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PubMedDate not supplied

A quantitative study of age-related changes in the vascular architecture of the rat cerebral cortex.

A quantitative study of age related changes in the vascular architecture of the rat cerebral cortex is described. A special vessel-filling technique, which allowed the simultaneous fixation of the vasculature, aided the identification of the vessels in histological sections. Vascular parameters, which included the total number of vessel fragments, a blood volume and a vessel wall-surface area index were obtained using a Quantimet 720 shape-analysing computer. In animals aged 13-83 weeks, there was an increase in the above vascular parameters which could mainly be attributed to an increase in the number of vessels with a diameter greater than 8 micrometers. In very old rats, aged 124 weeks, the vascularity of the cerebral cortex was severely reduced. These changes, which are very similar to those reported in the ageing human cerebral cortex, may be explained by either direct or indirect effects on the cerebral vasculature. Possible mechanisms are discussed in relation to similar changes observed in the cerebral vasculature after several different insults.

Aging↗

PubMed2002

Bilateral periventricular nodular heterotopia due to filamin 1 gene mutation: widespread glomeruloid microvascular anomaly and dysplastic cytoarchitecture in the cerebral cortex.

Bilateral periventricular nodular heterotopia (BPNH) is a neuronal migration disorder that is characterized by subependymal nodules of gray matter. Recently, a causative gene for BPNH, filamin 1, has been identified, and possible roles of the translated protein in cell migration and blood vessel development have been proposed. We report here the histopathological features of an autopsy case of BPNH with widespread glomeruloid microvascular anomaly and dysplastic cytoarchitecture in the cerebral cortex, in whom we found a novel exon 11 (Val528Met) filamin 1 mutation. Within the periventricular nodules, well-differentiated pyramidal neurons were randomly oriented. A small proportion of neurons were immunolabeled with antibodies raised against calbindin D-28k, parvalbumin, or calretinin. We used a carbocyanine dye (DiI) tracing technique to investigate the extent of fiber projections within and outside the nodules. The labeled fibers formed bundles that extended into the surrounding white matter. Connections between adjacent nodules were evident. Connections between the nodules and the cerebral cortex were also seen, with a small number of labeled fibers reaching the cortex. In the cerebral cortex, small closely packed vessels ran in a parallel fashion throughout all of the layers. Immunohistochemically, the inner rim of individual vessel lumina was labeled by an antibody against factor VIII, and the vessel walls were labeled by antibodies against actin and laminin. Astrocyte processes, labeled with an antibody to glial fibrillary acidic protein, invaded these vascular channels. Ultrastructurally, a network of basal lamina-like materials lined with endothelial cells was evident. The cytoarchitecture of the cerebral cortex was disturbed, in that the columnar neuronal arrangement was distorted around the malformed vessels. This case appears to represent an example of BPNH manifesting widespread developmental anomalies within the blood vessels and the cortical cytoarchitecture in the cerebrum.

Brain Diseases↗

PubMed2003

Optical analysis of acute spontaneous epileptiform discharges in the in vivo rat cerebral cortex.

We examined the spatiotemporal patterns of spontaneous epileptiform activity observed in the in vivo rat cerebral cortex using an optical recording technique of detecting transmembrane voltage changes. The surface of the cerebral cortex was exposed under anesthesia and stained with a fluorescent voltage-sensitive dye, RH414. Acute spontaneous epileptiform discharges were induced by application of a GABA(A) receptor antagonist, bicuculline. Changes in the intensity of fluorescence were recorded from the cerebral cortex using a 464-channel optic fiber photodiode system. We succeeded in recording spontaneous epileptiform discharges, and constructed their initiation-site maps. We found that the initiation site was neither unique nor randomly located, but exhibited a multimodal distribution pattern. The incidence of epileptiform discharges was different between the initiation sites, and some sites showed dominance in the induction of spontaneous epileptiform discharges.

Animals↗

PubMed1991

Appearance of putative amino acid neurotransmitters during differentiation of neurons in embryonic turtle cerebral cortex.

