of atropine, suggesting deviation of their antagonism from simple competition. However, after alkylation with propylbenzilylcholine mustard in the presence of low concentrations of pirenzepine, the response to carbamylcholine and oxotremorine-M showed monophasic inhibition curves by pirenzepine and linear Schild regression for this antagonist. These results support the interpretation that the formation of [3H]inositol phosphates is activated by multiple muscarinic receptor subtypes in rat cerebral cortex. The profile of affinities of muscarinic antagonists indicates that a major component of the response is activated by an M1 receptor subtype and a minor component is probably mediated by M3 muscarinic receptors when acetylcholine, carbamylcholine, or oxotremorine-M are used to stimulate the response. Conversely, pirenzepine inhibited the response induced by methacholine and bethanechol in a monophasic manner with high affinity (Ki = 13 nM), suggesting that these agonists can selectively stimulate phosphoinositide metabolism through activation of M1 muscarinic receptors in rat cerebral cortex.

Alkylating Agents↗
PubMed1985

Solubilization and characterization of high and low affinity pirenzepine binding sites from rat cerebral cortex.

An apparently monomeric form of the digitonin-solubilized muscarinic acetylcholine receptor from the rat cerebral cortex retains a high affinity of 7 X 10(7) M-1 for pirenzepine. Muscarinic receptor binding sites in the rat cerebral cortex with a low affinity for pirenzepine are solubilized with relatively little change in affinity. The ability of pirenzepine to distinguish between subtypes of muscarinic binding site in the cerebral cortex is manifest in both the membrane-bound and soluble state.

Animals↗
PubMed1996

Widespread programmed cell death in proliferative and postmitotic regions of the fetal cerebral cortex.

A key event in the development of the mammalian cerebral cortex is the generation of neuronal populations during embryonic life. Previous studies have revealed many details of cortical neuron development including cell birthdates, migration patterns and lineage relationships. Programmed cell death is a potentially important mechanism that could alter the numbers and types of developing cortical cells during these early embryonic phases. While programmed cell death has been documented in other parts of the embryonic central nervous system, its operation has not been previously reported in the embryonic cortex because of the lack of cell death markers and the difficulty in following the entire population of cortical cells. Here, we have investigated the spatial and temporal distribution of dying cells in the embryonic cortex using an in situ endlabelling technique called 'ISEL+' that identifies fragmented nuclear DNA in dying cells with increased sensitivity. The period encompassing murine cerebral cortical neurogenesis was examined, from embryonic days 10 through 18. Dying cells were rare at embryonic day 10, but by embryonic day 14, 70% of cortical cells were found to be dying. This number declined to 50% by embryonic day 18, and few dying cells were observed in the adult cerebral cortex. Surprisingly, while dying cells were observed throughout the cerebral cortical wall, the majority were found within zones of cell proliferation rather than in regions of postmitotic neurons. These observations suggest that multiple mechanisms may regulate programmed cell death in the developing cortex. Moreover, embryonic cell death could be an important factor enabling the selection of appropriate cortical cells before they complete their differentiation in postnatal life.

Animals↗
PubMed1982

The influence of bicuculline-induced seizures on free fatty acid concentrations in cerebral cortex, hippocampus, and cerebellum.

Using ventilated rats maintained on N2O-O2 (70:30, vol/vol) we induced continuous seizures with i.v. bicuculline and analysed free fatty acids (FFA) in cerebral cortex, hippocampus, and cerebellum after seizures durations of 1-120 min. In the cerebral cortex, peak FFA concentrations were observed after 5 min, with a threefold increase in total FFA content. The values then remained unchanged for the next 15-20 min, but decreased thereafter. At 60 and 120 min, total FFA contents were only moderately increased above control. In the initial period, arachidonic acid increased about 10-fold and stearic acid 2- to 3-fold, with little change in palmitic acid and linoleic acid concentrations. At all times, the docosahexenoic acid concentration was markedly increased. Following its massive accumulation at 1 min, arachidonic acid gradually decreased in concentration. Pretreatment of animals with indomethacin did not alter this behaviour. After 20 and 120 min of seizure activity, changes in total and individual FFA concentrations in the hippocampus were similar to those observed in the cerebral cortex. The cerebellum behaved differently. Thus, at 20 min the only significant change was a 5- to 10-fold increase in arachidonic acid concentration and, after 120 min, total and individual FFA concentrations were similar to control values. Furthermore, since the control values for arachidonic acid were much lower in the cerebellum, the 20-min values were only about 20% of those observed in the cerebral cortex and the hippocampus.

