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PubMed1985

Ammonia intoxication: effects on cerebral cortex and spinal cord.

The effect of an acute systemic ammonia intoxication on the metabolic states of the cerebral cortex and the spinal cord of the same animal was studied in the cat. The intravenous infusion of ammonium acetate (2 and 4 mmol/kg body weight/30 min) increased the gross levels of tissue NH4+, glutamine, glutamine/glutamate ratio, lactate, and the lactate/pyruvate ratio in the cerebral cortex and the spinal cord. Pyruvate increased, but significantly only in the spinal cord; aspartate decreased, but significantly only in the cerebral cortex. The infusion of ammonium acetate did not significantly change the levels of phosphocreatine, ATP, ADP, AMP, total adenine nucleotides, adenylate energy charge, glucose, glutamate, alpha-ketoglutarate, and malate in either tissue. The changes of NH4+, glutamine, and lactate levels as well as glutamine/glutamate and lactate/pyruvate ratios in the spinal cord correlated significantly with the corresponding changes of these metabolites in the cerebral cortex. Thus, cerebral cortex and spinal cord show certain specific and comparable metabolic changes in response to a systemic ammonia intoxication. The effect of ammonia intoxication on the increases of glutamine and lactate levels is discussed.

Acetates↗

PubMed2004

Transmitter receptors and functional anatomy of the cerebral cortex.

The currently available architectonic maps of the human cerebral cortex do not match the high degree of cortical segregation as shown by functional imaging. Such functional imaging studies have demonstrated a considerable number of functionally specialized areas not displayed in the architectonic maps. We therefore analysed the regional and laminar distribution of various transmitter receptors in the human cerebral cortex, because these signalling molecules play a crucial role in cortical functions. They may provide a novel and functionally more relevant insight into the regional organization of the cortex, which cannot be achieved by architectonic observations in cell body- or myelin-stained sections. Serial cryostat sections through whole human hemispheres were used for quantitative receptor autoradiography. The regional and laminar densities of numerous receptors of classic transmitter systems were analysed. Alternating sections were stained for comparisons based on cyto- or myeloarchitectonic criteria. Our results demonstrate that the regional distribution of transmitter receptors reflects well-established cyto- and myeloarchitectonically defined borders of cortical areas, but in addition enables the identification of more cortical areas than previously demonstrated. Moreover, the laminar distribution patterns of a given receptor type in different cortical areas as well as those of different receptor types in the same cortical area reveal novel and functionally relevant data concerning the intracortical organization in the human cerebral cortex.

Aged↗

PubMed1989

The determination of neuronal fate in the cerebral cortex.

During the embryonic development of the cerebral cortex, young neurons migrate out into characteristic laminar positions and form specific axonal connections with other neurons. The birthdate of a neuron, and its tangential location in the ventricular zone, can serve as markers that predict its normal laminar fate and pattern of connectivity. In order to test whether cells of the developing cerebral cortex are committed to their normal fates, several types of transplantation experiment have challenged young cortical neurons to alter their identities or connections in novel environments. Other recent experiments have employed retroviral vectors to trace neuronal lineages in the cortex. Together, these studies suggest that phenotypic commitment involves a series of decisions. Certain developmental restrictions--for example, commitment to a laminar identity--may occur at or around the time of the cell's final mitotic division, whereas the refinement of area-specific axonal projections occurs as the neuron differentiates within the cortex.

Animals↗

PubMed1989

Morphometric analysis of developing rat cerebral cortex following acute prenatal ethanol exposure.

Morphologic alterations of fetal rat cerebral cortex were quantified by morphometric analysis following acute ethanol exposure on Gestational Day 14, a critical period of development of cerebral cortex. Pregnant rats were intubated with a total dose of 9 g/kg of ethanol on Gestational Day 14. Maternal blood ethanol levels ranged from 51 to 202 mg% during the period of ethanol exposure. Fetal brains were examined on Gestational Day 15, 24 h after the last dose of ethanol. The acute morphologic changes associated with ethanol exposure include enlargement of subventricular zone nuclei, cortical swelling, and dilation of pial blood vessels over the affected cortex. In some fetuses, cortical swelling was accompanied by the protrusion into the lateral ventricles of cytoplasmic blebs of ventricular zone cells. It is concluded that maternal ethanol exposure during a critical period of brain development produces measurable morphologic changes in fetal rat cerebral cortex within 24 h after ethanol exposure.

Animals↗

PubMed2001

Transport of L-carnitine in isolated cerebral cortex neurons.

