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PubMed1998

Development of GAP-43 mRNA in the macaque cerebral cortex.

To estimate the extent of axonal growth in various areas of the cerebral cortex, we measured the amount of GAP-43 mRNA in the cerebral cortex of developing macaque monkeys. In four areas, i.e., the prefrontal area (FD delta), the temporal association area (TE), the primary somatosensory area (PC), and the primary visual area (OC), the amount of GAP-43 mRNA was measured from the intermediate fetal period [embryonic day 120 (E120)] to the adult stage. In two other areas, i.e., the parietal association area (PG) and the secondary visual area (OB), the amount of GAP-43 mRNA was measured during the postnatal period. The amount of GAP-43 mRNA was highest at E120, decreased roughly exponentially, and approached the asymptote by postnatal day 70 (P70). The amount of GAP-43 mRNA was higher in the association areas (FD delta, TE, and PG) than in the primary sensory areas (PC and OC) during development and at the adult stage. These findings suggest that axonal growth in the cerebral cortex is most exuberant before or during the intermediate fetal period and approximately ends by P70. Furthermore, axonal growth is evidently more intensive in the association areas than in the primary sensory areas during the stage following the intermediate fetal period.

Aging↗

PubMed1998

Functional and structural mapping of human cerebral cortex: solutions are in the surfaces.

The human cerebral cortex is notorious for the depth and irregularity of its convolutions and for its variability from one individual to the next. These complexities of cortical geography have been a chronic impediment to studies of functional specialization in the cortex. In this report, we discuss ways to compensate for the convolutions by using a combination of strategies whose common denominator involves explicit reconstructions of the cortical surface. Surface-based visualization involves reconstructing cortical surfaces and displaying them, along with associated experimental data, in various complementary formats (including three-dimensional native configurations, two-dimensional slices, extensively smoothed surfaces, ellipsoidal representations, and cortical flat maps). Generating these representations for the cortex of the Visible Man leads to a surface-based atlas that has important advantages over conventional stereotaxic atlases as a substrate for displaying and analyzing large amounts of experimental data. We illustrate this by showing the relationship between functionally specialized regions and topographically organized areas in human visual cortex. Surface-based warping allows data to be mapped from individual hemispheres to a surface-based atlas while respecting surface topology, improving registration of identifiable landmarks, and minimizing unwanted distortions. Surface-based warping also can aid in comparisons between species, which we illustrate by warping a macaque flat map to match the shape of a human flat map. Collectively, these approaches will allow more refined analyses of commonalities as well as individual differences in the functional organization of primate cerebral cortex.

Anatomy, Cross-Sectional↗

PubMed2001

Alterations of phospholipase C isozymes in rat cerebral cortex through hyperoxia.

The effect of hyperoxia on the level of three phospholipase C (PLC) isozymes (beta1, gamma1, delta1) was assessed in the rat cerebral cortex. When the rats were exposed to 100% oxygen for 60 h, there was a significant reduction in the catalytic activity of low molecular weight phosphotyrosine phosphatase, which was susceptible to activity loss under oxidative stress. The result suggests that oxidative stress is induced in the rat cerebral cortex through hyperoxia. The protein levels of PLC-beta1 and -delta1 were significantly increased in the cerebral cortex where oxidative stress had been induced, although that of PLC-gamma1 was not altered. There was no significant difference in the total PLC activity of the cerebral cortex between hyperoxia and control rats. Using gel filtration chromatography, it was revealed that the PLC-beta1 activity in the cerebral cortex of the hyperoxia rats was higher than that in the control rats, but the PLC-delta1 activity in the former did not differ from that in the latter, despite an increase in the PLC-delta1 protein level. These findings suggest that the PLC-beta1 and -delta1 protein levels of brain tissues are increased by oxidative stress, and that the increased PLC-delta1 molecule is less active.

Aerobiosis↗

PubMed2001

The changes in the ultrastructure of the cerebrovascular junction after traumatic injury of the cerebral cortex in rats.