Animals↗
PubMed1981

The release of endogenous GABA and glutamate from the cerebral cortex in the rat.

1. The release of endogenous GABA and glutamate from the cerebral cortex was measured using a cortical cup technique in unanaesthetized freely moving rats and anaesthetized rats by means of a sensitive and specific mass-spectrometric procedure. 2. GABA release was not affected by the presence of the dura mater or by anaesthesia. Glutamate output was reduced by urethane but not by pentobarbital anaesthesia and by the presence of the dura. 3. An isotonic solution containing 50 mM KCl placed epidurally within the cup elicited a significant short-lasting increase in glutamate output, a decrease in GABA output and a short-lasting electrocorticogram (ECoG) activation. 4. When the dura was removed, a high K+ solution placed on the exposed cerebral cortex elicited a 7--8 fold increase in GABA output accompanied by a marked decrease in glutamate output and by ECoG synchronization. The changes in GABA and glutamate output had parallel time-course and were prevented by the application within the cup of tetrodotoxin (3 X 10(-5) M). 5. Amphetamine at the doses of 3.7 and 7.4 mumol . kg-1 i.v. increased glutamate output and at the dose of 37 mumol . kg-1 i.v. increased GABA output. Both effects were prevented or reduced by haloperidol pretreatment (0.65 mumol . kg-1 i.v.). 6. It is concluded that GABA and glutamate released from the cerebral cortex and diffused into an epidural or cortical cup originate at least in part from the brain. The rate of their release is influenced by changes in neuronal activity. The measurement of their rate of release offers a useful tool for the study of the functional role of cortical GABA and glutamate-releasing neurons.

Amino Acids↗
PubMed1997

Effects of continuous low-dose prenatal irradiation on neuronal migration in mouse cerebral cortex.

We investigated the effects of continuous exposure to gamma-rays during corticogenesis on the migration of neuronal cells in developing cerebral cortex. Pregnant mice were injected with 0.5 mg of bromodeoxyuridine (BrdU) on day 14 of gestation to label cells in the S phase. The mice were then exposed to 137Cs gamma-rays (dose rates of 0.1, 0.3, and 0.94 Gy/day) continuously for 3 days. Brains from 17-day-old embryos and from offspring at 3 and 8 weeks after birth were processed immunohistochemically to track the movements of BrdU-labeled cells. Comparative analyses of the distribution pattern of BrdU-labeled cells in the cerebral cortex revealed that (1) the migration of neurons was delayed during the embryonic period in mice irradiated at 0.94 Gy/day, (2) in 3-week-old mice, there was a significant difference in the distribution pattern of BrdU-labeled cells in the cerebral cortex between the mice irradiated prenatally and control, and (3) in 8-week-old mice, there were no differences in the distribution pattern of BrdU-labeled cells between control and animals irradiated with 0.1 and 0.3 Gy/day. In contrast, in the animals irradiated with 0.94 Gy/day, the significant difference in the distribution pattern of the labeled cells relative to control was maintained. These results suggest that the migration of neuronal cells in mouse cerebral cortex is disturbed by continuous prenatal irradiation at low-dose and some modificational process occurred during the postnatal period.

Animals↗
PubMed1994

Alteration of tubulin-Gi protein interaction in rat cerebral cortex with aging.

The ability of the tubulin dimer to interact with and to modulate the Gi function inhibiting adenylyl cyclase was examined in cerebral cortex membranes from 2-month-old and 24-month-old rats. The hydrolysis-resistant GTP analogue 5'-guanylylimidodiphosphate (GppNHp)-dependent inhibition of adenylyl cyclase was significantly decreased in cerebral cortex membranes from 24-month-old rats. Tubulin, prepared from rat brains by polymerization with GppNHp, caused inhibition of adenylyl cyclase (approximately 28%) in 2-month-old rats. Tubulin-GppNHp-dependent inhibition of adenylyl cyclase in 24-month-old rats was significantly attenuated (approximately 15%). In 2-month-old rats, when tubulin, polymerized with the hydrolysis-resistant photoaffinity GTP analogue [32P]P3(4-azidoanilido)-P1-5'-GTP ([32P]AAGTP), was incubated with cerebral cortex membranes, AAGTP was transferred from tubulin to Gi alpha. Transfer of AAGTP from tubulin to Gi alpha was reduced in 24-month-old rats. Furthermore, photoaffinity labeling of [32P]AAGTP to Gi alpha in cortex membranes was significantly decreased in 24-month-old rats. No differences were observed in the amounts of Gs alpha, Gi alpha, or G beta subunits and tubulin, estimated by immunoblotting, in cortex membranes from 2-month-old and 24-month-old rats. These results suggest that the ability of tubulin to interact with Gi and thereby modulate the inhibitory regulation of adenylyl cyclase is reduced in the cerebral cortex of 24-month-old rats.