Pyramidal and nonpyramidal neurons can be recognized early in the development of the cerebral cortex in both reptiles and mammals, and the neurotransmitters likely utilized by these cells, glutamate and gamma-aminobutyric acid, or GABA, have been suggested to play critical developmental roles. Information concerning the timing and topography of neurotransmitter synthesis by specific classes of cortical neurons is important for understanding developmental roles of neurotransmitters and for identifying potential zones of neurotransmitter action in the developing brain. We therefore analyzed the appearance of GABA and glutamate in the cerebral cortex of embryonic turtles using polyclonal antisera raised against GABA and glutamate. Neuronal subtypes become immunoreactive for the putative amino acid neurotransmitters GABA and glutamate early in the embryonic development of turtle cerebral cortex, with nonpyramidal cells immunoreactive for GABA and pyramidal cells immunoreactive for glutamate. The results of controls strongly suggest that the immunocytochemical staining in tissue sections by the GABA and glutamate antisera corresponds to fixed endogenous GABA and glutamate. Horizontally oriented cells in the early marginal zone (stages 15-16) that are GABA-immunoreactive (GABA-IR) resemble nonpyramidal cells in morphology and distribution. GABA-IR neurons exhibit increasingly diverse morphologies and become distributed in all cortical layers as the cortex matures. Glutamate-immunoreactive (Glu-IR) cells dominate the cellular layer throughout development and are also common in the subcellular layer at early stages, a distribution like that of pyramidal neurons and distinct from that of GABA-IR nonpyramidal cells. The early organization of embryonic turtle cortex in reptiles resembles that of embryonic mammalian cortex, and the immunocytochemical results underline several shared as well as distinguishing features. Early GABA-IR nonpyramidal cells flank the developing cortical plate, composed primarily of pyramidal cells, shown here to be Glu-IR. The earliest GABA-IR cells in turtles likely correspond to Cajal-Retzius cells, a ubiquitous and precocious cell type in vertebrate cortex. Glutamate-IR projection neurons in vertebrates may also be related. The distinctly different topographies of GABA and glutamate containing cells in reptiles and mammals indicate that even if the basic amino acid transmitter-containing cell types are conserved in higher vertebrates, the local interactions mediated by these transmitters may differ. The potential role of GABA and glutamate in nonsynaptic interactions early in cortical development is reinforced by the precocious expression of these neurotransmitters in turtles, well before they are required for synaptic transmission.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1996

Alkylation of [3H]8-OH-DPAT binding sites in rat cerebral cortex and hippocampus.

The binding of tritiated 8-hydroxy-2-(di-n-propyl-amino)tetralin, or [3H]8-OH-DPAT, to membranes from rat cerebral cortex and hippocampus could be inhibited by serotonin (5-HT) and buspirone, and by the 5-HT antagonists propranolol, NAN-190, pindolol, pindobind-5-HT(1A), WAY1OO135, spiperone and ritanserin. All competition curves, except for ritanserin, best fitted a two-site model. In vitro treatment of the membranes with N-ethylmaleimide (NEM), to alkylate sulfhydryl groups, caused dose-dependent decreases of binding; the inhibition curves were biphasic, and the effects irreversible. Reduction of disulfide bonds with L-dithiothreitol (L-DTT) also decreased binding, but in a monophasic way; these effects were fully reversible in cortex, but only partially reversible in hippocampus. In the latter region, but not in cerebral cortex, previous occupancy by [(3)H]8-OH-DPAT partially protected binding from the effects of both L-DTT and NEM, suggesting that the thiol groups in the receptor recognition site(s) of this brain region are readily accessible. The binding characteristics were examined with the aid of saturation curves, carried out with increasing concentrations, up to 140 nM, of [(3)H]8-OH-DPAT. The saturation data were suggestive of a two-site receptor model incorporating a high-affinity site (K(H) of 0.3-0.5 nM) corresponding to the 5-HT(1A) receptor, and a low-affinity site (KL of ca 25 nM). After in vivo alkylations, carried out by treating rats with N-ethoxycarbonyl-2-ethoxy-1,2-dihydro-quinoline (EEDQ), the saturation curves from both control and EEDQ-treated rats were again best fitted to a two-site model. For EEDQ-treated animals, a drastic decrease of 5-HT(1A) receptor binding activity was noted; this loss was greater in hippocampus than in cerebral cortex. Since the decrease in 5-HT(1A) receptors was not associated with changes in low-affinity binding, the results suggest independent regulations of the two [(3)H]8-OH-DPAT binding proteins. Altogether, the present data further supports the notion that [(3)H]8-OH-DPAT, besides labelling 5-HT(1A) receptors, also binds to other structures in rat cerebral cortex and hippocampus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2004

Global optimization of cerebral cortex layout.