The accumulation of carnitine was measured in cerebral cortex neurons isolated from adult rat brain. This process was found to be lowered by 40% after preincubation with ouabain and with SH-group reagents (N-ethylmaleimide and mersalyl). The initial velocity of carnitine transport was found to be inhibited by 4-aminobutyrate (GABA) in a competitive way (Ki = 20.9 +/- 2.4 mM). However, of various inhibitors of GABA transporters, only nipecotic acid and very high concentrations of 1-[2-([(diphenylmethylene)amino]oxy)ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride (NO-711) acid decreased carnitine accumulation while betaine, taurine and beta-alanine had no effect. The GABA transporters expressed in Xenopus laevis oocytes did not transport carnitine. Moreover, carnitine was not observed to diminish the accumulation of GABA in cerebral cortex neurons, which further excluded a possible involvement of the GABA transporter GAT1 in the process of carnitine accumulation, despite the expression of this protein in the cells under study. The absence of carnitine transporter OCTN2 in rat cerebral cortex neurons (K. A. Nałecz, D. Dymna, J. E. Mroczkowska, A. Broër, S. Broër, M. J. Nałecz and R. Cecchelli, unpublished results), together with the insensitivity of carnitine accumulation towards betaines, implies that a novel transporting protein is present in these cells.

Animals↗

PubMed1998

Morphological characteristics and distribution pattern of the arterial vessels in human cerebral cortex: a scanning electron microscope study.

BACKGROUND: The human cerebral cortex is supplied by vessels that arise from the pial arteries. These vessels give rise to a dense vascular network that is highly interconnected. Cortical arteries have been classified in different categories. Both their angioarchitectonic pattern and anatomical structures involved in their regulation are not fully understood. METHODS: Twelve fresh human brains were studied by scanning electron microscopy of vascular corrosion casts. RESULTS: Four types of arterial vessels in the cerebral cortex--short, middle, long, and transcortical--were identified. The cortical vascular network was formed by several interconnected clusters of vessels, which were arranged in four vascular layers parallel to the pial surface and characterized by different vascular densities. The greatest vascular density corresponded to the middle and deep vascular layers. Circular constrictions were found at the origin of cortical arteries and at their branching sites, probably related to vascular sphincters. Connections between cortical arteries were observed at their initial course. Plastic strips, occasionally related to constrictions, were observed around both middle and long cortical arteries. Other plastic structures, morphologically similar to pericytes, were found around capillary vessels. CONCLUSIONS: The blood supply to the human cerebral cortex depends on the short, middle, and long cortical arteries, which give rise to a highly anastomosed capillary network. There exist vascular connections between pial arteries and occasionally between cortical arteries. Blood flow autoregulation is probably mediated by smooth muscle cells at the arteriolar level and by pericytes at the capillary level, through endothelial connections.

Adult↗

PubMed1983

Effects of thyroxine on methionine adenosyltransferase activity in rat cerebral cortex and cerebellum during postnatal development.

Methionine adenosyltransferase (MAT) activity was evaluated in cerebral cortex and cerebellum in controls and in rats treated with thyroxine. In controls the enzyme showed a different pattern in cerebral cortex and cerebellum during neonatal and late suckling periods. Hyperthyroid rats showed a significant increase of the enzyme in cerebral cortex only at the 2nd day of the neonatal period; in cerebellum the developmental pattern of MAT in neonatal period was anticipated temporally by 2-4 days. During the late suckling period thyroxine treatment produced in cerebellum a significant decrease in MAT activity at the 15th day after birth. From these data, we propose that hyperthyroidism may cause precocious induction of MAT both in cerebral cortex and in cerebellum and that the increased availability of S-adenosyl-L-methionine during the neonatal period could be related to its utilization also in polyamine biosynthesis.

Animals↗

PubMed1981

The effects of d-amphetamine and potassium on serotonin release and metabolism in rat cerebral cortex tissue.

Chopped rat cerebral cortex tissue released tritiated serotonin (3H-5HT) when exposed to d-amphetamine (d-A) (10(-5)-10(-3)M) or potassium ion (K) (24-60mM). The d-A-induced release was not dependent upon calcium, whereas, K-induced release was dependent upon calcium. Potassium caused a significant increase in the percentage of 3H-5-hydroxyindoleacetic acid (3H-5HIAA) released from the tissue. The increased metabolite was formed totally by oxidative deamination as shown by inhibition of the formation and release of 3H-5HIAA following inhibition of monoamine oxidase with clorgyline. The increased deamination as a result of incubation with K apparently occurred prior to release of 5HT from the nerve terminal, since incubation of the tissue with fluoxetine, a selective 5HT uptake inhibitor, did not alter the increased 3H-5IAA formation in response to K. These findings indicate that d-A and K apparently release 3H-5HT by different mechanisms and emphasize the importance of measuring metabolite formation in studies examining the effects of drugs on the release of 5HT in vitro.

