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PubMed1981

Metabolic changes in cerebral cortex, hippocampus, and cerebellum during sustained bicuculline-induced seizures.

The objective of the present experiments was to study metabolic correlates to the localization of neuronal lesions during sustained seizures. To that end, status epilepticus was induced by i.v. administration of bicuculline in immobilized and artificially ventilated rats, since this model is known to cause neuronal cell damage in cerebral cortex and hippocampus but not in the cerebellum. After 20 or 120 min of continuous seizure activity, brain tissue was frozen in situ through the skull bone, and samples of cerebral cortex, hippocampus, and cerebellum were collected for analysis of glycolytic metabolites, phosphocreatine (PCr), ATP, ADP, AMP, and cyclic nucleotides. After 20 min of seizure activity, the two "vulnerable" structures (cerebral cortex and hippocampus) and the "resistant" one (cerebellum) showed similar changes in cerebral metabolic state, characterized by decreased tissue concentrations of PCr, ATP, and glycogen, and increased lactate concentrations and lactate/pyruvate ratios. In all structures, though, the adenylate energy charge remained close to control. At the end of a 2-h period of status epilepticus, a clear deterioration of the energy state was observed in the cerebral cortex and the hippocampus, but not in the cerebellum. The reduction in adenylate energy charge in the cortex and hippocampus was associated with a seemingly paradoxical decrease in tissue lactate levels and with failure of glycogen resynthesis (cerebral cortex). Experiments with infusion of glucose during the second hour of a 2-h period of status epilepticus verified that the deterioration of tissue energy state was partly due to reduced substrate supply; however, even in animals with adequate tissue glucose concentrations, the energy charge of the two structures was significantly lowered. The cyclic nucleotides (cAMP and cGMP) behaved differently. Thus, whereas cAMP concentrations were either close to control (hippocampus and cerebellum) or moderately increased (cerebral cortex), the cGMP concentrations remained markedly elevated throughout the seizure period, the largest change being observed in the cerebellum. It is concluded that although the localization of neuronal damage and perturbation of cerebral energy state seem to correlate, the results cannot be taken as evidence that cellular energy failure is the cause of the damage. Thus, it appears equally probable that the pathologically enhanced neuronal activity (and metabolic rate) underlies both the cell damage and the perturbed metabolic state. The observed changes in cyclic nucleotides do not appear to bear a causal relationship to the mechanisms of damage.

Animals↗
PubMed2006

Effect of neuronal nitric oxide synthase inhibition on caspase-9 activity during hypoxia in the cerebral cortex of newborn piglets.

Previous studies have shown that cerebral hypoxia results in increased activity of caspase-9, a key initiator of programmed cell death. We have also shown increased nitric oxide (NO) free radical generation during hypoxia in the cerebral cortex of newborn piglets. The present study tests the hypothesis that hypoxia-induced increase in caspase-9 activity in the cerebral cortex of newborn piglets is mediated by NO derived from neuronal nitric oxide synthase (nNOS). To test this hypothesis, cytosolic caspase-9 activity was determined in 15 newborn piglets divided into three groups: normoxic (Nx, n=5), hypoxic (Hx, n=5), and Hx pretreated with 7-nitroindazole sodium salt (7-NINA), a selective nNOS inhibitor, 1mg/kg, i.p., 1h prior to hypoxia (Hx+7NI, n=5). The hypoxic piglets were exposed to an FiO(2) of 0.06 for 1h. Tissue hypoxia was documented by ATP and phosphocreatinine (PCr) levels. The cytosolic fraction was obtained from the cerebral cortical tissue following centrifugation at 100,000 x g for 1h and caspase-9 activity was assayed using Ac-Leu-Glu-His-Asp-amino-4-methyl coumarin, a specific fluorogenic substrate for caspase-9. Caspase-9 activity was determined spectroflourometrically at 460 nm using 380 nm as excitation wavelength. ATP levels (micromol/g brain) were 4.35+/-0.21 in the Nx 1.43+/-0.28 in the Hx (p<0.05 versus Nx), and 1.73+/-0.33 in the Hx+7-NINA group (p<0.05 versus Nx, p=NS versus Hx). PCr levels (micromol/g brain) were 3.80+/-0.26 in the Nx, 0.96+/-0.20 in the Hx (p<0.05 versus Nx), and 1.09+/-0.39 in the Hx+7 NINA group (p<0.05 versus Nx, p=NS versus Hx). Cytosolic caspase-9 activity (nmol/mg protein/h), increased from 1.27+/-0.15 in the Nx to 2.13+/-0.14 in the Hx (p<0.05 versus Nx) compared to 1.10+/-0.21 in the Hx+7-NINA group (p<0.05 versus Hx, p=NS versus Nx). Caspase-3 activity (nmol/mg protein/h) also increased from 9.39+/-0.73 in Nx to 18.94+/-3.64 in Hx (p<0.05 versus Nx) compared to 8.04+/-1.05 in the Hx+7-NINA group (p<0.05 versus Hx, p=NS versus Nx). The data show that administration of 7-NINA, an nNOS inhibitor, prevented the hypoxia-induced increase in caspase-9 activity that leads to increase in caspase-3 activity. Since nNOS inhibition blocked the increase in caspase-9 activity during hypoxia, we conclude that hypoxia-induced increase in caspase-9 activity is mediated by nNOS derived NO. We propose that the NO generated during hypoxia leads to activation of caspase-9 and results in initiation of caspase-cascade-dependent hypoxic neuronal death.

