The regeneration of peripheral nerves inserted into the cerebral cortex and the healing of cerebral lesions.
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Cerebral Cortex↗
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Generic model for the localization of the cerebral cortex and preoperative multimodal integration in epilepsy surgery.
In cerebral cortex neurosurgery and particularly in epilepsy surgery, the recognition of individual cortical anatomic landmarks is necessary for presurgical evaluation and planning. To overcome the classical great variability in the superficial aspect of the human cerebral cortex, we have developed an original generic description of the cerebral cortex in a three-dimensional structure. The result is a generic model matching the cortical topography of each brain regardless of inter- and intra-individual variability. In this model, sulcal roots (fundi) are separated by more or less superficial annectent gyrus, and buried by operculization during the gyrification. This original generic model of the cerebral cortex enabled us to develop a mathematical methodology for the construction of a structural representation of the cortical topography from a T1-weighted three-dimensional MR image. This program can provide automatic detection and recognition of the main cortical sulci.
Algorithms↗
Administration of FGF-2 to embryonic mouse brain induces hydrocephalic brain morphology and aberrant differentiation of neurons in the postnatal cerebral cortex.
Fibroblast growth factor-2 (FGF-2) was injected into mouse cerebral ventricles at embryonic day (E) 14 in utero and its effects on developing brain morphology and expression of various cell- or differentiation-associated protein markers in the cerebral cortex were examined. High doses of FGF-2 (200 or 300 ng) caused encephalic alternations such as deformation of the calvarium, enlargement of the ventricular spaces, and thinning of the cerebral cortex. There was no gross abnormality in the alignment of the cerebral neuronal layers, however, both cell number and cell density of the upper layers (II/III) and the lower layers (IV-VI) of the cerebral cortex were increased. Brain-derived neurotrophic factor (BDNF), tyrosine hydroxylase, nestin, and microtubule-associated protein 2 were aberrantly or ectopically expressed in the deep areas of the cerebral cortex. A substantial number of these cells coexpressed these antigens. These observations demonstrate that a subpopulation of neurons in the cortical deep layer abnormally differentiated or partly sustained their immature state following a single administration of FGF-2 at E14. Developmental analysis of localization of BDNF-positive cells suggested that the abnormality started around P5. Furthermore, cell migration was not affected by FGF-2 administration. FGF-2 seems to play predominant roles in the proliferation of neuronal precursors and in neuronal differentiation in the developing mouse cerebral cortex even at relatively late stages of brain neurogenesis.
Animals↗
Cerebral cortex ammonia and glutamine metabolism during liver insufficiency-induced hyperammonemia in the rat.
Hyperammonemia has been suggested to induce enhanced cerebral cortex ammonia uptake, subsequent glutamine synthesis and accumulation, and finally net glutamine release into the blood stream, but this has never been confirmed in liver insufficiency models. Therefore, cerebral cortex ammonia- and glutamine-related metabolism was studied during liver insufficiency-induced hyperammonemia by measuring plasma flow and venous-arterial concentration differences of ammonia and amino acids across the cerebral cortex (enabling estimation of net metabolite exchange), 1 day after portacaval shunting and 2, 4, and 6 h after hepatic artery ligation (or in controls). The intra-organ effects were investigated by measuring cerebral cortex tissue ammonia and amino acids 6 h after liver ischemia induction or in controls. Arterial ammonia and glutamine increased in portacaval-shunted rats versus controls, and further increased during liver ischemia. Cerebral cortex net ammonia uptake, observed in portacaval-shunted rats, increased progressively during liver ischemia, but net glutamine release was only observed after 6 h of liver ischemia. Cerebral cortex tissue glutamine, gamma-aminobutyric acid, most other amino acids, and ammonia levels were increased during liver ischemia. Glutamate was equally decreased in portacaval-shunted and liver-ischemia rats. The observed net cerebral cortex ammonia uptake, cerebral cortex tissue ammonia and glutamine accumulation, and finally glutamine release into the blood suggest that the rat cerebral cortex initially contributes to net ammonia removal from the blood during liver insufficiency-induced hyperammonemia by augmenting tissue glutamine and ammonia pools, and later by net glutamine release into the blood. The changes in cerebral cortex glutamate and gamma-aminobutyric acid could be related to altered ammonia metabolism.
