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PubMed1987

Citrate synthase and lactate dehydrogenase activities in rat cerebral cortex following the administration of the convulsants bicuculline and 3-mercaptopropionic acid.

Systemic administration of bicuculline (Bic) and 3-mercaptopropionic acid (MP) induces generalized seizure in laboratory animals. The effect of these convulsants on lactate dehydrogenase and citrate synthase activities in rat cerebral cortex was studied. Bic was administered i.p. at 1.0 mg/kg (subconvulsant dose) and 7.5 mg/kg (convulsant dose). MP was administered i.p. at 150 mg/kg (convulsant dose). Lactate dehydrogenase activity in cerebral cortex soluble and particulated fractions was not modified by the administration of Bic or MP. Citrate synthase activity in cerebral cortex homogenates increased about 40% by the administration of subconvulsant and convulsant doses of Bic. A similar increase was found after the injection of MP. No changes in the liver enzyme activity were found, suggesting tissue specificity. The finding of a higher activity of citrate synthase in cerebral cortex homogenates observed with the convulsants may be correlated with the increase in brain citrate levels reported in seizure states.

3-Mercaptopropionic Acid↗
PubMed1995

Prenatal cocaine exposure adversely affects development of the primate cerebral cortex.

This study was conducted to determine whether prenatal exposure to cocaine interferes with the development of the primate cerebral cortex. For this purpose, pregnant rhesus monkeys received cocaine orally (20 mg/kg/day in fruit or candy treats), twice a day from the 40th-102nd days of pregnancy (E40-E102), which is a period of corticogenesis in this species. The control group of pregnant animals received fruit or candy treats only. On E64 and E65, all animals received intravenous injections of [3H]thymidine. Monkeys were allowed to deliver at term. The offspring were sacrificed at age 2 months, and their brains were processed for histology and autoradiography. The analysis of cresyl violet-stained sections showed that prenatal treatment with cocaine significantly altered lamination of the primate cerebral cortex, in some cases completely blending distinction between individual layers. In addition, autoradiographic analysis revealed that in the control animals, [3H]thymidine labeling concentrated in cortical layers V and/or IV depending on the cytoarchitectonic area observed. In contrast, drug-treated animals displayed labeled cells in the white matter and cortical layer VI in addition to layers V and IV, suggesting inability of cortical cells to reach proper cortical layers. The number of labeled cells was also much lower in these animals. Finally, immunocytochemical studies with antisera directed toward glial fibrillary acidic protein showed that prenatal exposure to cocaine had dramatic effect on the glial fibers normally observed in the upper cortical layers. In many cortical regions of cocaine-treated animals, we observed practically no such fibers. This study demonstrates that cocaine administered during pregnancy can significantly affect the development of the primate cerebral cortex.

Animals↗
PubMed2002

Dynamic depolarization fields in the cerebral cortex.

Recent physiological evidence shows that in response to stimuli and preceding motor activity, large fields of the upper layers of the cerebral cortex depolarize. It is argued that this finding is a general one and that these dynamic depolarization fields represent the computational elements of the cerebral cortex. Each depolarization field engages many more neurons than do columns and hyper-columns. These fields can be explained by cooperative neuronal computing in layers I-III of the cortex. In these layers, the computing modes might be general for all parts of the cerebral cortex and be sufficiently flexible to handle all sorts of cortical computations, including perception, memory storage, memory retrieval, thought and the production of behavior.

Action Potentials↗
PubMed1991

Binding characteristics of a new 1,5-benzothiazepine, clentiazem, to rat cerebral cortex and skeletal muscle membranes.