Adenosine Triphosphate↗
PubMed1995

Differential changes in alpha- and beta-adrenoceptors in the cerebral cortex and hippocampus of the Mongolian gerbil after unilateral brain ischemia.

BACKGROUND AND PURPOSE: Changes in adrenoceptors in the cerebral cortex and hippocampus of Mongolian gerbils after brain ischemia were investigated. METHODS: Twenty-four hours after unilateral occlusion of the common carotid artery, alpha 1-, alpha 2-, and beta-receptors of the membrane fraction of the cerebral cortex or the hippocampus were analyzed by binding assay with the use of [3H]prazosin, [3H]p-aminoclonidine, and [125I]cyanopindolol as radioligands, respectively. RESULTS: In the cerebral cortex, the number of binding sites (Bmax) and the dissociation constant (Kd) of [3H]prazosin were not altered, whereas the Bmax value of [3H]p-aminoclonidine binding was decreased by 30% and that of [125I]cyanopindolol binding by 16% without a change in Kd values for the ligands. In the hippocampus, the Bmax values of [3H]prazosin, [3H]p-aminoclonidine, and [125I]cyanopindolol bindings were decreased by 21%, 53%, and 19%, respectively, but there was no change in the Kd values for the ligands. The bindings of [3H]prazosin and [3H]p-aminoclonidine of the contralateral side of the cerebral cortex and the hippocampus were not altered by ischemia, but that of [125I]cyanopindolol was decreased when compared with normal tissues. CONCLUSIONS: These results show that ischemia results in a decrease in brain alpha 1-, alpha 2-, and beta-adrenoceptors to various degrees, depending on the brain area and the types of receptors, and suggest that vulnerability of the brain to ischemia is different depending on brain areas and that the regulatory mechanisms of alpha 1-, alpha 2-, and beta-receptors are different.

Animals↗
PubMed1986

[Effect of beta-endorphin on catecholamine levels in the rat hypothalamus and cerebral cortex].

The present paper deals with the effect of beta-endorphin on catecholamine content in the hypothalamus and cerebral cortex of male rats. beta-endorphin was found to decrease catecholamine content in the rat brain, with the degree of reduction depending on the brain topography and the time following the peptide administration. 5 min later no changes in catecholamine content were observed either in the hypothalamus or in the cerebral cortex. 20 min later beta-endorphin induced a statistically significant fall of catecholamine concentration in the hypothalamus. A tendency towards its decrease was also observed in the cerebral cortex. 60 min later beta-endorphin produced an insignificant decrease in catecholamine level in both brain areas under study. It may be therefore suggested that beta-endorphin-induced decrease of catecholamine content in the hypothalamus and cerebral cortex represents one of the mechanisms underlying beta-endorphin stimulating action on a number of trophic functions of the hypophysis.

Animals↗
PubMedDate not supplied

Neuronal death in the development and aging of the cerebral cortex of the mouse.