Adenylyl Cyclase Inhibitors↗
PubMed1988

Serotoninergic innervation of the cat cerebral cortex.

Serotoninergic axons in the cat cerebral cortex were demonstrated immunohistochemically with a monoclonal antibody to serotonin (5-HT). Three types of 5-HT axons are distinguished at the light microscopic level by differences in their morphology. Small varicose axons are fine (less than 0.5 micron) and bear fusiform varicosities that are generally less than 1 micron in diameter. These axons extend throughout the width of the cortex and branch frequently, giving rise to widely spreading collaterals. Nonvaricose axons are smooth, show a relatively large and constant caliber (about 1 micron), travel in straight, horizontal trajectories, and branch infrequently. Large varicose axons are distinguished by large round or oval varicosities (1 micron or more in diameter) borne on fine-caliber fibers. These axons often form basket-like arbors around the somata of single neurons. In the simplest basket-like arbors, several large, round varicosities from a small number of axons contact the soma. In complex baskets intertwining collaterals contact the soma and apparently climb along and outline the cell's major dendrites. The patterns revealed by the climbing axons suggest that a variety of nonpyramidal cell types selectively receive dense 5-HT innervation. Serial reconstructions of the 5-HT axons within the cortex show that the large varicose axons arise as infrequent collaterals from the nonvaricose axons. A single nonvaricose parent axon gives rise to several large varicose axon collaterals that may contribute to different basket-like arbors. Conversely, a single basket-like arbor may be formed by large varicose axon collaterals from more than one nonvaricose parent axon. The small varicose axons do not appear to be related within the cortex to either the nonvaricose or large varicose axon types. The results support the hypothesis that the 5-HT projection to the cortex is organized into two subsystems, one of which may exert widespread influence in the cortex via highly divergent branches, while the other, with a more restricted distribution, acts on specific classes of cortical neurons.

Animals↗
PubMed1995

A quantitative immunocytochemical study of blood-brain barrier to endogenous albumin in cerebral cortex and hippocampus of senescence-accelerated mice (SAM).

The blood-brain barrier (BBB) to endogenous albumin was studied in the cerebral cortex and hippocampus of the senescence-accelerated prone (SAMP8) mouse and senescence-accelerated resistant (SAMR1) mouse strains in corresponding age groups by using a quantitative immunocytochemical procedure. Brain samples after immersion-fixation were embedded at low temperature in Lowicryl K4M and sectioned with an ultramicrotome. Thin sections were exposed to anti-mouse albumin antiserum followed by protein A-gold. Labeling density (gold particles per microns 2) was recorded over four compartments: vascular lumen, endothelium, subendothelial space, and brain parenchyma (neuropil). Morphometric analysis of the electron micrographs revealed that the barrier function of capillaries located in the cerebral cortex of SAMP8 mice was not significantly different from that in control (SAMR1) mice. Nevertheless, in SAMP8 mice, the percentage of leaking microvessels was higher than in control animals. In the older (11-month-old) group of control mice, the percentage of leaking microvessels was higher in the hippocampus than in the cerebral cortex. In SAMP8 mice, however, these differences were negligible. In contrast, in 4-month-old animals, the labeling density of the subendothelial space, which was considered an indicator of albumin escape, was significantly higher in SAMP8 than in SAMR1 mice. Also, the labeling density of the neuropil in the hippocampus of both groups of mice was significantly higher than that in the cerebral cortex. This finding suggests that albumin has an access to the parenchyma of the hippocampus in normal conditions, and that this phenomenon becomes more pronounced during the process of senescence.

Aging↗
PubMed2003

Vasoactive intestinal peptide (VIP) and VIP mRNA decrease in the cerebral cortex of nNOS knock-out(-/-) mice.