OBJECTIVES: The effect of the traumatic injury of the cerebral cortex on the ultrastructure of the cerebrovascular junction was studied in rats. The aim of the present study is to describe the ultrastructural alterations in the cerebrovascular junction in rat cerebral cortex after traumatic injury. We were particularly interested in the alterations in endothelium, pericytes and the differentiated population of cerebral macrophages. MATERIAL AND METHODS: The observations were conducted four days (group I-five animals) and seven days (group II-five animals) after induction of cortical trauma. Traumatic injury was induced in the fronto-temporal region of cerebral cortex in general anesthesia with 20 mg/kg ketamine hydrochloride. RESULTS: In the first group we found the features of damage of the blood-brain barrier and migration of the morphological blood components to the perivascular space. The trauma caused necrosis and apoptosis within brain tissue. An important observation was the presence of numerous brain macrophages that participated in phagocytosis of damaged cellular elements. Additionally, we found an increase in the connective tissue ground substance around brain capillaries. In the second experimental group we noted an increased number of pericytes (1-3) near capillary walls. In some instances, the basement membrane surrounding the pericytes was interrupted and these cells were also located beyond the rim of the vessel wall. Some pericytes showed numerous phagolysosomes indicating that these cells belonged to perivascular macrophages. Moreover, we observed a population of phagocytes residing in close contact with neurons. These cells were different from the typical perivascular macrophages. CONCLUSIONS: These observations indicate that the traumatic injury of the brain results in mobilization of a heterogeneous population of brain macrophages. This study indicates that different subpopulations of macrophages emerge in the region of traumatic brain damage, and that the morphology and dynamics of these phagocytes changes and depends on the time elapsed after the initial traumatic incident.

Animals↗

PubMed1999

Modulation of NMDA receptor by huperzine A in rat cerebral cortex.

AIM: To investigate the effects of huperzine A (Hup A) on NMDA receptors in rat cerebral cortex. METHODS: 1) The effect of hup A on NMDA-induced current was studied in acutely dissociated rat hippocampal pyramidal neurons using whole-cell recording. 2) The effect of Hup A on NMDA receptor binding was assessed using [3H] dizocilpine (Diz) binding assay in synaptic membrane preparation of rat cerebral cortex. RESULTS: 1) Hup A reversibly inhibited NMDA-induced current in a concentration-dependent manner with IC50 of 45.4 mumol.L-1. 2) Hup A inhibited the specific binding of [3H]MK-801 to extensively washed synaptic membrane of rat cerebral cortex in a concentration-dependent manner with IC50 of 0.5 (0.1-1.9) mumol.L-1 (n = 4). 3) L-Glutamate 10 mumol.L-1 markedly increased [3H] MK-801 binding. In the presence of L-glutamate, Hup A 0.001-0.1 mumol.L-1 caused a further increase of the binding, whereas Hup A 1-300 mumol.L-1 inhibited the binding in a concentration-dependent manner with IC50 of 12.3 (5.8-26.3) mumol.L-1 (n = 5). CONCLUSION: Hup A acted as an antagonist of NMDA receptor in cerebral cortex in addition to its inhibitory effect on acetylcholinesterase.

Alkaloids↗

PubMed1985

Serotonin release in human cerebral cortex and its modulation via serotonin receptors.

Human cerebral cortex slices were prepared from brain tissue which had to be removed in order to gain access to deep-seated tumours. Subsequent to incubation with [3H]serotonin, the slices were superfused with physiological salt solution containing paroxetine, and 3H overflow was evoked by electrical field stimulation. The evoked tritium overflow (86% of which was accounted for by unmetabolized [3H]serotonin) was abolished by tetrodotoxin or omission of calcium from the superfusion fluid. Unlabelled serotonin decreased, and the serotonin receptor antagonist metitepin increased, the evoked overflow. The inhibition produced by serotonin was antagonized by metitepin. It is concluded that serotonin release in human cerebral cortex is modulated by inhibitory serotonin receptors, which may be localized presynaptically on the serotoninergic nerve fibers themselves. There are marked similarities between human and rat brain cortex with respect to action potential-induced, Ca2+-dependent serotonin release and its modulation via serotonin receptors.

