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PubMedDate not supplied

[Structural and functional reorganization of neurons and glia in the sensomotor cortex of the cerebral cortex in experimental neurosis].

Histological and hypoxic changes in different tissue elements (neurones and glia), testifying to active disturbances of metabolic processes, are observed in the sensorimotor cerebral cortex of rabbits with experimental neurosis. These changes indicate a complex structural-metabolic rearrangement, occuring with this form of CNS pathology. The results of the study may be used for investigation of mechanisms compensating disturbances in the higher nervous activity and for pathogenetically grounded therapy.

Animals↗
PubMed1994

Elevated immunoreactivity for glutamic acid decarboxylase in the rat cerebral cortex following transient middle cerebral artery occlusion.

We investigated the expression of glutamic acid decarboxylase (molecular weight 67,000; GAD67) immunohistochemically in the rat cerebral cortex following transient middle cerebral artery occlusion (MCAO) capable of producing slowly progressive neuronal damage. An increase in GAD67 immunoreactivity was observed in the cerebral cortex ipsilateral to the ischemic insult, most prominent in lamina IV, 3 to 14 days after MCAO. At this stage, light microscopy showed GAD67-positive puncta to be larger and more strongly immunoreactive in the ipsilateral cortex than those in the contralateral side. The elevated expression of GAD67 in the insulted cortex may reflect part of the adaptive functional changes in GABA transmission with slowly progressive cortical ischemic damage.

Animals↗
PubMed2001

Focal ischemia in the cerebral cortex has an effect on the neurohypophysis. II. Angiogenesis in the neurohypophysis is a consequence of the focal ischemia in the cerebral cortex.

OBJECTIVES: Focal ischemia in the cerebral cortex has an effect on neurohypophysis. The morphological changes of microvessels of neurohypophysis were evaluated in a model of the cerebral infarction initiated by a photochemical reaction in the cerebral cortex. After photochemically induced platelet aggregation, we observed the morphological features of angiogenesis. METHOD: The model of photochemically-induced cerebral ischemia was used. Seven days after intravenous injection of rose bengal and irradiation from a halogen lamp source through an intact cranium, the sampled material from neurohypophysis is processed for transmission electron microscopy using standard procedures. RESULTS: We observed morphological features of the new vessel formation: the alterations in the endothelium and extracellular matrix during separation of the endothelial cell from each other in a "mother" vessel, the migration of the endothelial cells in the extracellular matrix, the communication of the lumen of the new and the "mother" vessels. CONCLUSION: We observed development of the angiogenic phenotype in the neurohypophysis after focal ischemia in the cerebral cortex. The endothelium, basement membrane and extracellular matrix undergo morphological alterations which lead to new blood vessel formation.

Animals↗
PubMed2005

A tracking approach to parcellation of the cerebral cortex.

The cerebral cortex is composed of regions with distinct laminar structure. Functional neuroimaging results are often reported with respect to these regions, usually by means of a brain "atlas". Motivated by the need for more precise atlases, and the lack of model-based approaches in prior work in the field, this paper introduces a novel approach to parcellating the cortex into regions of distinct laminar structure, based on the theory of target tracking. The cortical layers are modelled by hidden Markov models and are tracked to determine the Bayesian evidence of layer hypotheses. This model-based parcellation method, evaluated here on a set of histological images of the cortex, is extensible to 3-D images.

Algorithms↗
PubMed1988

Effects of nifedipine and felodipine on adenosine and inosine release from the hypoxemic rat cerebral cortex.

The cerebral cortical cup technique has been used to study the effects of nifedipine and felodipine on adenosine and inosine release from the rat brain. After basal and hypoxia (8% 02)-evoked control levels of purine release had been established, these 1,4-dihydropyridine calcium antagonists were administered intraperitoneally (1 mg/kg). Both agents depressed basal levels of purine efflux and suppressed the hypoxia-evoked release of adenosine and inosine. An inhibition of the transporter that mediates purine efflux from brain cells is likely to account for the suppression of release from the cerebral cortex. A reduced release of adenosine into the interstitial space also explains the ability of both agents to block the increase in CBF evoked by hypoxic challenges.

Adenosine↗
PubMed1992

Amino acid release from cerebral cortex in experimental acute liver failure, studied by in vivo cerebral cortex microdialysis.