Ammonia↗
A developmental decrease in NMDA-mediated spontaneous firing in cultured rat cerebral cortex.
In primary cultures of fetal rat cerebral cortex chronic manipulation of the level and/or pattern of bioelectric activity leads to plastic changes in bioelectric activity, opposite to those seen during the manipulation. This suggests the presence of adaptive mechanisms which regulate functional development in the neuronal network. Since NMDA receptors play an important role in early postnatal bioelectric activity and have been implicated in activity-dependent plasticity in vivo, the involvement of NMDA and non-NMDA receptors in spontaneously occurring bioelectric activity was investigated in cultured rat cerebral cortex by assaying the effects of NMDA and non-NMDA antagonists on neuronal firing. In addition, the physiological consequences of chronic suppression of bioelectric activity were investigated following development in the presence of tetrodotoxin. NMDA receptors appeared at all ages to be more crucial for spontaneous bioelectric activity than non-NMDA receptors, although their relative importance decreased during the first 3 weeks. Whereas the NMDA antagonist APV strongly reduced burst firing, the non-NMDA antagonist DNQX tended to increase burst firing slightly. Following chronic suppression of bioelectric activity, non-variable burst firing was increased, thus replicating previous findings in cerebral cortex culture grown under different conditions. The prominence of NMDA receptor activation in spontaneous bioelectric activity in early cultures suggests a role for these receptors in activity-dependent functional plasticity, as found in vivo.
2-Amino-5-phosphonovalerate↗
Mild hypercapnia induces vasodilation via adenosine triphosphate-sensitive K+ channels in parenchymal microvessels of the rat cerebral cortex.
BACKGROUND: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex. METHODS: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 microm) was monitored using computerized videomicroscopy. RESULTS: During contraction to prostaglandin F2alpha (5 x 10(-7) m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10(-6) m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10(-7) m) as well as the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (10(-4) m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10(-8) to 3 x 10(-7) m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide. CONCLUSION: These results suggest that in parenchymal microvessels of the rat cerebral cortex, decreased pH corresponding with hypercapnia, but not hypercapnia itself, contributes to cerebral vasodilation produced by carbon dioxide and that ATP-sensitive K+ channels play a major role in vasodilator responses produced by mild hypercapnia.
Adenosine Triphosphate↗
Patterning and specification of the cerebral cortex.
Regionalization of the cerebral cortex occurs during development by the formation of anatomically and functionally discrete areas of the brain. Descriptive evidence based on expression of molecules and structural features suggests that an early parcelation of the cerebral wall may occur during fetal development. Experimental strategies using tissue transplants and cell culture models have explored the nature of the timing of areal specification. New signaling systems displaying the sensitivity of precursor cells to environmental cues that define the fate of neurons destined for specific areas of the cortex have been discovered. Studies in the field now suggest mechanisms of regulating cell phenotype in the cortex that are common to all parts of the neuraxis.
Animals↗
Transient ipsilateral blood flow reduction in the thalamus and cerebral cortex after pontine infarction.
Remote cerebral hypoperfusion associated with pontine lesions is rare. We describe a patient who showed transient ipsilateral hypoperfusion in the thalamus and cerebral cortex after a pontine infarct. This resolved within 8 days after onset. Anatomical considerations strongly suggested involvement of the cerebellothalamocortical pathway in this case.
Aged↗
Immunohistochemistry of neural markers for the study of the laminar architecture in celloidin sections from the human cerebral cortex.