The numbers of neurons and glial cells in the cerebral cortex of the mouse have been estimated during its whole life-span (5 to 720 days), taking into account both the cellular densities of several areas and the cortical volumes. The results clearly demonstrate that there is a massive neuronal loss in the cerebral cortex during early postnatal development, greater in layers II-IV than in layers V-VI. In contrast, aging is characterized by a discrete neuronal loss in the cerebral cortex, purely restricted to layers II-IV. The number of glial cells increases continuously from 5 to 720 days. We emphasize here the need to obtain volumetric measure together with cellular densities in order to get interpretable quantitative data on cellular death and proliferation.

Aging↗
PubMed2000

[The cerebral cortex: structure, interrelations of neurons, functional columnar organization].

The cerebral cortex develops from a portion of the telencephalic vesicle. Cells originating from the germinal zone surrounding the lumen migrate peripherally to form the cortical mantle. During the fetal life, cortical neurons begin to form six horizontal layers. Cells formed at the same time migrate to the same cortical layer, cells migrating later pass through deep layers to form more superficial laminae. A six layer cellular organization is characteristic of the entire neopallium, which is referred to as the neocortex. The paleopallium--olfactory cortex--and the archipallium--hippocampal formation and dentate gyrus--have three basic layers and collectively constitute the allocortex. Through the course of evolution, the cerebral cortex has increased enormously in surface area but not in thickness, a trend that can be seen even in the relatively short period of primate evolution. The human cortex is only about 15% thicker than that of the macaque monkey but is at least 10 times greater in area. To understand how this complex structure functions we need to examine its unique internal cellular arrangement.

Cell Movement↗
PubMedDate not supplied

[Clinico-experimental research on the electrophysiological and polarographic characteristics of the cerebral cortex in hypoxia].

Electrocorticography, measurement of tissue PO2, local cerebral blood flow, and sodium ion concentration in the extracellular fluid of the cerebral cortex, as well as study of dynamics of the response of the cortex to its direct electrical stimulation, conducted during neurosurgical operations on patients with tumors of the brain and in experiment revealed two stages in the changes of excitability of the cortex: first stage--its sharp increase and second stage--its suppression. Electrophysiological and polarographic characteristics of these stages of edema and excitability of the cerebral cortex are shown. The results of the research are discussed from the standpoint of the pathomechanisms of the occurrence and cessation of epileptic seizures in the development of brain edema.

Animals↗
PubMed1983

Effects of various pathological conditions on the nuclear T3 receptors of rat cerebral cortex: comparison with liver.

The binding capacity and relative affinities of the nuclear triiodothyronine receptors were measured in the cerebral cortex and liver tissues of the rat under several conditions involving energy deprivation. Protracted hypothyroidism caused significant increases in binding capacity in both brain and liver representing a probable direct tissue response to this specific thyroidal dysfunction. Three conditions affecting glucose homeostasis: fasting, glucagon administration and insulin-induced acute hypoglycemia, caused a significant decrease in nuclear binding capacity measured by in vitro binding assay in liver but did not affect brain receptors indicating a tissue specific response to these altered energy states. Lowering of available oxygen (hypoxia) also appeared to cause a slight decrease in binding capacity in the cerebral cortex measured in vitro. On the other hand, total depletion of oxygen (anoxia) showed a progressive increase in binding of a lower affinity nature in the cerebral cortex and liver. A similar change in binding and affinity was seen in the progression of the post-mortem condition in the cerebral cortex and liver resulting from a probable general alteration of the chromosomal material. These results illustrate the degree and nature of alterations of a specific nuclear regulatory component, the thyroid hormone receptor, under several pathological conditions.

Animals↗
PubMed1999

Effect of pre- and postnatal ethanol exposure on protein tyrosine kinase activity and its endogenous substrates in rat cerebral cortex.