Functional areas of mammalian cerebral cortex seem positioned to minimize costs of their interconnections, down to a best-in-a-billion optimality level. The optimization problem here, originating in microcircuit design, is: Given connections among components, what is the physical placement of the components on a surface that minimizes total length of connections? Because of unfeasibility of measuring long-range "wire length" in the cortex, a simpler adjacency cost was validated. To deal with incomplete information on brain networks, a size law was developed that predicts optimization patterns in subnetworks. Macaque and cat cortex rank better in this connection optimization than the wiring of comparably structured computer chips, but somewhat worse than the macroeconomic commodity-flow network among U.S. states. However, cortex wiring conforms to the size law better than the macroeconomic patterns, which may indicate cortex optimizing mechanisms involve more global processes.

Animals↗

PubMed1973

A membrane-bound activity catalysing phosphatidylinositol breakdown to 1,2-diacylglycerol, D-myoinositol 1:2-cyclic phosphate an D-myoinositol 1-phosphate. Properties and subcellular distribution in rat cerebral cortex.

1. Breakdown of phosphatidylinositol was studied in homogenates and subcellular fractions of rat cerebral cortex by using both membrane-bound and externally added [(32)P]phosphatidylinositol as substrate. 2. In the presence of deoxycholate breakdown followed first-order kinetics at low substrate concentrations ([unk]1mm) and zero-order kinetics at higher concentrations (6-9mm). 3. Maximum breakdown by cerebral-cortex homogenates was approximately 0.5mumol/h per mg of protein and occurred at pH7.0 in the presence of 8mm-phosphatidylinositol, 2mm-CaCl(2) and 2mg of deoxycholate/ml. Activity was abolished by 1mm-ethanedioxybis(ethylamine)tetra-acetate. 4. The products of phosphatidylinositol breakdown were 1,2-diacylglycerol and a mixture of d-myoinositol 1:2-cyclic phosphate (55%) and d-myoinositol 1-phosphate (45%). The two phosphate esters appeared to be produced together and in constant proportions. 5. Some 51% of the activity was particle-bound, with the highest activities in small nerve endings, microsomal material and two synaptic membrane fractions (fractions Mic(20), Mic(100), M(1) 1.0 and M(1) 0.9 respectively), all of which were also rich in acetylcholinesterase and which have been shown to be rich in other surface-membrane enzymes. Much of the particle-bound activity therefore appears to be present in cerebral-cortex plasma membranes. 6. The results are discussed in relation to previously described soluble activities that catalyse the same reaction, and to a possible role of the membrane-bound enzyme in enhanced phosphatidylinositol turnover in externally stimulated cells.

Acetylcholinesterase↗

PubMed2002

Spatial eigenmodes and synchronous oscillation: co-incidence detection in simulated cerebral cortex.

Zero-lag synchronisation arises between points on the cerebral cortex receiving concurrent independent inputs; an observation generally ascribed to nonlinear mechanisms. Using simulations of cerebral cortex and Principal Component Analysis (PCA) we show patterns of zero-lag synchronisation (associated with empirically realistic spectral content) can arise from both linear and nonlinear mechanisms. For low levels of activation, we show the synchronous field is described by the eigenmodes of the resultant damped wave activity. The first and second spatial eigenmodes (which capture most of the signal variance) arise from the even and odd components of the independent input signals. The pattern of zero-lag synchronisation can be accounted for by the relative dominance of the first mode over the second, in the near-field of the inputs. The simulated cortical surface can act as a few millisecond response coincidence detector for concurrent, but uncorrelated, inputs. As cortical activation levels are increased, local damped oscillations in the gamma band undergo a transition to highly nonlinear undamped activity with 40 Hz dominant frequency. This is associated with "locking" between active sites and spatially segregated phase patterns. The damped wave synchronisation and the locked nonlinear oscillations may combine to permit fast representation of multiple patterns of activity within the same field of neurons.

Cerebral Cortex↗

PubMed1989

Stimulation of the nucleus basalis of Meynert increases acetylcholine release in the cerebral cortex in rats.