Morphometric studies of the cerebral cortex in celloidin sections provide reliable quantitative estimates of cytoarchitectural features in individual brain regions. To increase our knowledge about the morphology and distribution of neuronal and glial cell types using specific cellular markers, we compared two methods of celloidin removal/antigen recovery, and subsequent immunohistochemical staining of free floating sections with specific antibodies. The method based on methanol and NaOH for celloidin removal was the most adequate for optimal recovery of immunoreactivity of the neural markers NF200, MAP2, GFAP, calretinin, parvalbumin, calbindin-D28kD, and synaptophysin. The other method, based on a treatment with ethanol/ether and formic acid, gave good results in the immunostaining of NF200, GFAP and MAP2, but not the other markers named above. The immunostained sections were compared with nearby sections stained with cresyl violet in order to assign the immunoreactive structures to individual layers in the prefrontal cortex. Sections from blocks not embedded in celloidin showed a comparable distribution of all the antigens included in the present study. The present paper provides an antigen recovery technique for celloidin sections that can be applied to optimize studies on the cytoarchitecture and distribution of specific neural elements in the human cerebral cortex.
Collodion↗
Schilder's disease. A study of the cerebral cortex with Golgi's method.
The cerebral cortex of a patient with Schilder's disease was studied with the Golgi method. The number of synaptic spines, basal dendrites, branching points, and dendritic intersection points of 5th layer pyramids are similar to those of controls, in spite of almost complete loss of extrinsic fibers. These data illustrate the probable remodeling of intrinsic cortical circuits and neuronal plasticity in the human cerebral cortex.
Cerebral Cortex↗
[On representation of the internal organs in the cerebral cortex and cerebellar cortex in cats and dogs. Communication V Individual variations in localizations of the zones of specific projections in the cortex of the greater hemispheres in cats and dogs].
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Animals↗
Dose-dependent effects of acute in vivo ethanol exposure on extracellular glutamate concentration in the cerebral cortex of the near-term fetal sheep.
The cerebral cortex is a target site of ethanol teratogenesis. L-Glutamate is a major excitatory neurotransmitter that plays an important neurotrophic role in brain development. It has been proposed that optimal function of the glutamate neuronal system is required for normal brain development; overactivation could lead to excitotoxic-induced neuronal injury, whereas underactivation could delay/restrict brain development. The objective of this study was to test the hypothesis that acute in vivo ethanol exposure alters basal glutamate release in the fetal cerebral cortex. The experimental approach involved measuring fetal cortical extracellular glutamate concentration using the technique of in vivo microdialysis. Near-term fetal sheep were chronically instrumented with a microdialysis probe placed in the parasagittal cortex. At 124 +/- 3 days of gestation, the effects of maternal intravenous infusion of 2 g or 4 g ethanol/kg maternal body weight or an equivalent volume of saline, given as four equally divided doses over 5 hr, on fetal cerebral cortical extracellular glutamate concentration were determined. None of the three treatment regimens produced fetal or maternal demise during the time course of the study. There was an ethanol dose-dependent increase, p = 0.005, in extracellular glutamate concentration in the fetal cerebral cortex. This increase was paroxysmal in nature and was not directly related to the fetal blood ethanol concentration. In view of the proposed role for glutamate in neuronal development, this apparent ethanol-induced increase in glutamate release may be important in the pathogenesis of ethanol teratogenesis involving the cerebral cortex.
Alcohol Drinking↗
Effects of substances affecting protein kinase C on histamine-evoked stimulation of cyclic AMP formation in chick cerebral cortex.
In membrane preparation of chick cerebral cortex, HA (histamine) did not affect both basal and forskolin-stimulated adenylyl cyclase activity. However, in slices of chick cerebral cortex prelabeled with [3H]adenine, HA, as well as 2-methylHA, 4-methylHA, and N alpha-methylHA, potently increased [3H]cyclic AMP accumulation in a concentration-dependent manner. The stimulatory effect of the HA-ergic compounds on cyclic AMP formation was antagonized by HA H2-receptor blockers (aminopotentidine, ranitidine), and by chelerythrine (50 microM), a potent and selective inhibitor of PKC (protein kinase C). Of the two other tested PKC inhibitors H-7 (100 microM) significantly reduced the HA action, while the effect of staurosporine (1 microM) did not reach the level of statistical significance. Preincubation of chick cerebral cortical slices with a PKC activator, PDB (4 beta-phorbol 12,13-dibutyrate, 1 microM), markedly enhanced the accumulation of cyclic AMP evoked by HA, 2-methylHA, 4-methylHA and N alpha-methylHA. 4 beta-Phorbol, inactive on PKC, was ineffective. A possible role of PKC in the regulation of HA-induced cyclic AMP synthesis in chick cerebrum has been discussed.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
An anatomical study of cholinergic innervation in rat cerebral cortex.