Animals↗

PubMed1989

Characteristics and displaceability of neurotensin binding sites in the rat cerebral cortex and corpus striatum.

1. Neurotensin binding to synaptosomes isolated from the rat cerebral cortex and corpus striatum reached saturation after 4 min of incubation. 2. The rates of binding were found to be higher in the corpus striatum than in the cerebral cortex. 3. Concentration study revealed the presence of two different and independent classes of neurotensin binding sites with a negative cooperative interaction within each class of binding sites. 4. At saturation levels, the low affinity binding component was found to have a flat regional difference, while the high affinity binding component showed regional differences in terms of maximal binding capacity, suggesting a higher number of high affinity binding sites in the striatum than in the cortex. 5. In the competition related experiments, dopamine was found to displace around 70% of neurotensin binding sites in the corpus striatum and the cerebral cortex. 5. Substance P displaced around 50% of [3H]neurotensin in the cerebral cortex. Whereas, 50% and 70% displacement were observed in the striatum at high and low affinity binding sites, respectively. 6. These results show the overlap in the binding sites of neurotensin, dopamine and substance P.

Animals↗

PubMed1995

Low intensity areas observed on T2-weighted magnetic resonance imaging of the cerebral cortex in various neurological diseases.

The cerebral cortex of patients with Alzheimer's disease (AD) or amyotrophic lateral sclerosis (ALS) may show low signal intensity on T2-weighted magnetic resonance images (MRI). Since these low intensity areas (LIA) are also often observed in aged patients with other diseases, we suspected that they might be a non-specific finding. We conducted a retrospective study of LIA in 139 patients with various diseases of the central and peripheral nervous systems, and evaluated their relationship to age and other MRI findings. Brain atrophy, ventricular dilatation, white matter lesions, and LIA were visually evaluated on axial images of the spin echo sequences obtained with a 1.5 tesla (T) system. We found that LIA appeared after age 50 and became more common with advancing age. Their presence correlated with brain atrophy and white matter lesions. They were most frequent in the motor cortex, followed by the occipital and sensory cortices. Their incidence in the motor cortex was significantly higher in patients with central nervous system diseases than in those with peripheral neuropathy. We conclude that LIA are common in old patients with various neurological diseases and suggest that the deposition of iron in the cerebral cortices causes their development.

Adolescent↗

PubMed1993

Formation of synapses between basal forebrain afferents and cerebral cortex neurons: an electron microscopic study in organotypic slice cultures.

Co-cultures of rat basal forebrain and cerebral cortex were maintained from 1 to 5 weeks in vitro with serum-free defined medium. The formation of synaptic connections between basal forebrain afferent fibres and cortical neurons was studied by specific labelling with three staining techniques, including (i) neuronal tract tracing with the fluorescent dye 1,1'-dioctodecyl-3,3,3'3'- tetramethylindocarbocyanine perchlorate, (ii) acetylcholinesterase histochemistry, and (iii) choline acetyltransferase immunocytochemistry. Both basal forebrain and cerebral cortex tissue displayed organotypic characteristics in culture. Cerebral cortex revealed a dense innervation by axonal projections from the basal forebrain. All three labelling techniques produced similar results at the light microscopic level, with densest innervation located in the marginal zone. At the fine structural level, the 1,1'-dioctodecyl-3,3,3'3'-tetramethylindocarbocyanine perchlorate-, acetylcholinesterase- and choline acetyltransferase-stained basal forebrain afferents all revealed a number of synaptic contacts with cortical neurons. The contacts displayed consistent synaptic features, including presynaptic accumulation of small round vesicles, cleft widening, and postsynaptic densities forming symmetric synapses. These morphological characteristics of connections formed in vitro are similar to basal forebrain cholinergic projections to cerebral cortex in normal brain. Based on these results, this tissue culture model appears to be an useful tool for investigations of the development of cholinergic innervation of cerebral cortex.

Acetylcholinesterase↗

PubMed1990

Three-dimensional structural organization of layer I of the human cerebral cortex: a Golgi study.