Both increased gamma-aminobutyric acid (GABA)-ergic and decreased glutamatergic neurotransmission have been suggested relative to the pathophysiology of hepatic encephalopathy. This proposed disturbance in neurotransmitter balance, however, is based mainly on brain tissue analysis. Because the approach of whole tissue analysis is of limited value with regard to in vivo neurotransmission, we have studied the extracellular concentrations in the cerebral cortex of several neuroactive amino acids by application of the in vivo microdialysis technique. During acute hepatic encephalopathy induced in rats by complete liver ischemia, increased extracellular concentrations of the neuroactive amino acids glutamate, taurine, and glycine were observed, whereas extracellular concentrations of aspartate and GABA were unaltered and glutamine decreased. It is therefore suggested that hepatic encephalopathy is associated with glycine potentiated glutamate neurotoxicity rather than with a shortage of the neurotransmitter glutamate. In addition, increased extracellular concentration of taurine might contribute to the disturbed neurotransmitter balance. The observation of decreasing glutamine concentrations, after an initial increase, points to a possible astrocytic dysfunction involved in the pathophysiology of hepatic encephalopathy.

Acute Disease↗
PubMed2005

Patterning and plasticity of the cerebral cortex.

The cerebral cortex of the human brain is a sheet of about 10 billion neurons divided into discrete subdivisions or areas that process particular aspects of sensation, movement, and cognition. Recent evidence has begun to transform our understanding of how cortical areas form, make specific connections with other brain regions, develop unique processing networks, and adapt to changes in inputs.

Animals↗
PubMed1993

Spreading depression can be restricted to distinct depths of the rat cerebral cortex.

In cerebral cortex of rats recurrent and single spreading depressions (SDs) were elicited by KCl application and by needle prick, respectively. SDs were monitored by recording changes of DC (direct current) potentials and of K+ concentration ([K+]o) in the extracellular space using K(+)-selective microelectrodes. Profiles of DC potential and of [K+]o were obtained by stepwise lowering a microelectrode array consisting of up to four electrodes into the brain cortex. Recurrent SDs propagating from the site of KCl application had lower frequencies and longer duration in superficial compared to deeper cortical structures. Single SD elicited by needle prick 3 mm away from the recording sites usually invaded the whole grey matter and showed DC potential shifts that differed in shape from the recurrent SDs. At a depth restricted to 1000 microns SD-related DC potential shifts and rises in [K+]o were drastically diminished. In 2 of 8 experiments prick-elicited SD was absent either above or below cortical depths of 800-1000 microns. The results suggest a barrier for vertical SD propagation in cortical depth between 800 and 1200 microns. The observations are relevant for application of noninvasive techniques (DC electroencephalography, magnetoencephalography) to detect SD in the brain.

Animals↗
PubMed1999

Activation of serotonin receptors modulates synaptic transmission in rat cerebral cortex.

The cerebral cortex receives an extensive serotonergic (5-hydroxytryptamine, 5-HT) input. Immunohistochemical studies suggest that inhibitory neurons are the main target of 5-HT innervation. In vivo extracellular recordings have shown that 5-HT generally inhibited cortical pyramidal neurons, whereas in vitro studies have shown an excitatory action. To determine the cellular mechanisms underlying the diverse actions of 5-HT in the cortex, we examined its effects on cortical inhibitory interneurons and pyramidal neurons. We found that 5-HT, through activation of 5-HT(2A) receptors, induced a massive enhancement of spontaneous inhibitory postsynaptic currents (sIPSCs) in pyramidal neurons, lasting for approximately 6 min. In interneurons, this 5-HT-induced enhancement of sIPSCs was much weaker. Activation of 5-HT(2A) receptors also increased spontaneous excitatory postsynaptic currents (sEPSCs) in pyramidal neurons. This response desensitized less and at a slower rate. In contrast, 5-HT slightly decreased evoked IPSCs (eIPSCs) and eEPSCs. In addition, 5-HT via 5-HT(3) receptors evoked a large and rapidly desensitizing inward current in a subset of interneurons and induced a transient enhancement of sIPSCs. Our results suggest that 5-HT has widespread effects on both interneurons and pyramidal neurons and that a short pulse of 5-HT is likely to induce inhibition whereas the prolonged presence of 5-HT may result in excitation.

Animals↗
PubMed1998

Cyclin-dependent kinase 5-deficient mice demonstrate novel developmental arrest in cerebral cortex.