The rat brain contains high levels of tyrosine-specific protein kinases (PTKs) that specifically phosphorylate the tyrosine-containing synthetic peptide poly(Glu4Tyr1). Using this peptide as a substrate, we have measured the protein tyrosine kinase activity in membrane and cytosolic fractions from the cerebral cortices of pre- and postnatal ethanol-exposed rats at time intervals of 8, 30, and 90 days. During the course of development of the cerebral cortex, PTK activity decreased both in the membrane and cytosolic fractions from 8 and 90 days of age. Maximum activity was associated at the age of 8 days and gradually declined in the later ages (30 and 90 days) of postnatal development. However, PTK activity in the ethanol exposed rat cerebral cortex was further decreased when compared to controls in all the ages of postnatal development in membrane as well as in cytosolic fractions. In the presence of vanadate, a specific inhibitor of protein tyrosine phosphatases (PTPs), the PTK activity increased, indicating that the balance between protein tyrosine kinase and protein tyrosine phosphatase might be lost during ethanol exposure. In addition, when using an antibody specific for phosphotyrosine, endogenous substrates for protein tyrosine kinases were identified on an immunoblot of membrane and cytosolic fractions from the ethanol-exposed rat cerebral cortex. The immunoblot showed several phosphotyrosine-containing proteins with molecular weights of 114, 70, 36, 34, 32, 20, and 14 kDa that were present in the cerebral cortex. However, higher levels of immunoreactivity of these proteins were found in the ethanol-exposed membrane fractions when compared to control fractions-particularly at the age of 30 and 90 days. Two phosphotyrosine proteins with molecular weights of 38 and 40 kDa showed decreased immunoreactivity at the age of 90 days in the cytosolic fraction of an ethanol-exposed rat's cerebral cortex. The differences in tyrosine-specific protein kinase activity and in phosphotyrosine-containing proteins observed during pre- and postnatal ethanol exposure may reflect specific functional defects in the cerebral cortex which could possibly underlie the mechanism contributing to fetal alcohol syndrome (FAS).

Aging↗
PubMed1982

Subcellular distribution of iodothyronine 5'-deiodinase in cerebral cortex from hypothyroid rats.

We have examined iodothyronine deiodination in subcellular fractions of cerebral cortex obtained from hypothyroid rats. Enzymatic activities were measured at 37 degrees C in the presence of 20 mM dithiothreitol with 125I-labeled T4 and 125I-labeled rT3 as substrates for 5'-deiodination and 131I-labeled T3 as the substrate for the 5-deiodinase. Reaction products were separated by descending paper and/or ion-exchange chromatography. Cerebral cortex subcellular fractions were also characterized by marker enzyme analysis and electron microscopy. Under optimal reaction conditions more than 80% of the 5'-deiodinase was recovered after fractionation. Both 5'-deiodinase and (Na+ + K+)-ATPase showed similar subcellular distributions and were enriched approx. 3-fold in the easily sedimenting membrane fraction and nerve terminal plasma membranes. Crude microsomal membranes (6 X 10(6) g X min pellet) also showed 2-fold enrichment of these enzymes. Nuclei and isolated mitochondria were devoid of deiodinating activity. T4 and T3 5-deiodinating activity was absent in the easily sedimenting membranes and present but not enriched in particulate fractions containing microsomal membranes. These data suggest that iodothyronine 5'-deiodinase is associated with plasma membrane fractions in the cerebral cortex.

Animals↗
PubMed1991

Neuronal loss in layers V and VI of cerebral cortex in Huntington's disease.

Neuronal loss in the cerebral cortex in Huntington's disease (HD) has not been well documented, nor has its laminar pattern been definitively established. We therefore counted neurons in individual cortical laminae in the dorsal frontal cortex of 5 HD and 5 control autopsy brains. Significant neuronal loss (to 57% of control, P = 0.002) was found in layer VI of HD brains. These cells project principally to the thalamus, the claustrum and other regions of cerebral cortex; thus their loss is unlikely to be the result of retrograde degeneration secondary to striatal pathology. Layer V neurons were also decreased (to 71% of control, P = 0.034). Degeneration of cerebral cortical neurons may be at least partly responsible for some of the non-choreic symptoms of HD, such as dementia, irritability, apathy, and depression.

Autopsy↗
PubMed1991

Guidance of callosal axons by radial glia in the developing cerebral cortex.