The cholinergic innervation of rat cerebral cortex was studied by immunohistochemical localization of choline acetyltransferase. Stained bipolar cells, fibers and terminals were found in all areas of cortex. The density of cholinergic terminals was similar in all cortical areas with the exception of entorhinal and olfactory cortex, which showed a marked increase in the number of stained terminals. A laminar distribution of cholinergic terminals was found in many cortical areas. In motor and most sensory areas, terminal density was high in layer 1 and upper layer 5, and lowest in layer 4. Visual cortex, in contrast to other cortical areas, was characterized by a dense band of innervation in layer 4. It has been known that the majority of cortical cholinergic structures derive from a projection to cortex from large, multipolar neurons in the basal forebrain, which stain heavily for choline acetyltransferase. In this study, stained fibers were observed to take three different pathways from basal forebrain to cortex. The first, confined to medial aspects of forebrain and cortex, was observed to originate in the septal area, from where fibers formed a discrete bundle, swinging forward around the rostral end of the corpus callosum, then travelling caudally in the cingulate bundle. The second was found to consist of fibers fanning out laterally from the area of the globus pallidus, travelling through the caudate, then continuing for various distances in the corpus callosum before finally turning into the cortex. A third pathway appeared to innervate olfactory and entorhinal cortex. Ibotenic acid injections were made in the area of the globus pallidus to study the effect of lesioning the lateral pathway on the cholinergic innervation in cortex. A major loss of choline acetyltransferase positive terminals was observed in neocortex, but retrosplenial, cingulate, entorhinal and olfactory cortex showed a normal density of cholinergic innervation. The borders separating areas with lesioned cholinergic input from non-lesioned areas were precise. The distribution of stained terminals remaining in cortical areas with lesioned basal forebrain innervation suggests that the basal forebrain projection to cerebral cortex, and not the intrinsic cortical cholinergic neurons, give rise to the laminar distribution of cholinergic terminals observed in normal cortex. To compare the relative densities of different cholinergic cortical systems, the distribution of choline acetyltransferase staining was compared with that of vasoactive intestinal polypeptide and substance P, which are co-localized in some choline acetyltransferase-positive neurons innervating cortex.
Animals↗
[Decisive role of the activity of cerebral cortex in the regulation of the adreno-pituitary system].
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Adrenal Cortex↗
Characterization of alpha-1 adrenergic receptors linked to [3H]inositol metabolism in rat cerebral cortex.
The properties of alpha-1 adrenergic receptors in rat cerebral cortex were examined by measuring increases in [3H]inositol metabolism in brain slices. Slices of rat cerebral cortex were incubated in the presence of 0.23 microM [3H]inositol in Krebs-Ringer-bicarbonate buffer containing 10 mM lithium chloride, and the production of water-soluble [3H]inositol phosphates was monitored after extraction and anion-exchange chromatography. Norepinephrine caused a 4- to 6-fold increase in [3H]inositol metabolism in cerebral cortical slices, and this response was blocked much more potently by the alpha-1-selective antagonist prazosin than by the alpha-2-selective antagonist yohimbine. Epinephrine and norepinephrine were both full agonists and stimulated [3H]inositol metabolism to the same extent in this system. The synthetic drugs phenylephrine and methoxamine were both partial agonists at these receptors, with intrinsic activities only 56 to 58% of epinephrine and norepinephrine. A variety of imidazoline and other partial agonists caused no measurable stimulation of [3H]inositol metabolism in this preparation. The response to norepinephrine was completely blocked by alpha adrenergic receptor antagonists with the potency order prazosin greater than BE 2254 greater than indoramin = phentolamine greater than azapetine greater than piperoxan greater than yohimbine. In the absence of calcium, basal [3H]inositol metabolism was increased, but norepinephrine caused the same 5-fold stimulation as in the presence of 2.5 mM CaCl2. The potencies of both antagonists and agonists in inhibiting or activating [3H]inositol metabolism in slices of rat cerebral cortex were highly correlated with their ability to displace the alpha-1 adrenergic receptor selective radioligand [125I]BE 2254 from specific binding sites in membrane preparations of rat cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic alpha-Antagonists↗
Pharmacological characterisation of human cerebral cortex somatostatin SRIF1 and SRIF2 receptors.