The cerebral cortex of mice with a targeted disruption in the gene for cyclin-dependent kinase 5 (cdk5) is abnormal in its structure. Bromodeoxyuridine labeling reveals that the normal inside-out neurogenic gradient is inverted in the mutants; earlier born neurons are most often found superficial to those born later. Despite this, the early preplate layer separates correctly and neurons with a normal, pyramidal morphology can be found between true marginal zone and subplate. Consistent with their identity as layer VI corticothalamic neurons, they can be labeled by DiI injections into thalamus. The DiI injections also reveal that the trajectories of the cdk5(-/-) thalamocortical axons are oblique and cut across the entire cortical plate, instead of being oriented tangentially in the subcortical white matter. We propose a model in which the cdk5(-/-) defect blocks cortical development at a heretofore undescribed intermediate stage, after the splitting of the preplate, but before the migration of the full complement of cortical neurons.

Animals↗
PubMed1997

Light and electron microscope study of nerve cells in traumatic oedematous human cerebral cortex.

The cerebral cortex of eight patients with complicated head and brain traumatic injuries has been examined with light and transmission electron microscopes. The neuronal and neuroglial cell bodies and their processes have been examined to study the changes induced by the brain injury and the associated vasogenic and cytotoxic, moderate or severe, brain oedema. Light microscopy study showed oedematous and ischaemic neurons and neuroglial cells in both moderate and severe oedema, and breakdown of the blood-brain barrier with perivascular and parenchymatous haemorrhagic foci. Astrocytes and oligodendrocytes exhibited oedematous and reactive changes. At the electron microscope level oedematous changes were found in intraneuronal and glial somatic compartment. Myelinated axons showed clear and dark degenerative features. Beaded dendrites and clear and dense synaptic degeneration were also found. The extracellular space appeared distended, with the presence of clear and electron-dense haematogenous oedema fluid and fibrinous organization. Phagocytosis of degenerated myelinated axons and synaptic endings by neuroglial cells and non-nervous invading cells were observed. The clinical evolution time of traumatic brain injuries was considered in relation to nerve cell degenerative features.

Adolescent↗
PubMed1986

Subunit interactions of native and ADP-ribosylated alpha 39 and alpha 41, two guanine nucleotide-binding proteins from bovine cerebral cortex.

Bovine cerebral cortex contains two major substrates for ADP-ribosylation by pertussis toxin: a 39-kDa protein, alpha 39, and a 41-kDa protein, alpha 41 (Neer, E. J., Lok, J. M., and Wolf, L. G. (1984) J. Biol. Chem. 259, 14222-14229). Both of these proteins bind guanosine 5'-(3-O-thio)triphosphate (GTP gamma S) with a similar affinity (Kd = 30 +/- 10 nM for alpha 39, Kd = 32 +/- 14 nM for alpha 41). Both proteins associate with a beta X gamma subunit made up of a 36-kDa beta component and a 6-kDa gamma component. We have previously shown that the beta X gamma unit is required for pertussis toxin-catalyzed ADP-ribosylation (Neer et al. (1984)). By measuring the amount of beta X gamma required for maximal incorporation of ADP-ribose, we now find that the EC50 for beta X gamma in this reaction is 3 +/- 1 times lower for alpha 41 than for alpha 39. ADP-ribosylation by pertussis toxin does not prevent dissociation of alpha 41 X beta X gamma or alpha 39 X beta X gamma by GTP gamma S. GTP gamma S decreases the sedimentation coefficient of ADP-ribosylated alpha 41 from 4.2 S to 3.0 S and the sedimentation coefficient of ADP-ribosylated alpha 39 from 4.3 S to 2.9 S. The conclusion that GTP gamma S dissociates both ADP-ribosylated heterotrimers was confirmed by the observation that GTP gamma S blocks precipitation of ADP-ribosylated alpha 39 or alpha 41 by anti-beta antibody. Neither alpha 41 X beta X gamma nor alpha 39 X beta X gamma is dissociated by GTP whether or not the proteins are ADP-ribosylated. The observation that alpha 41 more readily associates with beta X gamma than does alpha 39 may explain our earlier observation that alpha 41 is more readily ADP-ribosylated than alpha 39. In most intact membranes, only a 41-kDa ADP-ribosylated protein is seen. However, alpha 39 is also present in most tissues since we can detect it with anti-alpha 39 antibody. The functional consequences of pertussis toxin treatment may depend on whether one or both proteins are ADP-ribosylated. This in turn may depend on the ratio of alpha 41 and alpha 39 to beta X gamma in a given tissue.