Although there is much evidence showing that NO regulates the release of VIP in several areas, there is no report about the influence of NO on VIP in the cerebral cortex. We therefore examined changes in VIP expression in the cerebral cortex of nNOS knock-out(-/-) mice using immunohistochemistry and in situ hybridization. The nNOS((-/-)) mice had significantly fewer VIP-immunoreactive neurons than the control mice and the VIP mRNA as well as the VIP-immunoreactivity of the individual neuron was decreased in the nNOS((-/-)) mice. The first demonstration of decrease in VIP expression in the cerebral cortex of nNOS((-/-)) mice may provide useful data for investigating the relation between NO and VIP in the cerebral cortex and the mechanisms of many functions of these two neurotransmitters.

Animals↗
PubMed1968

Factors affecting the glucose 6-phosphate inhibition of hexokinase from cerebral cortex tissue of the guinea pig.

1. The inhibition of hexokinase by glucose 6-phosphate has been investigated in crude homogenates of guinea-pig cerebral cortex by using a sensitive radio-chemical technique for the assay of hexokinase activity. 2. It was observed that 44% of cerebral-cortex hexokinase activity did not sediment with the microsomal or mitochondrial fractions (particulate fraction), and this is termed soluble hexokinase. The sensitivities of soluble and particulate hexokinase, and hexokinase in crude homogenates, to the inhibitory actions of glucose 6-phosphate were measured; 50% inhibition was produced by 0.023, 0.046 and 0.068mm-glucose 6-phosphate for soluble, particulate and crude homogenates respectively. 3. The optimum Mg(2+) concentration for the enzyme was about 10mm, and this appeared to be independent of the ATP concentration. In the presence of added glucose 6-phosphate, raising the Mg(2+) concentration to 5mm increased the activity of hexokinase, but above this concentration Mg(2+) potentiated the glucose 6-phosphate inhibition. When present at a concentration above 1mm, Ca(2+) ions inhibited the enzyme in the presence or absence of glucose 6-phosphate. 4. When the ATP/Mg(2+) ratio was 1.0 or below, variations in the ATP concentration had no effect on the glucose 6-phosphate inhibition; above this value ATP inhibited hexokinase in the presence of glucose 6-phosphate. ATP had an inhibitory effect on soluble hexokinase similar to that on a whole-homogenate hexokinase, so that the ATP inhibition could not be explained by a conversion of particulate into soluble hexokinase (which is more sensitive to inhibition by glucose 6-phosphate). It is concluded that ATP potentiates glucose 6-phosphate inhibition of cerebral-cortex hexokinase, whereas the ATP-Mg(2+) complex has no effect. Inorganic phosphate and l-alpha-glycerophosphate relieved glucose 6-phosphate inhibition of hexokinase; these effects could not be explained by changes in the concentration of glucose 6-phosphate during the assay. 5. The inhibition of hexokinase by ADP appeared to be independent of the glucose 6-phosphate effect and was not relieved by inorganic phosphate. 6. The physiological significance of the ATP, inorganic phosphate and alpha-glycerophosphate effects is discussed in relation to the control of glycolysis in cerebral-cortex tissue.

Adenine Nucleotides↗
PubMedDate not supplied

Effects of histamine on phosphoinositide metabolism in chick cerebral cortex.

Effects of histamine (HA) and agonists of HA receptors on phosphoinositide metabolism in chick cerebral cortex have been studied using two approaches - measurement of inositol 1,4,5-trisphosphate (IP3) level by a specific and sensitive IP3 receptor radioassay, and analysis of [3H]inositol phosphates accumulation in cortical slices prelabeled with myo-[3H]inositol. HA concentration-dependently elevated IP3 levels in slices of chick cerebral cortex. The effect of HA was mimicked by 2-methylHA, a selective agonist of H1-HA receptors, and blocked by mepyramine, an H1 receptor antagonist. 4-MethylHA and Ralpha-methylHA, selective agonists of H2- and H3-HA receptors, respectively, did not affect IP3 level in the chick cerebrum. In cerebral cortical slices prelabeled with myo-[3H]inositol, 2-methylHA significantly stimulated [3H]inositol phosphates accumulation, whereas HA only slightly and non-significantly increased phosphoinositide metabolism. It is suggested that phospholipase C-coupled H1-HA receptors are present in the chick cerebral cortex, yet their number seems to be a small one.

Animals↗
PubMed1999

Common binding sites for beta-amyloid fibrils and fibroblast growth factor-2 in heparan sulfate from human cerebral cortex.