Calcium↗

PubMed1984

Preferential uptake of norepinephrine into dopaminergic terminals of a synaptosomal preparation from rat cerebral cortex.

In a synaptosomal preparation from male rat cerebral cortex only 34% of total norepinephrine (NE) uptake could be inhibited by nanomolar concentrations of desmethylimipramine (DMI) with an apparent IC50 value of 0.37 nM. The residual uptake was efficiently inhibited by micromolar concentrations of DMI (IC50 = 4.0 microM). In synaptosomes from the hypothalamus, 74% of total NE uptake could be blocked by DMI with an IC50 of 0.1 nM whereas in synaptosomes from the striatum the IC50 for DMI inhibition was 3.8 microM. It is concluded that in synaptosomes from rat cerebral cortex only 34%, and in synaptosomes from the hypothalamus 74% of total NE are taken up by noradrenergic nerve terminals whereas the residual NE uptake occurs in dopaminergic nerve endings.

Animals↗

PubMed1980

In vivo biosynthesis of cholecystokinin in rat cerebral cortex.

The biosynthesis of cholecystokinin (CCK) in the cerebral cortex of rats was studied by intracisternal pulse injections of [35S]methionine. The rats were killed with intervals varying from 15 min to 10 h after the injections. Cortical CCK extracted in boiling water and acetic acid was immunoabsorbed using an antiserum specific for the COOH-terminal sequence of CCK. After displacement from the immunoabsorbent by heptadecapeptide gastrin, which contains the same COOH-terminal sequence as CCK, chromatography on Sephadex G-50 columns showed four molecular forms of CCK with elution constants (Kav) of 0.08, 0.50 (corresponding to the tritriacontapeptide amide, CCK-33), 1.10 (corresponding to the COOH-terminal octapeptide amide, CCK-8) and 1.40 (a component which may correspond to the COOH-terminal tetrapeptide of rat CCK). Chasing with methionine demonstrated a biosynthetic pathway from the largest molecular form to the octapeptide-like form. The results indicate that a rapid and extensive synthesis of CCK takes place in the cerebral cortex, and that a precursor relationship exists between CCK-8 and the larger molecular forms of CCK.

Animals↗

PubMed1982

Effect of magnocellular forebrain nuclei lesions on acetylcholine output from the cerebral cortex, electrocorticogram and behaviour.

ACh output from the cerebral cortex, electrocortical activity, spontaneous alternation and the acquisition of a conditioned avoidance response have been investigated in rats 20 days after the placement of a unilateral lesion of the magnocellular forebrain nuclei (MFN). ACh output from the hemisphere ipsilateral to the lesion was 40% lower than in sham operated rats. Electrocortical activity quantified with a frequency analyzer supplemented by a period and power spectrum analysis showed a marked asymmetry between the two hemispheres of the lesioned rats. The total electrical activity was strongly reduced over the lesioned hemisphere. The reduction involved all frequencies but was more evident in the high frequencies. In the lesioned rats spontaneous alternation was not impaired and spontaneous motility was enhanced while the acquisition of a conditioned active avoidance in a two-way shuttle box was significantly hampered. The possibility is envisaged that the destruction of cholinergic fibres impinging upon the cerebral cortex may decrease cortical activation and impair the selective awareness necessary for information acquisition and exclusion of irrelevant output.

Acetylcholine↗

PubMed1982

[An autopsy case of Parkinson's disease associated clinically with dementia terminating in akinetic mutism and pathologically with multiple Lewy's Bodies in the cerebral cortex].