The effect of focal stimulation of the magnocellular nucleus of the basal forebrain (nucleus basalis of Meynert; NBM) on acetylcholine (ACh) release in the cerebral cortex in the parietal lobe was examined in halothane-anesthetized rats. ACh was measured using a microdialysis method. Focal electrical stimulation of the unilateral NBM increased ACh release in the ipsilateral cerebral cortex in stimulus intensity and frequency dependently. Microinjection of L-glutamate (100 nmol) into the unilateral NBM also increased ACh release in the ipsilateral cerebral cortex. The ACh release in the contralateral cerebral cortex was not affected by these unilateral stimulations of the NBM. It was concluded that focal stimulation of the NBM releases ACh from cortical terminals of cholinergic fibers originating in the NBM.

Acetylcholine↗

PubMed1989

Methylmercury-induced movement and postural disorders in developing rat: high-affinity uptake of choline, glutamate, and gamma-aminobutyric acid in the cerebral cortex and caudate-putamen.

Subcutaneous administration of methylmercuric chloride to neonatal rats resulted in movement and postural disorders during the fourth postnatal week. Sodium-dependent high-affinity uptake of radiolabeled choline, glutamate, and gamma-aminobutyric acid (GABA) was measured in homogenates of cerebral cortex and caudate-putamen. There was a significant decrease in the uptake of [3H]choline in the cerebral cortex, but not in the caudate-putamen, at the onset of neurological impairment (73-75%) and at one subclinical stage of toxicity (58-64%). No significant differences in [3H]glutamate uptake were detected in either region. The uptake of [3H]GABA in the presence of 1 mM beta-alanine, which was employed to inhibit the glial uptake process, was reduced significantly in both the cerebral cortex and caudate-putamen at the onset of neurological impairment (50-62%) and at one subclinical stage (40-51%). This decrease in [3H]GABA uptake is consistent with the results of previous studies using this animal model, which demonstrated a preferential degeneration of GABAergic neurons in the cerebral cortex and caudate-putamen of methylmercury-treated animals. Because the high-affinity uptake of choline is the rate-limiting step for acetylcholine synthesis by cholinergic neurons, the decrease in [3H]choline uptake may reflect an abnormal development of cholinergic innervation of the cerebral cortex.

Animals↗

PubMed1986

Spatial correlation between sensory regions and the drainage fields of pial veins in rat cerebral cortex.

Visual and somatosensory evoked potentials were mapped in the cerebral cortex of adult rats and, after filling the cerebral arteries and veins with dye, the mappings were then compared to the distribution of pial veins. A close relationship was found between the position, size and shape of the occipital venous drainage field and the distribution of visual evoked potentials with high amplitudes and short latencies. Accordingly, such potentials evoked by stimulation of the forepaw and tailroot were confined to the fronto-parietal drainage field. In the case of individual variations in the expansion and shape of sensory areas, the medial and lateral borders of the occipital drainage field and the medial border of the fronto-parietal drainage field covaried. Only at the common border between these two drainage fields, visual evoked potentials with small amplitudes and long latencies extended into the parietal drainage field and overlapped with somatosensory evoked potentials. This overlapping area corresponds in position to the anterior part of the peristriate cortex. A comparison between the vascular organization and cytoarchitectonic maps of the rat cortex indicates that other parts of the characteristic pattern of venous drainage fields may also correlate with the cytoarchitectonic and functional organization of the cerebral cortex. These observations suggest that during morphogenesis the formation of sensory projections to the cerebral cortex may interact with the angiogenesis, mainly with the development of veins.

Animals↗

PubMed1986

The lamination and connectivity of embryonic cerebral cortex transplanted into newborn rat cortex.

Sheets of frontal or occipital cerebral cortex were taken from embryonic day (E) 15 rat embryos and placed in shallow depressions made in the occipitoparietal region of newborn rats. These transplants developed normal patterns of lamination, which could be in an inverted orientation if the transplant itself was placed upside down. Irrespective of the cortical area of origin of the grafted tissue, the transplants consistently received projections from those host thalamic nuclei that were normally found to innervate the adjacent host cortex. This indicates that immature cortical tissue, up to at least E15, may not contain the information necessary to define the specific thalamocortical connections characteristic of individual areas. On the contrary, the observed input pattern may be the result of sprouting of fibers that normally innervated host cortical regions adjacent to the transplant. Similarly, callosal afferents to transplants seemed to be a direct extension of the callosal input to the host cortex immediately beneath the transplant. Results from HRP studies of callosal connections indicated that transplant efferents to the contralateral cortex are smaller in magnitude than their afferents. This may be related to the superficial location of the transplants, which may limit the access transplant efferents have to the white matter. This study suggests that, while the cortical lamination is largely determined intrinsically, the innervation of the cortex is influenced by the context in which it develops.