Heparan sulfate found in the cerebral plaques of Alzheimer's disease binds to beta-amyloid (Abeta) fibrils. This interaction has been proposed to enhance fibril deposition and mediate Abeta-induced glia activation and neurotoxicity. On the other hand, heparan sulfate augments signaling of fibroblast growth factor-2 (FGF-2), a neuroprotective factor that antagonizes the neurotoxic effects of Abeta. We defined structures in heparan sulfate from human cerebral cortex that bind Abeta fibrils. The minimal binding site is found in N-sulfated hexasaccharide domains and contains critical 2-O-sulfated iduronic acid residues. By contrast, binding of Abeta monomers requires, in addition, 6-O-sulfate groups on glucosamine residues. The binding specificity of fibrillar Abeta is shared by FGF-2, and we here show that cerebral heparan sulfate domains selected for binding to Abeta-(1-40) fibrils bind also to FGF-2. These data suggest that neurotoxic and neuroprotective signals may converge by competing for the same binding sites on the heparan sulfate chain.

Amyloid beta-Peptides↗
PubMed1994

Purinergic modulation of the evoked release of [3H]acetylcholine from the hippocampus and cerebral cortex of the rat: role of the ectonucleotidases.

Modulation by exogenous and endogenous adenine nucleotides and adenosine of [3H]acetylcholine release evoked by veratridine (10 microM) was compared in synaptosomal fractions from the hippocampus and the cerebral cortex of the rat. In both brain areas, exogenously added ATP or adenosine (10-100 microM) inhibited the evoked tritium release. In the hippocampus, ATP gamma S, an ATP analogue more resistant to catabolism than ATP, was virtually devoid of effect on tritium release, and the effect of ATP was prevented by the ecto-5'-nucleotidase inhibitor alpha,beta-methylene ADP (100 microM), by adenosine deaminase (2 U/ml) and by the A1 adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 20 nM). In contrast, in the cerebral cortex, the effect of ATP on tritium release was not prevented by either alpha,beta-methylene ADP (100 microM) or adenosine deaminase (2 U/ml), and several ATP analogues (30 microM) inhibited release. The order of intensity of the inhibitory effects of the ATP analogues was: ATP gamma S > ATP > beta,gamma-imido ATP > beta,gamma-methylene ATP >> 2-methyl-S-ATP, alpha,beta-methylene ATP. The effect of ATP gamma S in the cerebral cortex was prevented by DPCPX (20 nM) and was not affected by the P2 purinoceptor antagonist suramin (100 microM). In the hippocampus, alpha,beta-methylene ADP (100 microM) increased the evoked release of tritium, and adenosine deaminase (2 U/ml) produced an even greater increase; when adenosine deaminase was added in the presence of alpha,beta-methylene ADP, adenosine deaminase still increased the evoked release of tritium. In the cerebral cortex, DPCPX (20 nM) and adenosine deaminase (2 U/ml) increased the evoked tritium release by a similar magnitude, but the effect of adenosine deaminase was smaller than in the hippocampus. It is concluded that in the cerebral cortex ATP as such presynaptically inhibits acetylcholine release, whereas in the hippocampus the role of adenine nucleotides is as a source of endogenous extracellular adenosine that tonically inhibits acetylcholine release. The results also show that besides formation of adenosine from adenine nucleotides, released adenosine as such contributes in nearly equal amounts to the pool of endogenous adenosine that presynaptically inhibits acetylcholine release in the hippocampus.

Acetylcholine↗
PubMed1992

Divergent effects of glucocorticoid on the gene expression of vasoactive intestinal peptide in the rat cerebral cortex and pituitary.

We investigated the effects of glucocorticoid on the expression of the vasoactive intestinal peptide (VIP) gene, a neuropeptide and an established prolactin (PRL)-releasing factor, in the rat brain and pituitary. The mRNA and peptide contents of VIP in the cerebral cortex, hypothalamus and anterior pituitary of male Sprague-Dawley rats were quantitated 4 weeks after adrenalectomy or sham-operation. Following adrenalectomy, VIP mRNA content increased in the anterior pituitary but showed no significant change in the cerebral cortex and hypothalamus. Dexamethasone treatment for 10 days abolished the effect of adrenalectomy and decreased significantly pituitary VIP mRNA content in sham-operated rats. In the cerebral cortex, however, dexamethasone treatment resulted in an enhancement in VIP mRNA levels in both sham-operated and adrenalectomized animals. Hypothalamic VIP mRNA content remained unchanged. These changes in VIP mRNA levels were accompanied by parallel changes in VIP concentrations in the tissues studied, suggesting that glucocorticoid regulates the synthesis of VIP in the cerebral cortex and anterior pituitary. On the other hand, serum PRL level increased after adrenalectomy but became suppressed following dexamethasone administration, in parallel with changes in pituitary VIP synthesis. These findings suggest that the effect of glucocorticoid on PRL secretion may be mediated, at least in part, via changes in VIP synthesis and secretion. We conclude that glucocorticoid regulates the expression of VIP in the rat brain, resulting in divergent changes in the cerebral cortex and pituitary. Changes in VIP synthesis and secretion may contribute to the disturbances in brain function and PRL secretion in conditions of glucocorticoid excess.