The three-dimensional structural organization of layer I of the developing and adult human cerebral cortex has been investigated by using sagittal, transverse, and tangential rapid Golgi and Klüver-Barrera preparations. The actual morphology of its fundamental neuron--the Cajal-Retzius cell (C-R)--is established. These large and solitary cells are horizontal multipolar neurons characterized by: (1) long horizontal dendrites that radiate in all directions within a tangential plane parallel to the pial surface, (2) long horizontal axonic collaterals that radiate in all directions within layer I middle level, and (3) a descending axonic process that reaches the lower level, becomes a long tangential fiber--and eventually a myelinated one--and projects in any direction within this level. In cortical ontogenesis, its dendrites, axonic collaterals and terminal axon undergo a progressive multipolar "horizontalization" extending throughout the surface of the expanding cerebral cortex. The neuron's body and main dendrites will be found only in some areas, whereas its axonic collaterals and terminal tangential axon should be found throughout the cerebral cortex. This developmental feature explains the presence of two--middle and lower--plexuses in layer I, composed of the axonic collaterals and the terminal tangential axons of C-R cells, respectively. It is emphasized that the basic morphology of the C-R cell remains essentially unchanged in the course of cortical ontogenesis and that the neuron persists in the adult cerebral cortex. Whereas the C-R cell is the basic neuron of layer I, the pyramidal cells dendritic bouquets represent its larger and main receptive surface (the only one early in development). By the 30th week of gestation, a C-R cell could establish: (1) proximal contacts, through its axonic collaterals, with all dendritic bouquets within a approximately 350 microns radius, and (2) distant contacts, through its tangential axon, with dendritic bouquets within a narrow sagittal, transverse, or diagonal territory several mm long. In cortical ontogenesis, the C-R cells' functional territories continue to expand throughout the surface of the cerebral cortex and possibly overlap with each other. It is proposed that the C-R cell receives inputs from primitive (mesencephalic?) corticipetal fibers and that it transmits the same kind of information (perhaps a basal tone?) to the dendritic bouquets of all pyramidal neurons throughout the cerebral cortex regardless of their location, cortical depth, or functional role.

Adolescent↗

PubMed1985

Comparative effects of topical perfusions of pentylenetetrazol in the mesencephalon and cerebral cortex of cats.

Push-pull perfusions of pentylenetetrazol (PTZ) were carried out in the mesencephalon and cerebral cortex (orbitofrontal, motor, and suprasylvian) of "encéphale isolé" cats, while EEG recordings from motor cortices and EMG of facial muscles were obtained. There were significant differences between perfusions in the mesencephalic reticular formation (MRF) and in the cerebral cortex: (i) EEG spikes not accompanied by muscular contractions occurred during perfusion of cerebral cortex (motor cortex included), but never with perfusions in MRF. (ii) In some instances muscular tonic and clonic contractions occurred in the absence of EEG spikes when perfusing the mesencephalon, but never with cortical perfusions. (iii) Both MRF and cortical perfusions induced EEG spikes accompanied by myoclonic seizures; however, muscular seizures were practically of the same amplitude in both sides after perfusion of the MRF and were predominant in the contralateral side after cortical perfusions. In addition, significantly less perfusion time (total dose) of PTZ was needed to induce such events in the MRF than in the cerebral cortex. (iv) Generalized seizures induced by cortical perfusions showed a clear predominance of contractions in the muscles contralateral to the perfusion site, whereas perfusions in the MRF induced generalized seizures indistinguishable from those produced by i.v. administration of PTZ. Results suggest that PTZ generalized seizures, closely resembling the so called "primary generalized seizures," result from activation of the MRF, whereas PTZ acting in the cerebral cortex produces a model of focal convulsions that may become secondarily generalized.

Administration, Topical↗

PubMed1979

Structural abnormalities in the cerebral cortex of chronic schizophrenic patients.

Enlarged cerebral ventricles in chronic schizophrenic patients suggest a process of mild cerebral atrophy occurs in some. To see if this process involves the cerebral cortex, the widths of the Sylvian fissure, the interhemispheric fissure, and three cortical sulci were measured blindly on computerized tomography (CT) scans of 75 chronic psychiatric patients and 62 asymptomatic volunteers, all less than 50 years of age. A total of 19 of the 60 patients with chronic schizophrenia had at least one abnormality. All 15 patients with other diagnoses were within the control range. Comparing those chronic schizophrenic patients with abnormalities to those without them, there were no significant differences in age, length of illness or treatment, and length of hospitalization. From this and ventricular size data, two thirds of the chronic schizophrenics had some cerebral structural abnormality. Ventricular enlargement did not correlate significantly with cortical abnormalities. Therefore, more than one etiology may account for the structural abnormalities found in chronic schizophrenic patients.

Adult↗

PubMedDate not supplied

Developmental expression of estrogen receptor mRNA in the rat cerebral cortex: a nonisotopic in situ hybridization histochemistry study.