Animals↗

PubMed1989

Effects of chronic chlorpromazine treatment on peripheral benzodiazepine binding sites in heart, kidney, and cerebral cortex of rats.

Daily intraperitoneal administration to rats of 5 mg/kg of chlorpromazine (CPZ) for 21 days induced a significant up-regulation (51%) of peripheral benzodiazepine binding sites (PBSs) in cerebral cortex and a down-regulation of PBSs in the heart (25%) and kidney (14%), whereas no alteration in [3H]flunitrazepam binding in cerebral cortex was observed. [3H]PK 11195 binding to cerebral cortex returned to normal following 5 days of CPZ withdrawal, whereas the density of PBSs in the heart and kidney remained reduced. The affinity of PBSs for the ligand [3H]PK 11195 in the cerebral cortex and heart was not affected by the drug treatment or withdrawal. The CPZ-induced alterations in PBSs may be relevant to the effects of the drug on CNS and/or peripheral organs.

Animals↗

PubMed2002

Histamine H(2) -like receptors in chick cerebral cortex: effects on cyclic AMP synthesis and characterization by [(3) H]tiotidine binding.

In this study, histamine (HA) receptors in chick cerebral cortex were characterized using two approaches: (1) analysis of the effects of HA-ergic drugs on the cAMP-generating system, and (2) radioreceptor binding of [(3) H]tiotidine, a selective H(2) antagonist. HA was a weak activator of adenylyl cyclase in a crude membrane preparation of chick cerebrum. On the other hand, HA (0.1-1000 microm) potently and concentration dependently stimulated cAMP production in [(3) H]adenine pre-labelled slices of chick cerebral cortex, displaying an EC(50) value (concentration that produces 50% of maximum response) of 2.65 microm. The effect of HA was mimicked by agonists of HA receptors with the following rank order of potency: HA >or= 4-methylHA (H(2)) >or= N alpha,N alpha-dimethylHA (H(3) >> H(2) = H(1)) >> 2-methylHA (H(1)) >> 2-thiazolylethylamine (H(1)) >or= R alpha-methylHA (H(3)) >> amthamine, dimaprit (H(2)), immepip (H(3), H(4)). The HA-evoked increase in cAMP production in chick cerebral cortex was antagonized by selective H(2) receptor blockers (aminopotentidine >or= tiotidine > ranitidine >> zolantidine), and not significantly affected by mepyramine and thioperamide, selective H(1) and H(3) /H(4) receptor blockers, respectively. A detailed analysis of the antagonistic action of aminopotentidine (vs. HA) revealed a non-competitive mode of action. The binding of [(3) H]tiotidine to chick cortical membranes was rapid, stable and reversible. Saturation analysis resulted in a linear Scatchard plot, suggesting binding to a single class of receptor binding site with high affinity [equilibrium dissociation constant (K (d)) = 4.42 nm] and high capacity [maximum number of binding sites (B (max) ) = 362 fmol/mg protein]. The relative rank order of HA-ergic drugs to inhibit [(3) H]tiotidine binding to chick cerebrum was: antagonists - tiotidine >> aminopotentidine = ranitidine >or= zolantadine >> thioperamide - triprolidine; agonists - HA >or= 4-methylHA >> 2-methylHA >or=R alpha-methylHA - dimaprit. In conclusion, chick cerebral cortex contains H(2) -like HA receptors that are linked to the cAMP-generating system and are labelled with [(3) H]tiotidine. The pharmacological profile of these receptors is different from that described for their mammalian counterpart. It is suggested that the studied receptors represent either an avian-specific H(2) -like HA receptors or a novel subtype of HA receptors.

Adenylyl Cyclases↗

PubMed1980

Monoamines and related enzymes in cerebral cortex and basal ganglia following transient ischemia in gerbils.