An autopsy case of a 50 year-old male with Parkinson's disease associated with multiple Lewy bodies in the cerebral cortex was reported. His clinical symptoms began at the age of 26 with the speech and actions indicative of a persecution complex accompanied by irritability and were followed by progressive dementia from the age of 37 and Parkinsonism since the age of 41. He was in a state of akinetic mutism thereafter till his death at the age of 50. Autopsy disclosed in addition to the typical findings of Parkinson's disease in the brain stem multiple intracytoplasmic Lewy bodies in medium-sized neurons of the fifth and sixth layers of the cerebral cortex. They were atypical in the sense that they did not have any haloes. They were especially numerous in the cingulate gyrus. In addition, findings of non-specific neuronal degeneration were obtained in the cerebral cortex such as cellular atrophy with massive deposition of lipofuscin pigments, central chromatolysis, cell loss and cellular gliosis in the third, fifth and sixth layers. These neuronal findings were also prominent in the cingulate gyrus. Such senile changes as senile plaques or granulo-vacuolar degeneration were not found, although there were a few foci of neurofibrillary degeneration in the hippocampal gyrus. Histochemically and electron microscopically, no difference was observed in the constituents of Lewy bodies between the brain stem and the cerebral cortex. Such autopsy findings and a review of the literature indicate that the dementia in this case may be related not only to the presence of Lewy bodies but also to the above-described, non-specific neuronal degeneration in the bilateral cingulate gyri and surrounding frontal gyri. The standpoint of regarding a Parkinson's disease with multiple Lewy bodies in the cerebral cortex as an independent disease entity was criticized.

Akinetic Mutism↗

PubMed1998

Salient features of synaptic organisation in the cerebral cortex.

The neuronal and synaptic organisation of the cerebral cortex appears exceedingly complex, and the definition of a basic cortical circuit in terms of defined classes of cells and connections is necessary to facilitate progress of its analysis. During the last two decades quantitative studies of the synaptic connectivity of identified cortical neurones and their molecular dissection revealed a number of general rules that apply to all areas of cortex. In this review, first the precise location of postsynaptic GABA and glutamate receptors is examined at cortical synapses, in order to define the site of synaptic interactions. It is argued that, due to the exclusion of G protein-coupled receptors from the postsynaptic density, the presence of extrasynaptic receptors and the molecular compartmentalisation of the postsynaptic membrane, the synapse should include membrane areas beyond the membrane specialisation. Subsequently, the following organisational principles are examined: 1. The cerebral cortex consists of: (i) a large population of principal neurones reciprocally connected to the thalamus and to each other via axon collaterals releasing excitatory amino acids, and, (ii) a smaller population of mainly local circuit GABAergic neurones. 2. Differential reciprocal connections are also formed amongst GABAergic neurones. 3. All extrinsic and intracortical glutamatergic pathways terminate on both the principal and the GABAergic neurones, differentially weighted according to the pathway. 4. Synapses of multiple sets of glutamatergic and GABAergic afferents subdivide the surface of cortical neurones and are often co-aligned on the dendritic domain. 5. A unique feature of the cortex is the GABAergic axo-axonic cell, influencing principal cells through GABAA receptors at synapses located exclusively on the axon initial segment. The analysis of these salient features of connectivity has revealed a remarkably selective array of connections, yet a highly adaptable design of the basic circuit emerges when comparisons are made between cortical areas or layers. The basic circuit is most obvious in the hippocampus where a relatively homogeneous set of spatially aligned principal cells allows an easy visualization of the organisational rules. Those principles which have been examined in the isocortex proved to be identical or very similar. In the isocortex, the basic circuit, scaled to specific requirements, is repeated in each layer. As multiple sets of output neurones evolved, requiring subtly different needs for their inputs, the basic circuit may be superimposed several times in the same layer. Tangential intralaminar connections in both the hippocampus and isocortex also connect output neurones with similar properties, as best seen in the patchy connections in the isocortex. The additional radial superposition of several laminae of distinct sets of output neurones, each representing and supported by its basic circuit, requires a co-ordination of their activity that is mediated by highly selective interlaminar connections, involving both the GABAergic and the excitatory amino acid releasing neurones. The remarkable specificity in the geometry of cells and the selectivity in placement of neurotransmitter receptors and synapses on their surface, strongly suggest a predominant role for time in the coding of information, but this does not exclude an important role also for the rate of action potential discharge in cortical representation of information.

Action Potentials↗

PubMed1967

Effects of fatty acids, ketone bodies, lactate and pyruvate on glucose utilization by guinea-pig cerebral cortex slices.