The binding properties of a new 1,5-benzothiazepine, clentiazem (TA-3090), were investigated in rat cerebral cortex and skeletal muscle membranes with [3H]diltiazem and [3H]nitrendipine as radioligands. Clentiazem inhibited [3H]diltiazem binding to cerebral cortex membranes at the same concentrations as diltiazem at 2 degrees C. However, at 37 degrees C clentiazem was 3 times more potent to inhibit binding than diltiazem. [3H]Nitrendipine binding was modulated by clentiazem in a temperature-dependent manner. At 37 degrees C clentiazem significantly enhanced [3H]nitrendipine binding to rat cerebral cortex membranes, whereas it has an inhibitory effect on [3H]nitrendipine binding at 0 degree C and no effect at 25 degrees C. Of two optical isomers of clentiazem and four of diltiazem, only d-cis isomers (clentiazem and diltiazem) increased [3H]nitrendipine binding, indicating that both compounds have the same stereoselectivity for increasing [3H]nitrendipine binding. These results suggest that clentiazem binds to the same 1,5-benzothiazepine binding sites as diltiazem but with greater affinity.

Animals↗
PubMed2002

Amino acid and monoamine alterations in the cerebral cortex and hippocampus of mice submitted to ricinine-induced seizures.

The alkaloid ricinine isolated from the plant Ricinus communis, when administered to mice at high doses, induces clonic seizures accompanied by electroencephalographic alterations in the cerebral cortex and hippocampus. The lethal nature of ricinine-induced seizures is considered to be a good model for the study of the events that cause death during clonic seizures, particularly those related to respiratory spasms. The initial signs (pre-seizure period) were marked by exophthalmus and decreased locomotor behavior. Animals killed during the preseizure period presented an increased utilization rate (HVA/DA) of dopamine (DA), an increased concentration of noradrenaline (NA), and a decreased concentration of glutamate (Glu), glutamine (Gln), taurine (Tau), and serotonin (5-HT) in the cerebral cortex. The seizure period is characterized by the occurrence of hind limb myoclonus and respiratory spasms, which are followed by death. Alterations in the cerebral cortex concentration of these neurotransmitters persisted during the seizure period. These alterations are only partially observed in the hippocampus, mainly during the seizure period. The present results suggest that an increased release of Glu in the cerebral cortex can be implicated in the genesis of the ricinine-induced seizure and that it triggers many anticonvulsive mechanisms, like the release of Tau, DA, 5-HT, and NA.

Alkaloids↗
PubMed1999

Reconstruction of the human cerebral cortex from magnetic resonance images.

Reconstructing the geometry of the human cerebral cortex from MR images is an important step in both brain mapping and surgical path planning applications. Difficulties with imaging noise, partial volume averaging, image intensity inhomogeneities, convoluted cortical structures, and the requirement to preserve anatomical topology make the development of accurate automated algorithms particularly challenging. In this paper we address each of these problems and describe a systematic method for obtaining a surface representation of the geometric central layer of the human cerebral cortex. Using fuzzy segmentation, an isosurface algorithm, and a deformable surface model, the method reconstructs the entire cortex with the correct topology, including deep convoluted sulci and gyri. The method is largely automated and its results are robust to imaging noise, partial volume averaging, and image intensity inhomogeneities. The performance of this method is demonstrated, both qualitatively and quantitatively, and the results of its application to six subjects and one simulated MR brain volume are presented.

Algorithms↗
PubMed1996

Eosinophilic bodies in the cerebral cortex of Alzheimer's disease cases.

The light microscopical, immunohistochemical and ultrastructural aspects of eosinophilic bodies in the cerebral cortex from patients with Alzheimer's disease (AD) are described, based on a study of 16 cases of AD, 5 elderly non-demented controls and, as disease controls, 5 cases of Pick's disease, 9 with progressive supranuclear palsy, 5 with Creutzfeldt-Jakob disease and 1 with Binswanger's disease. At the light microscopy level, the bodies were clearly separated from the surrounding tissues and were mostly round or elliptic with a diameter of 5-30 microns and a central, intensely eosinophilic core. Ultrastructurally, they consisted of a central homogeneous electron-dense body (HDB), and filamentous structures (resembling either neurofilaments or paired helical filaments) or other small organelles in the periphery. Immunohistochemically, some of these bodies exhibited ring-shaped rims which were positive with antibodies against paired helical filaments, tau-2, phosphorylated neurofilaments and ubiquitin. The bodies were widely distributed throughout the cerebral cortex, but were not observed in the white matter. These bodies were thought to be compatible with one type of axonal dystrophy in the gracile nucleus (termed 'old' spheroid by Jellinger), and are here referred to as the HDB-type spheroid based on their ultrastructure. In this study HDB-type spheroids were found in high incidence in the AD cases, but only two HDB-type spheroids were seen in one case of Pick's disease, and none in any of the other cases of neurodegenerative diseases or in the elderly non-demented controls. It seems plausible that the incidence of HDB-type spheroids in the cerebral cortex might be related to a pathological process and not to a physiological ageing phenomenon, and might be characteristic of, but not unique to, AD.