During development, columns of the mammalian cerebral cortex are formed by migration of neurons along fascicles of radial glia. Subsequently, axons of the corpus callosum connect reciprocal regions of each cerebral hemisphere. To determine whether the radial growth of callosal afferents through the developing cortex may be guided by particular cellular elements, we examined the ultrastructural relationship between callosal afferents and radial fibers in the early postnatal hamster sensorimotor cortex. Developing callosal axons and their growth cones were labeled with HRP injected into the cortex at 3 d postnatal when the growth cones have extended across the callosum and are just entering the contralateral cortex. An EM analysis of 30 HRP-labeled axons and their growth cones revealed that they extended upon fascicles of radial processes associated with migrating neurons. Reconstruction of seven of these growth cones, serially sectioned in their entirety, showed that growth cones were associated with the same radial fascicle as their axon. Growth cones also touched other cellular elements such as axons. However, the finding that callosal afferents, from the point at which they enter the cortex to their growth cones, were apposed to a continuous fascicle of radial fibers suggests that callosal axons are tracking along radial processes. We conclude that the majority of the radial processes within fascicles are likely to be glial, based on their relatively large diameters, electron-lucent cytoplasm with a regular array of microtubules, the presence of glycogen granules, occasional cytoplasmic protrusions lacking microtubules, and their consistent association with migrating neurons. We propose therefore that radial glia may serve a guidance function for growing callosal axons in their radial trajectory through the developing cerebral cortex.

Animals↗
PubMed2005

Receptors for VIP and PACAP in guinea pig cerebral cortex: effects on cyclic AMP synthesis and characterization by 125I-VIP binding.

Receptors for vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) in guinea pig cerebral cortex were characterized by (1) radioreceptor binding of 125I-labeled VIP (human/rat/porcine), and (2) cyclic AMP (cAMP) formation. Saturation analysis of 125I-VIP binding to membranes of guinea pig cerebral cortex resulted in a linear Scatchard plot, suggesting the presence of a single class of high-affinity receptor-binding sites, with a Kd of 0.63 nM and a B(max) of 77 fmol/mg protein. Various peptides from the PACAP/VIP/secretin family displaced the specific binding of 125I-VIP to guinea pig cerebrum with the relative rank order of potency: chicken VIP (cVIP) > or = PACAP38 approximately PACAP27 approximately guinea pig VIP (gpVIP) > or = mammalian (human/rat/porcine) VIP (mVIP) > peptide histidine-methionine (PHM) > peptide histidine-isoleucine (PHI) > secretin. Analysis of the competition curves revealed displacement of 125I-VIP from high- and lower-affinity binding sites, with IC50 values in the picomolar and the nanomolar range, respectively. About 70% of the specific 125I-VIP-binding sites in guinea pig cerebral cortex were sensitive to Gpp(NH)p, a nonhydrolyzable analog of GTP. Pituitary adenylate cyclase-activating polypeptide 38 (PACAP38), PACAP27, cVIP, gpVIP, mVIP, PHM, and PHI stimulated cAMP production in [3H]adenine-prelabeled slices of guinea pig cerebral cortex in a concentration-dependent manner. Of the tested peptides, the most effective were PACAP38 and PACAP27, which at a 1 microM concentration produced a 17- to 19-fold rise in cAMP synthesis, increasing the nucleotide production to approx 11% conversion above the control value. The three forms of VIP (cVIP, mVIP, and gpVIP) at the highest concentration used, i.e., 3 microM, produced net increases in cAMP production in the range of 8-9% conversion, whereas 5 microM PHM and PHI, by, respectively, 6.7% and 4.9% conversion. It is concluded that cerebral cortex of guinea pig contains VPAC- type receptors positively linked to cAMP formation. In addition, the observed stronger action of PACAP (both PACAP38 and PACAP27), when compared to any form of VIP, on cAMP production in this tissue, suggests its interaction with both PAC1 and VPAC receptors.

Amino Acid Sequence↗
PubMed2002

The surface of the developing cerebral cortex: still special cells one century later.