Adenosine Diphosphate Ribose↗
PubMed1996

Ketamine antagonizes nitric oxide release from cerebral cortex after middle cerebral artery ligation in rats.

BACKGROUND AND PURPOSE: Ischemia or hypoxia activates N-methyl-D-aspartate (NMDA) receptors and results in nitric oxide (NO) production. The purpose of this study was to investigate whether an NMDA channel blocker can inhibit NO production during ischemia. METHODS: Temporary cerebral ischemia was induced by middle cerebral artery ligation while common carotid arteries were clamped bilaterally for 40 minutes in urethane-anesthetized rats. Extracellular NO concentration in the cortex was recorded through Nafion- and porphyrine-coated carbon fiber electrodes. Ketamine, and NMDA channel blocker, was administered (50 mg/kg) intraperitoneally 15 minutes before the cerebral artery ligation. RESULTS: During middle cerebral artery ligation, cortical NO was increased to its peak (18.76+/-3.36 nmol/L) in 7 minutes and then declined. The overflow of NO can be antagonized by pretreatment with ketamine, dizocilpine maleate (MK801), or N(G)-nitro-L-arginine methyl ester (L-NAME). Local application of nitroprusside also induced NO production. However, this effect was not antagonized by ketamine. CONCLUSIONS: These findings demonstrated that NO release induced by short-term cerebral ischemia can be attenuated by pretreatment with NMDA antagonists.

Animals↗
PubMedDate not supplied

[Protein synthesis in cerebral cortex cells of rats exposed to hypoxia during interparenchymal administration of protein isolated from embryonal nerve tissue into the cerebral cortex].

The stage-specific activator protein CF was studied for effects on protein biosynthesis in the fractions rich in nerve and glial cells of the brain cortex of rats which had been exposed to hypoxia. Protein was isolated from the cortex of embryos or from the cerebellum of 8-10-day rats, the period being of the most active nerve cell proliferation. Following 4 days of the interparenchymal administration of SF into the cerebral cortex of the animals exposed to hypoxia there was an increase in the rate of 3-H-leucine incorporation into the nerve cells up to the values observed in the neurons of the cerebral cortex of intact animals. The level of protein synthesis in the glial cells remained unchanged. There were no increases in protein synthesis either in nerve or glial cells 120 days after single administration of SF. The findings were compared with the experimental evidence for the biosynthesis of macromolecules in various cerebral cortical cells from rats exposed to hypoxia and undergone transplantation of embryonal nerve tissue.

Animals↗
PubMed2004

Local field potential oscillations in primate cerebellar cortex: synchronization with cerebral cortex during active and passive expectancy.

Many brain regions, such as the cerebellum, primary somatosensory cortex (SI), and primary motor cortex (MI), interact to produce coordinated actions. Synchronization of local field potentials (LFPs) in sensorimotor cerebral areas has been related to motor performance, often through 10- to 25-Hz oscillatory LFPs. The macaque cerebellar paramedian lobule (PM) also shows 10- to 25-Hz LFP oscillations, which are modulated in a stimulus-response lever press task to get reward (active condition), but also, albeit differently, in a similarly timed stimulus-reward relation (passive condition). This study focuses on simultaneous LFP activity in primate SI or MI and the PM cerebellum during the active (left- or right-hand lever presses) and passive conditions. Results show a similar modulation pattern of 10- to 25-Hz oscillations in the cerebellum, MI, and SI during the active condition (left or right hand), decreasing after stimulus onset, returning, and again decreasing after movement onset. In the passive condition, when the monkey did not move but got reward, all 3 areas show an oscillatory profile where oscillations increase after stimulus onset and last until reward, denoting a role for these oscillations in passive expectancy. However, synchronization between cerebellar LFPs and SI LFPs is higher during the active condition than during the passive condition, and highest for the interested hand. This greater PM-SI synchronization, when the monkey had to press the lever, could represent a form of cerebro-cerebellar communication, perhaps to serve somatosensory processing to accomplish the task; PM-MI synchronization was less selective for the hand used and might carry a more general type of information.

Animals↗