Radioligand binding studies were performed in membranes of human cerebral cortex using [125I]Tyr3-octreotide in the presence of 5 mM MgCl2, [125I]SRIF-14 ([125I]Tyr11-SRIF-14) and [125I]CGP 23996 ([125I]c[Asu- Lys-Asn-Phe-Phe-Trp-Lys-Thr-Tyr-Thr-Ser]) both in the presence of 120 mM NaCl, to characterise the nature of the somatostatin (SRIF) receptors. The pharmacological profile of human brain SRIF recognition sites was compared with that of recombinant human SRIF1 (sst2-sst3-sst5) or SRIF2 receptors (sst1-sst4) and with that of native rat sst1, sst2, and sst4 receptors. [125I]Tyr3-octreotide labelled binding sites in human cerebral cortex: Bmax = 238 +/- 36 fmol/mg protein and pKd = 9.73 +/- 0.08. The pharmacological profile of [125I]Tyr3-octreotide labelled sites correlated very significantly with that of recombinant human sst2 receptors (r = 0.98) and much less with those of recombinant human sst3 (r = 0.65) or sst5 receptors (r = 0.72). The correlation between [125I]Tyr3-octreotide binding to native sst2 receptors in human and rat cerebral cortex was also highly significant (r = 0.97). [125I]SRIF-14 and [125I]CGP 23996 binding (performed in the presence of 120 mM NaCl) in the human cerebral cortex identified very similar populations of sites Bmax = 44 +/- 7 and 36 +/- 5 fmol/mg protein and pKd = 9.44 +/- 0.08 and 9.48 +/- 0.10, respectively. The pharmacological profiles of the sites labelled with [125I]SRIF-14 and [125I]CGP 23996 correlated highly significantly with those of recombinant human sst1 (r = 0.97-0.99) or sst4 receptors (r = 0.91-0.94). Similarly, the correlations between [125I]SRIF-14 or [125I]CGP 23996 binding in human cortex and [125I]SRIF-14 binding to native sst1 sites in rat cerebral cortex were also highly significant (r = 0.97 and 0.94, respectively). Finally, the pharmacological profile of native rat lung sst4 sites determined with [125I]LTT-SRIF-28 ([Leu8,D-Trp22, 125I-Tyr25]SRIF-28) correlated with [125I]SRIF-14 and [125I]CGP 23996 binding in human cortex; r = 0.91 and 0.87, respectively. The present data show that in human cerebral cortex, [125I]Tyr3-octreotide labels SRIF1 receptor sites which are best characterised as of the sst2 type, whereas [125I]SRIF-14 and [125I]CGP 23996 (both in the presence of 120 mM NaCl), label sites which fit almost equally well with sst1 or sst4 receptors and therefore are best described as of the SRIF2 type. Under the conditions used, there was no evidence that either of these ligands would label sst3 or sst5 receptors in human cerebral cortex.
Animals↗
[Effect of cerebral hypoxia and hyperventilation hypocapnia on the epileptiform activity of the cerebral cortex of the cat].
Influence of cerebral hypoxia and hyperventilatory hypocapnia on the ECoG and focal epileptiform activity of the cerebral cortex induced with local application of strychnine was studied in cats with transection of spinal cord at C1. Although both hypoxia and hypocapnia produced synchronization of the cerebral cortex electrical activity, i.e. exerted the same effects on the ECoG, their influence on cortical excitability was quite different: hypoxia suppressed the epileptiform activity whereas hypocapnia facilitated it.
Animals↗