The marginal zone of the developing cerebral cortex is formed by different types of neurons, some of which were described more than one century ago. It is the case of Cajal-Retzius cells, which are known to synthesize and secrete Reelin, an extracellular matrix glycoprotein critically involved in the radial migration and early cortical cytoarchitectonic organization. These cells do not emit projection axons, a characteristic that bespeaks against these cells being considered as pioneer neurons. The true pioneer neurons of the marginal zone are part of a distinct cell entity: these are cells that emit the earliest descending axonal projection from the cerebral cortex into the subpallium, even before than subplate neurons, the other population of pioneer neurons in the cortical anlage. Finally, the marginal zone is a territory where cohorts of undifferentiated cortical interneurons migrate into the upper layers of the cerebral cortex. Marginal zone neurons, including Cajal-Retzius cells, tend to distribute non-uniformly over the cortical surface. Such a mosaic structural configuration points towards more complexities regarding their possible functions during cortical development.

Animals↗
PubMed2000

Decrease of adenosine A-1 receptor gene expression in cerebral cortex of aged rats.

Changes of adenosine A-1 receptor (A1-AR) gene expression in aging were investigated in cerebral cortex using the rat aged from 2 months (adult) to 24 months (aged). Quantification of A1-AR protein level by immunoblotting analysis showed an age-related decrease of A1-AR in cerebral cortex of Wistar rats. Compared to the preparations from 2-month-old animals, the levels of A1-AR in the 6-, 12-, and 24-month-old rats were reduced by 14.3+/-5.2, 32.5+/-4.5 and 28.2+/-5.7%, respectively. Similar decrease of mRNA level in A1-AR was also obtained using Northern blotting analysis. Two representative spots of mRNA, a 3.4-kb transcript and a 5.6-kb transcript, were observed in X-ray film from cerebral cortex of rat hybridized with rat A1-AR cDNA probe. Compared to the 2 month-old rats, levels of the 5.6-kb transcript were decreased by 17.9+/-2.5, 27.4+/-3.2 and 23.1+/-2.1% in the 6-, 12- and 24-month-old rats, respectively. These results indicated an age-related decrease of A1-AR in cerebral cortex of the rat that seems responsible for the change of response to adenosine.

Aging↗
PubMed1988

Asymmetrical activation of GABA-gated chloride channels in cerebral cortex.

A pronounced left/right asymmetry of GABA-gated chloride channels was observed in rat cerebral cortex. This asymmetry was manifest as a higher apparent affinity and density of binding sites for the "cage" convulsant [35S]t-butylbicyclophosphorothionate (TBPS) in the right compared to left cortex. Asymmetries in [35S]TBPS binding were not observed in other brain areas, and were restricted to the occipital and entorhinal/pyriform areas of cerebral cortex. Evaluation of other components of the benzodiazepine/GABA receptor chloride ionophore complex in cerebral cortex suggests that this asymmetry is not present in either benzodiazepine receptors or that population of GABA receptors linked to benzodiazepine receptors. Brief restraint-stress significantly increased both the apparent affinity and number of [35S]TBPS binding sites in cortex, but the left/right asymmetry was no longer apparent. These findings indicate a time-dependent, asymmetric response of cortical GABA-gated chloride channels to stress rather than an anatomical hemispheric difference, and suggest that GABA-gated chloride channels may be involved in a differential processing of stressful stimuli by the cerebral hemispheres.

Animals↗
PubMed1992

The generation of cellular diversity in the cerebral cortex.

We have studied cell lineage in the rat cerebral cortex using retroviral vectors. With this technique, the virus is used to introduce a marker gene into dividing precursor cells such that their fate can be followed. We have studied cell lineage by using this method in the following ways. First, we have labelled germinal cells of the cerebral cortex in vivo during the period of neurogenesis. Second, we have grown cortical precursor cells in dissociated cell culture, and used the viral labelling technique to follow their development in vitro. Both types of study have shown that by the time neurogenesis is under way, the majority of precursor cells are restricted to the production of a single cell type: neurones, astrocytes, or oligodendrocytes. The only exception is a cell we call the N-O cell because it has the ability to generate both neurones and oligodendrocytes. These data suggest that the ventricular zone, the germinal layer of the embryonic cortex, is a mosaic of different precursor cells each with a different restricted potential. However, this restriction of potential of cortical precursor cells does not extend to their ability to contribute to more than one cortical lamina or cytoarchitectonic area. The precursors of both neurones and grey matter astrocytes contribute cells to multiple layers of the cortex. Moreover, in the hippocampal formation, neuronal precursors can contribute cells to more than one hippocampal field.

Aging↗