Adrenalectomy↗
PubMed1975

Brain tissue transplanted to the anterior chamber of the eye: 3. Substitution of lacking central noradrenaline input by host iris sympathetic fibers in the isolated cerebral cortex developed in oculo.

Fetal parietal cerebral cortex was homologously transplanted to the anterior chambers of the eyes of adult rats. The transplants got vascularized, proliferated, as measured by in vivo stereoscopic inspections, and differentiated into brain tissue similar to cortex cerebri in situ and survived for long times, greater than 41/2 months. Fibers from the intact sympathetic adrenergic ground plexus of the iris were able to innervate the transplants in an organotypic way regarding fluorescence morphology, pattern of distribution of the nerve terminals and, to a certain extent, density of innervation, the only variable parameter being density of innervation. Thus, in unpretreated or MAO inhibited transplants only rather few to scattered terminals could be found, while after preincubation in 10(-5)M alpha-methyl-noradrenaline the number of visible terminals was normal or slightly less than normal, as compared to cortex cerebri in situ. When superior cervical ganglia (SCG) were transplanted together with fetal cortex tissue to sympathetically denervated eyes the ingrowth in the cortex tissue was similar to that after single cortex transplantation combined with 5 day old SCG, while a marked hyperinnervation was encountered when combined with adult SCG. It is concluded that the developing cortex cerebri, deprived of its normal CNS source of adrenergic nerves, is able to receive sympathetic adrenergic nerves from the iris in an organotypic way upon transplantation to the anterior chamber of the eye.

Animals↗
PubMed2003

Focal thinning of the cerebral cortex in multiple sclerosis.

Brain atrophy as determined by quantitative MRI can be used to characterize disease progression in multiple sclerosis. Many studies have addressed white matter (WM) alterations leading to atrophy, while changes of the cerebral cortex have been studied to a lesser extent. In vivo, the cerebral cortex has been difficult to study due to its complex structure and regional variability. Measurement of cerebral cortex thickness at different disease stages may provide new insights into grey matter (GM) pathology. In the present investigation, we evaluated in vivo cortical thickness and its relationship to disability, disease duration, WM T2 hyper-intense and T1 hypo-intense lesion volumes. High-resolution MRI brain scans were obtained in 20 patients with clinically definite multiple sclerosis and 15 age-matched normal subjects. A novel method of automated surface reconstruction yielded measurements of the cortical thickness for each subject's entire brain and computed cross-subject statistics based on the cortical anatomy. Statistical thickness difference maps were generated by performing t-tests between patient and control groups and individual thickness measures were submitted to analyses of variance to investigate the relationship between cortical thickness and clinical variables. The mean overall thickness of the cortical ribbon was reduced in multiple sclerosis patients compared with controls [2.30 mm (SD 0.14) versus 2.48 mm (SD 0.11)], showing a significant main effect of group (controls versus patients). In patients, we found significant main effects for disability, disease duration, T2 and T1 lesion volumes. The visualization of statistical difference maps of the cortical GM thickness on inflated brains across the cortical surface revealed a distinct distribution of significant focal thinning of the cerebral cortex in addition to the diffuse cortical atrophy. Focal cortical thinning in frontal [2.37 mm (SD 0.17) versus 2.73 mm (SD 0.25)] and in temporal [2.65 mm (SD 0.15) versus 2.95 mm (SD 0.11)] brain regions was observed, even early in the course of the disease or in patients with mild disability. Patients with longstanding disease or severe disability, however, presented additionally with focal thinning of the motor cortex area [2.35 mm (SD 0.19) versus 2.74 mm (SD 0.15)]. We conclude that in vivo measurement of cortical thickness is feasible in patients suffering from multiple sclerosis. The data provide new insight into the cortical pathology in multiple sclerosis patients, revealing focal cortical thinning beside an overall reduction of the cortical thickness with disease progression.

Adult↗