1. Starvation did not affect the rates of glucose utilization or lactate formation by guinea-pig cerebral cortex slices. 2. Palmitate (1mm), butyrate (5mm) or acetoacetate (5mm) did not affect glucose utilization or lactate formation by cerebral cortex slices from guinea pigs starved for 48hr. 3. dl-beta-Hydroxybutyrate (10mm) increased the formation of lactate without affecting glucose utilization by cerebral cortex slices from guinea pigs starved for 48hr. This implies that beta-hydroxybutyrate decreased the rate of glucose oxidation. 4. Metabolism of added ketone bodies can account for 20-40% of observed rates of oxygen consumption. 5. Lactate or pyruvate (5mm) decreased the rates of glucose utilization by guinea-pig cerebral cortex slices.

Acetoacetates↗

PubMed1997

Localization of V1a vasopressin receptor mRNA expression in cultured neurons, astroglia, and oligodendroglia of rat cerebral cortex.

Previous studies suggested the existence of V1a vasopressin receptors (V1aR) in the cerebral cortex. Here, we investigated the cellular and regional localization of V1aR in the E18 rat cerebral cortex using RT-PCR and Southern blot analysis of V1aR mRNA derived from enriched cultures of neurons, astroglia, and oligodendroglia from four cortical regions (rostral, caudal, dorsal and ventral). V1aR mRNA was detected in each of the cell types within each of the regions studied. These data indicate that V1aR is broadly distributed throughout the cerebral cortex and suggest that vasopressin plays an important role in cortical functions.

Animals↗

PubMed1972

Effect of etorphine, morphine and diprenorphine on neurones of the cerebral cortex and spinal cord of the rat.

1. The actions of etorphine, morphine and diprenorphine were investigated on neurones of the cerebral cortex and spinal cord of rats anaesthetized with pentobarbitone.2. In the cerebral cortex, intravenous etorphine increased the latency of the primary evoked response to a peripheral nerve stimulus and suppressed the rhythmical after-discharge. Diprenorphine reversed this effect. These actions were demonstrated on both field potentials and unit firing.3. Morphine had no effect on the primary response but the frequency of after-discharge bursts was reduced and there was an increase in firing between bursts.4. In the cerebral cortex, electrophoretically applied etorphine reduced after-discharges when applied for long periods but had no effect on the depressant actions of glycine and gamma-aminobutyric acid (GABA) nor on the excitant action of acetylcholine and L-glutamate. Similarly there was no alteration by etorphine of the effects of glycine, GABA and L-glutamate on spinal cord neurones.5. It is concluded that etorphine may act pre-synaptically in the cerebral cortex.

Analgesics↗

PubMed1992

Development of AChE-positive neuronal projections from basal forebrain to cerebral cortex in organotypic tissue slice cultures.

Development of the innervation of the cerebral cortex by acetylcholinesterase (AChE)-stained basal forebrain neurons was studied in vitro using the roller tube technique. Slice cultures were maintained from 3 days to 4 weeks either in serum based medium or in chemically defined medium, each supplemented in some cases with nerve growth factor (NGF). The distribution of AChE and choline acetyltransferase (CAT)-containing neurons was investigated using histo- and immunocytochemical techniques. Slice cultures of basal forebrain revealed the presence of large and medium sized AChE-positive neurons. Within one week of cultivation, numerous AChE-labeled fibers could be seen growing out from the basal forebrain toward the cortex. After entering cortical tissue most of the afferent basal forebrain fibers projected either radially or obliquely into the cortical layers. Many afferent axons initially also travelled tangentially within the white matter, and turned then to grow into the cortical layers. Cerebral cortex tissue maintained a coarse laminar organization. Ramifications of basal forebrain fibers were visible within the subplate region, the deep and superficial cortical layers, and within the marginal zone; greatest density occurred in the subplate region and in marginal zones. Many of these processes exhibited branching patterns markedly similar to those observed during cortical development in vivo. Cortex slices placed with the pial surface adjacent to the basal forebrain revealed AChE-stained fibers that entered the cortical tissue through the marginal surface and gave off ramifications within the superficial layers and, less frequently, the deeper cortical layers. CAT-immunostaining revealed labeled cell bodies and neurites only in the basal forebrain, not in the cortex tissue. Control experiments with co-cultures of basal forebrain and cerebellum slices showed no AChE-positive fiber ingrowth into the cerebellum tissue. The results of these studies demonstrate that basal forebrain projections to cerebral cortex in vitro appear similar to the projections that develop in vivo, and indicate that organotypic co-cultures provide a valuable model for studies of developing cortical afferents.