The post-ischemic effects on cerebral cortex and basal ganglia monoamine levels and monoamine oxidase (MAO A and B) and catechol-O-methyl transferase (COMT) activities were evaluated in Mongolian gerbils (Meriones unguiculatus) subjected to bilateral common carotid arteries of occlusion for 15 min and reflow for 7 days. Disorders of monoamine metabolism was found in ischemic brain which persisted during the long-term post-ischemia. A rebound increase of norepinephrine and serotonin appeared in early stages (up to 1 h) of post-ischemia both in cerebral cortex and basal ganglia; a rebound increase of dopamine as found only in cerebral cortex. Thereafter, the serotonin level ws enhanced over the control level during the whole post-ischemic period whereas the levels of catecholamines were reduced particularly in basal ganglia. With respect to monoamine content and activities of monoamine degraded enzymes an oscillatory behavior was observed in the post-ischemia. Disorder of the monoamine metabolism found during post-ischemic period possibly contributes to neurological dysfunction after an ischemic insult.

Animals↗

PubMed1989

Cortical spectroscopy: localized spectroscopy of the cerebral cortex in rats.

A method for obtaining nuclear magnetic resonance (NMR) spectroscopic signals confined to the cerebral cortex in rat using a cortical coil constructed based on the principles of the zig-zag coil is described. We obtained 31P NMR spectra of normal cerebral cortex and cold-induced injured cortex using this cortical coil. The cortical coil clearly demonstrated an increase in inorganic phosphate (Pi) confirmed to cerebral cortex which, by contrast, the conventional planar surface coil failed to detect. There are significant metabolic differences between cortex and subcortical tissues. The technique described here, capable of assessing cortical metabolism in vivo without contamination by the underlying tissue, has substantial application to studies of cerebral metabolism.

Animals↗

PubMed1989

Serotonin innervation of the cerebral cortex in lizards.

The serotonin (5-HT) innervation of the cerebral cortex in two species of lizards has been studied. Results show no differences between both species. Most of the cerebral cortex of these lizards is innervated by serotoninergic fibers, which are fine and varicose. Their density varies greatly from one cortical region to another: the areas with higher density of serotoninergic fibers and terminals are parts of the medial and dorsal cortices. There is a laminar pattern of distribution of serotoninergic fibers. In the medial cortex, 5-HT fibers are found preferentially in both plexiform layers just above and below the cellular layer. In the dorsomedial cortex, there is an immunoreactive plexus in the outermost third of the superficial plexiform layer and another in the depth of the layer, whereas 5-HT fibers are distributed evenly in the deep plexiform layer of this cortex. In the pars medialis of the dorsal cortex, serotoninergic fibers are abundant in all layers, whereas in the pars lateralis, fibers are found predominantly in the external third of the superficial plexiform layer. The lateral cortex is almost devoid of immunoreactive fibers. These results show a different organization of the cortical serotonin innervation between lizards and turtles.

Animals↗

PubMed2003

[Increase of LTB4 level and expression of LTA4-hydrolase mRNA in lung tissue and cerebral cortex in asthmatic rats].

OBJECTIVE: To investigate antigen-induced changes of leukotriene B(4)(LTB(4))content and LTA(4)-hydrolase mRNA expression in lung tissue and cerebral cortex in sensitized rats. METHODS: The contents of LTB(4) in lung tissue and cerebral cortex homogenates and LTA(4)-hydrolase mRNA expression after antigen challenge by aerosol were respectively detected by reverse-phase high performance liquid chromatography(RP-HPLC) and semi-quantitative RT-PCR. RESULT: The LTB(4) levels in lung tissue and cerebral cortex homogenates in asthmatic rats were significantly higher than those in control (P%0.05), and LTA4-hydrolase mRNA expression was also increased in asthmatic group. Dexamethason(DXM, 0.5 mg/kg, i.p.) decreased the LTB(4) content and inhibited the LTA(4)-hydrolase mRNA expression significantly in asthmatic rats(P%0.05). CONCLUSION: LTB(4) content and LTA(4)-hydrolase mRNA expression in cerebral cortex and lung tissue are increased in asthmatic rats, and there may exist neuroimmunological cross-talking between central nervous system and lung tissue in asthma.

Animals↗