Aged↗
PubMed2004

Binding of the prototypical adenosine A(2A) receptor agonist CGS 21680 to the cerebral cortex of adenosine A(1) and A(2A) receptor knockout mice.

1. 2-p-(2-carboxyethylphenethylamino-5'-ethylcarboxamidoadenosine) (CGS 21680) is considered the reference compound to study adenosine A(2A) receptors. However, CGS 21680 binding in the cerebral cortex, where adenosine A(1) receptors are predominant, displays a mixed A(2A)/A(1) receptor pharmacology. We now use adenosine A(1) and A(2A) receptor knockout mice to investigate the characteristics of cortical [(3)H]CGS 21680 binding. 2. [(3)H]CGS 21680 binding to the cerebral cortex was strongly reduced in adenosine A(1) receptor knockout mice, but only slightly reduced in A(2A) receptor knockout mice compared with the corresponding wild-type littermates. 3. Another selective A(2A) receptor ligand, [(3)H]-5-amino-7-(2-phenylethyl)-2-(2-furyl)-pyrazolo[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine ([(3)H]SCH 58261), displayed a saturable binding to mouse cortical membranes, albeit with a binding density 20 times lower than that of striatal membranes, and this [(3)H]SCH58261 binding was abolished in both striatal and cortical membranes of A(2A) receptor knockout mice and unchanged in A(1) receptor knockout mice. 4. The presence of A(2A) receptors in cortical neurons was further confirmed by Western blot in mouse cortical nerve terminal membranes. 5. It is concluded that, although A(2A) receptors are present in the cerebral cortex, the purportedly selective A(2A) receptor agonist [(3)H]CGS 21680 binds in the cerebral cortex to an entity that requires the presence of adenosine A(1) receptors. Thus, CGS 21680 should be used with care in all preparations where adenosine A(1) receptors out-number A(2A) receptors.

Adenosine↗
PubMed1996

Neurons in the cerebral cortex are most susceptible to DNA-damage in aging rat brain.

Using nick translation type of incubation and terminal deoxynucleotidyl transferase catalyzed 3 -end labeling, single and double strand breaks in genomic DNA of permeabilised neurons from different regions of young, adult and the aged rat brain were assessed. A steady increase in both types of breaks is noted with advancement of age in all of the brain regions studied. However, the number of SSB encountered in the cerebral cortex was the maximum and was also markedly higher than that in other brain regions. When the neuronal cells were exposed to MNNG or Glutamate the damage was aggravated in all the regions and at all ages but the most severe SSB damage is present in the cerebral cortex of older animals. Both cerebral cortex and the hippocampus showed equally higher DSB in comparison with the other regions. It is concluded that with advancement of age, DNA-damage accumulates in neurons and the cerebral cortex is the most vulnerable region.

Age Factors↗
PubMed1985

Altered myelinated fiber trajectory at various postnatal days in the cerebral cortex of reeler mice by immunohistochemical stain with MBP antiserum.

The cerebral cortex of reeler mutant mice characterized by the derangement of cell position was analyzed by an immunohistochemical staining technique using antiserum against myelin basic protein. All the myelins of the myelinated fibers were stained, so that the fiber trajectories could be clearly traced. In the present study the changes in the fiber trajectories were accompanied by changes in myelination sites. Myelinated fibers were localized in the central white matter and gradually became sparser toward the surface of the normal cerebral cortex, while in the reeler myelinated fibers were observed throughout the cortical plane. From the immunohistochemical analysis of the changes occurring in the myelinated fiber pathways in developmental sequence, it was also shown that the fiber bundle accumulation was thin at the earlier stages (e.g. the 15th postnatal day) and became thick as the animal grew, and the timing of myelination in the reeler was similar to that of the control.