Acetylcholinesterase↗

PubMed1979

Histochemical and morphological evaluation of cerebral cortex of newborn rat in the course of joint ethanol and pyrazole administration.

The object of the study was the cerebral cortex of newborn rat. Tissue material was collected from the 2-nd to the 8-th hour after birth both from control animals and newborns whose mothers had been given both ethanol and pyrazole throughout gestation period, and also either ethanol alone or pyrazole. The drug were administered by gastric tube, in doses: ethanol 8.0 g/kg body weight, pyrazole 36 mg/kg body weight. Histochemical studies revealed variation in the intensity of reaction of the respiratory enzymes during examination of the cortex of newborns whose mothers had been fed with ethanol alone, or pyrazole alone. A strong inhibition of enzymatic reaction was observed in the examined cerebral cortex of newborns after a joint ethanol and pyrazole administration. Morphological studies showed an inhibition of maturing process of the cerebral cortex cells of animals treated with ethanol alone, whereas the cerebral cortex of animals whose mothers had been given both ethanol and pyrazole, presented symptoms allowing to diagnose encephalitis congenita symptomatica.

Animals↗

PubMed1979

The activity of cerebellar neurones during epileptiform activity induced by penicillin in the cerebral cortex of the rat.

In urethane anaesthetized rats an epileptiform focus was made in one cerebral cortex with penicillin (25 U). The relationship between epileptiform spikes in the cerebral cortex and the activity of cerebellar cortical and nuclear neurones have been investigated by means of extracellular recording techniques and computation of peri-event histograms and 'CUSUMs' (cumulative sums of differences from the mean). In the cerebellar cortex two distinct patterns of evoked activity were recorded: (a) In units showing little or no spontaneous activity, a brief evoked discharge followed the epileptiform spike. (b) In units showing steady spontaneous activity, a period of evoked inhibition followed the epileptiform spike. These included Purkinje cells and probably inhibitory interneurones. In the intracerebellar nuclei, cells with marked spontaneous activity showed a prolonged period of increased discharge following the epileptiform spike. It is concluded that the output of the intracerebellar nuclei is increased by epileptiform activity in the cerebral cortex. The significance of these results is discussed.

Animals↗

PubMed1999

Inhibiting neuronal migration by blocking NMDA receptors in the embryonic rat cerebral cortex: a tissue culture study.

To investigate the role of the NMDA receptor on neuronal migration in the cerebral cortex, we performed a tissue culture study using embryonic rat brain. After we labeled progenitor cells in the ventricular zone of E16 cerebral cortex explants by [3H]thymidine, the explants were cultured for 48 h. Then distribution of labeled cells was evaluated autoradiographically. Blocking NMDA receptors by adding the NMDA receptor antagonist, (+)-5-methyl-10, 11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801: 1 or 10 microM) or d(-)-2-amino-5-phosphonopentanoic acid (d-AP5: 100 microM) to the culture medium, caused significantly decreased distribution of labeled cells in the outer intermediate zone (control 14.2+/-5.5%, 1 microM MK-801 5.8+/-7.2%, 10 microM MK-801 3.6+/-1.4%, and d-AP5 8.6+/-4.0%; mean+/-S.D.). This suggests that blocking NMDA receptors inhibits neuronal migration in the cerebral cortex. Furthermore, the influence of decreased intracellular Ca2+ concentration on neuronal migration was examined by adding intracellular Ca2+ chelator, 1, 2-bis-(o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid tetra-(acetoxymethyl)-ester (BAPTA-AM: 5 or 25 microM). This also resulted in inhibited neuronal migration. Therefore, it seems that neuronal migration in the cerebral cortex is regulated by intracellular Ca2+ concentration, which the NMDA receptor may influence.

2-Amino-5-phosphonovalerate↗