The distribution of estrogen receptor mRNA expression was studied in the developing rat cerebral cortex by in situ hybridization histochemistry. We used a specific, nonisotopically (digoxigenin) labeled, synthetic oligodeoxyribonucleotide complementary to a 48 base sequence in the region of the estrogen-binding domain of rat uterine estrogen receptor cDNA. During development, estrogen receptor mRNA was observed in all forebrain regions previously reported to bind estrogen, as determined by steroid autoradiography or nuclear binding assay. In the developing cerebral cortex, estrogen receptor mRNA was extensively expressed in the ventricular zone, primitive plexiform layer, and immature cortical plate at least as early as embryonic day 16. During the first 3 postnatal weeks, cortical mRNA expression was increasingly restricted to the upper third of the cerebral cortex and to the neurons of the cortical subplate (layer VIb/VII) and decreased to low levels by postnatal day 28. In the cerebral cortex, the spatial distribution of estrogen receptor mRNA expression overlapped that reported for the encoded protein. The extensive distribution of estrogen receptor mRNA throughout the late prenatal and early postnatal cerebral cortex points to an important role for estrogen in the differentiation and maturation of the cerebral cortex.

Aging↗

PubMed1976

Distribution of dopamine in the rat cerebral cortex.

The rat cerebral neocortex was sectioned by 3 transverse cuts and analyzed for dopamine and noradrenaline. Dopamine concentration decreased gradually from the rostral (97 +/- 4 ng/g) to the caudal (59 +/- 2 ng/g) end of the neocortex. Also, the noradrenaline concentration was highest in the rostral part (269 +/- 6 ng/g) and decreased gradually reaching a concentration of 238 +/- 3 ng/g in the caudal part. Since the quotient dopamine/noradrenaline showed similar changes in the neocortex parts investigated the data support the view that dopamine serves as a transmitter in cortical neurons apart from being a precursor for noradrenaline.

Animals↗

PubMed2004

Effects of 1alpha,25 dihydroxyvitamin D3 on the expression of HO-1 and GFAP in glial cells of the photothrombotically lesioned cerebral cortex.

In ischemic cerebral injuries a cascade of degenerative mechanisms, all participating in the development of oxidative stress, influence the condition of the tissue. The survival of viable tissue affected by secondary injury largely depends on the balance between endogenous protective mechanisms and the ongoing degenerative processes. The inducible enzyme, heme oxygenase-1 metabolizes and thus detoxifies free heme to the powerful endogenous antioxidants biliverdin and bilirubin therefore enhancing neuroprotection. The secosteroid 1alpha,25-dihydroxyvitamin D3 (1,25-D3) is a modulator of the immune system and also exhibits a strong potential for neuroprotection as recently shown in the MCAO model of cerebral ischemia. We studied the effects of 1,25-D3 treatment on heme oxygenase-1 expression following focal cortical ischemia elicited by photothrombosis. Postlesional treatment with 1,25-D3 (4 microg/kg body weight) resulted in a transient, but significant upregulation of glial heme oxygenase-1 immunoreactivity concomitant with a reduction in glial fibrillary acidic protein immunoreactivity in remote cortical regions affected by a secondary spread of injury, whereas the size of the lesion's core remained unaffected. 1,25-D3 did not produce a temporal shift or extension of injury-related heme oxygenase-1 responses, indicating that 1,25-D3 did not prolong ischemia-related heme oxygenase-1 expression. In contrast to glial heme oxygenase-1 upregulation, glial fibrillary acidic protein, a sensitive marker for reactive gliosis, was significantly reduced. These findings support an additional protective action of 1,25-D3 at the cellular level in regions affected by secondary injury-related responses.

Animals↗

PubMed2004

Structural patterns of injured mitochondria in human oedematous cerebral cortex.

PRIMARY OBJECTIVE: Cerebral cortical biopsies of 37 patients with clinical diagnosis of congenital malformations, brain trauma and tumours were studied to establish mitochondrial morphological alterations. METHODS AND PROCEDURES: Cortical biopsies obtained in the surgical room were immediately processed by conventional technique for transmission electron microscopy. RESULTS: Three injured mitochondrial morphological patterns were found: swollen clear, (SCM), swollen dense (SDM) and dark degenerated (DDM) mitochondria. SCM were predominantly found in traumatic brain oedema. SDM and DDM were frequently observed in sustained permanent ischaemia induced by brain tumours, vascular anomaly and congenital hydrocephalus. SCM exhibited low electron dense mitochondrial matrix, enlarged intracristal space and continuity of outer and inner mitochondrial membranes. SDM showed high electron dense matrix and swollen intact or fragmented cristae. DDM displayed overall high electron density of matrix and mitochondrial membranes. CONCLUSION: The injured mitochondrial patterns are related with nerve cell death and considered markers of lethal nerve cell injury.

Adolescent↗