Animals↗
PubMed1988

Biochemical mapping of cholecystokinin-, substance P-, [Met]enkephalin-, [Leu]enkephalin- and dynorphin A (1-8)-like immunoreactivities in the human cerebral cortex.

The distribution of immunoreactive cholecystokinin, substance P, [Met]enkephalin, [Leu]-enkephalin and dynorphin was determined in the cerebral cortex of the human brain post mortem. Peptide radioimmunoassays in three selected zones of the cortical gray mantle (frontal, temporal, occipital) revealed significant regional differences, prompting to the development of a new dissection procedure for the complete mapping of peptide-like materials throughout the entire cerebral cortex. For this purpose, frozen cerebral hemispheres were cut rostrocaudally in 21 verticofrontal serial sections, from which the cortical gray matter was divided into 4-5 distinct zones. The peptides could be measured in each of the 93 dissected pieces of tissue, but their distribution was uneven. The most abundant was cholecystokinin, particularly in the anterior part of the frontal lobe and in the temporal cortex, where its levels reached 0.5 ng/mg of tissue. The regional distribution of cholecystokinin resembled that of substance P with a decreasing gradient from the frontal to the occipital pole, but absolute levels of substance P were hardly one tenth of cholecystokinin levels. The mean concentrations of the three opioid peptides were even less than those of substance P, and their regional distributions were markedly different. [Met]Enkephalin was concentrated in the occipital cortex, and [Leu]enkephalin in the temporal cortex. Dynorphin was the least abundant, even in the temporal cortex where the highest levels were found. The widespread and heterogeneous distribution of these peptides strongly suggests that each of them exerts specific functions in the human cerebral cortex.

Aged↗
PubMed1986

Enhancement of histamine H1-receptor agonist activity by 1,4-dithiothreitol in guinea-pig cerebellum and cerebral cortex.

The disulphide bond-reducing agent 1,4-dithiothreitol (1 mM) produced a marked potentiation of histamine-stimulated accumulation of [3H]inositol phosphates in lithium-treated slices of guinea-pig cerebellum and cerebral cortex. This was seen as a parallel shift of the concentration-response curve for histamine to lower agonist concentrations, with no significant effect on the maximal response or Hill coefficient. Dithiothreitol similarly potentiated the augmentation of adenosine-stimulated cyclic AMP accumulation elicited by histamine in guinea-pig cerebral cortex. Studies with partial agonists suggested that this potentiating effect was associated with an increase in agonist efficacy rather than a change in agonist binding affinity. Thus, dithiothreitol increased the maximal accumulation of [3H]inositol phosphates produced by both 2-pyridylethylamine and 2-methylhistamine, which appeared to act as partial agonists in guinea-pig cerebral cortex. Dithiothreitol similarly increased the maximal extent of the augmentation of adenosine-stimulated accumulation of cyclic AMP produced by 2-methylhistamine. The site of action of dithiothreitol is not known; however, a comparison of the effect of dithiothreitol on muscarinic and histamine H1-receptor-mediated phosphoinositide responses in guinea-pig cerebral cortex suggests that it is before the stage at which the receptor-effector pathways are shared by these two receptor systems.

Animals↗
PubMed2003

Characterization of vasoactive intestinal peptide/pituitary adenylate cyclase-activating polypeptide receptors in chick cerebral cortex.

In this study receptors for vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) were characterized in chick cerebral cortex by an in vitro binding technique, using 125I-labeled VIP ([125I]-VIP) as a ligand. The specific binding of [125I]-VIP to chick cerebral cortical membranes was found to be rapid, stable, saturable, reversible, and of high affinity. Saturation analysis resulted in a linear Scatchard plot, suggesting binding to a single class of receptor binding sites with high affinity (Kd = 0.21 nM) and low capacity (Bmax = 19.5 fmol/mg protein). The relative rank order of potency of the tested peptides to inhibit [125I]-VIP binding to chick cerebrum was VIP (chicken) > or = VIP (mammalian) > or = PACAP27 > or = PACAP38 >> VIP6-28 (mammalian) > PHI (porcine) >> neurotensin6-11-chicken VIP7-28 > neurotensin6-11-mammalian VIP7-28 >>> VIP16-28 (chicken; inactive) approximately secretin (inactive). About 60% of [125I]-VIP-binding sites in chick cerebral cortex were sensitive to Gpp(NH)p, a nonhydrolyzable analog of GTP. It has been concluded that the cerebral cortex of chick, in addition to PAC1 receptors, contains a population of VPAC-type receptors.

Animals↗
PubMed1993

Potassium-evoked efflux of transmitter amino acids and purines from rat cerebral cortex.

Repeated applications of elevated K+ (50 or 75 mM) in cerebral cortical cup superfusates was used to evoke an efflux of gamma-aminobutyric acid (GABA), glutamate, aspartate, glycine, adenosine, and inosine from the in vivo rat cerebral cortex. K+ (50 mM) significantly elevated GABA levels in cup superfusates but had little effect on the efflux of glutamate, aspartate, glycine, adenosine, or inosine. K+ (75 mM) significantly enhanced the efflux of GABA, aspartate, adenosine, and inosine and caused nonsignificant increases in glutamate and glycine efflux. The adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA), applied in cup superfusates at a concentration of 10(-10) M had no effect on either basal or K(+)-evoked release of any of the amino acids or purines measured. At 10(-6) M CPA significantly enhanced aspartate release, and depressed GABA efflux. The selective A2 adenosine receptor agonist 2-p(2-carboxyethyl) phenethylamino-5'-N-ethyl-carboxamidoadenosine (CGS 21680) (10(-8) M) was without effect on either basal, or K(+)-evoked, efflux of amino acids or purines. The enhancement of aspartate (an excitotoxic amino acid) efflux by higher concentrations of CPA is likely due to activation of adenosine A2b receptors. This observation may be of relevance when selecting adenosinergic agents to treat ischemic or traumatic brain injuries. Overall, the results suggest that effects of adenosine receptor agonists on K(+)-evoked efflux of transmitter amino acids from the in vivo rat cerebral cortex may not be comparable to those observed with in vitro preparations.

Adenosine↗
PubMed1992

Epileptiform activity in chronically isolated cerebral cortex in humans.

The ability of neuronally isolated human cerebral cortex to sustain epileptiform rhythms over long time intervals is unknown. We report here two patients after functional hemispherectomy for infantile hemiplegia and infantile meningoencephalitis. Both patients had intractable seizures. EEG performed early and up to 3 years after surgery showed persistent epileptiform activity in the isolated frontal cortex in both cases. This indicates that human isolated cortex retains its epileptogenic potential for years, independently of subcortical influences. Previous related animal and human studies are briefly reviewed.

Cerebral Cortex↗
PubMed2002

Region-specific alterations in insulin-like growth factor receptor type I in the cerebral cortex and hippocampus of aged rats.

In the present study, we investigated age-related changes in IGF-I receptor localization in the cerebral cortex and hippocampus of Sprague-Dawley rats using immunohistochemistry. In the cerebral cortex of adult rats, weakly stained cells were seen in layers II-III and layer V/VI in several cortical regions. In aged rats, there was a significant increase in IGF-I receptor immunoreactivity in the pyramidal cells in the same cortical regions. In the hippocampus of adult rats, several moderately stained neurons were seen in CA1-3 areas and the dentate gyrus. Levels of IGF-I receptor protein increased substantially with age in the CA3 area of the hippocampus. Our first morphological data concerning the differential regulation of IGF-I receptors in aged cerebral cortex and hippocampus may provide insights into age-related changes in trophic support as well as basic knowledge required for the study of neurodegenerative diseases such as Alzheimer's disease.

Aging↗