[Observations and considerations on the fine structure of capillaries of the cerebral cortex (with reference to cerebral edema and swelling)].
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Animals↗
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Results for “Cerebral Cortex”
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[Synergism between folic acid and strychnine at the level of the cerebral cortex and the cerebellar cortex].
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Animals↗
[Phospholipid and malondialdehyde content in the cerebral cortex of rats with incomplete ischemia and in the postischemic period].
During severe incomplete brain ischemia caused by combined bilateral ligation of the general carotid arteries and blood pressure reduction to 50 Hg by blood withdrawal from the femoral artery, the cortex of cerebral hemispheres demonstrates, by the 60th minute of ischemia, a 15.4%-lowering of the content of total phospholipids (PL) and a 33.3%-increase in the content of malonyl dialdehyde (MDA). By the 30th minute of the postischemic period the content of total PL remains decreased, the content of monophosphoinositides (MPI) rises by 110.2%, whereas the content of MDA remains high. By the 60th minute of postischemia the content of total PL and MDA returns to the initial levels. However the content of MDA remains high as before.
Animals↗
[Interrelationship between the auditory, parietal and sensomotor regions of the dog cerebral cortex during a defensive conditioned reflex].
Interrelations between projection (auditory), associative (parietal) and integrative-triggering (sensorimotor) cortical areas were studied in dogs by EP parameters and localization during formation of defensive conditioned reflex to clicks. These interrelations were studied in intact animals and after ablation of either T3 areas or PI2 area of the auditory cortex. It was found that in intact animals auditory cortical areas are constantly involved in brain integrations whereas parietal ones show periodical participation (EPs in the parietal cortical area accompany some pairings of signal stimulus with reinforcement). Integrative-triggering cortical structures are involved in the systemic processes in the period of stabilisation of defensive reaction. After ablation of T3 area integrative-triggering cortical structures are turned on within a large exitation system from the beginning of the defensive reaction formation. After ablation of PI2 area parietal areas constantly participate in brain integrations. The nature of their participation in the forming of a given functional system is determined by the state of the auditory system or location of its injury.
Animals↗
[Spectral-correlation analysis of high-frequency EEG components of the rabbit cerebral cortex during orienting and defensive responses].
A change was shown in the EEG power spectra of the sensorimotor, visual and auditory neocortical areas and the dorsal hippocampus, and corresponding coherence functions in the range of 14.6-110 c/s during an orienting reaction and the formation of a defensive conditioned reflex in rabbits. It was suggested that the rhythm of about 5 c/s appearing during formation of the conditioned reflex, serves for the functional integration of the brain structures which is specific for a certain functional state.
Animals↗
Topography of inhibitory actions from the cerebral cortex on the climbing fibre input to cerebellar Purkinje cells.
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Afferent Pathways↗
[Ultrastructure of the blood-brain barrier in the cerebral cortex in atherosclerotic dementia].
Ultrastructural changes of blood-brain barrier elements were studied in the cortex of cerebral superior frontal and medial temporal gyri in atherosclerotic dementia. Destructive changes in endotheliocytes, pericytes, basement membrane and increase in number, swelling and edema of astrocyte peduncles with the inconstant approximation of astrocyte body to the capillary basement membrane were demonstrated along with signs of blood circulation decline in cortical capillaries. Lipofuscin and lipids accumulation and aggregation of homogenous material of high electron density, probably plasma proteins, were characteristic for changes in blood-brain barrier in atherosclerotic dementia, which is important in pathogenesis of this type of the disease.
Aged↗
Cerebral cortex ammonia and glutamine metabolism in two rat models of chronic liver insufficiency-induced hyperammonemia: influence of pair-feeding.
Enhanced cerebral cortex ammonia uptake, subsequent glutamine synthesis, and glutamine release into the bloodstream have been hypothesized to deplete cerebral cortex glutamate pools. We investigated this hypothesis in rats with chronic liver insufficiency-induced hyperammonemia and in pair-fed controls to rule out effects of differences in food intake. Cerebral cortex plasma flow and venous-arterial concentration differences of ammonia and amino acids, as well as cerebral cortex tissue concentrations, were studied 7 and 14 days after surgery in portacaval-shunted/bile duct-ligated, portacaval-shunted, and sham-operated rats, while the latter two were pair-fed to the first group, and in normal unoperated ad libitum-fed control rats. At both time points, arterial ammonia was elevated in the chronic liver insufficiency groups and arterial glutamine was elevated in portacaval shunt/biliary obstruction rats compared to the other groups. In the chronic liver insufficiency groups net cerebral cortex ammonia uptake was observed at both time points and was accompanied by net glutamine release. Also in these groups, cerebral cortex tissue glutamine, many other amino acid, and ammonia levels were elevated. Tissue glutamate levels were decreased to a similar level in all operated groups compared with normal unoperated rats, irrespective of plasma and tissue ammonia and glutamine levels. These results demonstrate that during chronic liver insufficiency-induced hyperammonemia, the rat cerebral cortex enhances net ammonia uptake and glutamine release. However, the decrease in tissue glutamate concentrations in these chronic liver insufficiency models seems to be related primarily to nutritional status and/or surgical trauma.
Amino Acids↗
Age-related increase in presynaptic noradrenergic markers of the rat cerebral cortex.
Age-related alterations in the noradrenergic innervation of the cerebral cortex were investigated in young (3-4 months) and aged (28-29 months) Fischer-344 rats. The concentration of noradrenaline and the activity of tyrosine hydroxylase, the probable rate-limiting step in catecholamine biosynthesis, were significantly higher in the aged cerebral cortex, but no differences in L-3,4-dihydroxyphenylalanine decarboxylase activity were observed. The specific high-affinity uptake of noradrenaline by homogenates of the aged cerebral cortex exhibited higher maximal uptake, but lower affinity, than those of young rats. These results suggest increased presynaptic noradrenergic activity in the cerebral cortex of aged Fischer-344 rats.
Aging↗
Expression and potential role of phospholipase D1 in cryoinjured cerebral cortex of rats.
The expression and potential role of phospholipase D1 (PLD1) were studied in the cerebral cortex of rats after freeze injury. Histopathologically, cryoinjury, by exposing cerebral cortex to a prechilled rod for 1 minute, produced consistent pathological lesions, specifically neuronal death, infiltration of macrophages into the center of the cryoinjury, and reactive astrogliosis at the periphery, which caused the lesion site to become encased. Western blot analysis showed that PLD1 expression in the ipsilateral cerebral cortex increased significantly during days 1 to 3 after cryoinjury and declined slightly at post-injury day 7. PLD1 immunoreactivity was very low in the brains of sham-operated control adults. After cryoinjury, there was substantial PLD1 immunostaining of numerous inflammatory cells in the ipsilateral cortex, which were identical to ED1-positive macrophages. In addition, PLD1 immunoreactivity was increased in some neurons and astrocytes at the periphery of the cryoinjury at post-injury days 3 and 7. These findings suggest that cryoinjury by means of prechilled rods induced consistent histopathological changes in the cerebral cortex. In addition, expression of a cell activation signal, PLD1, was upregulated in macrophages and astrocytes in the ipsilateral cerebral cortex after cryoinjury.
Animals↗
Investigation of the subtypes of alpha2-adrenoceptor mediating prejunctional inhibition in rat atrium and cerebral cortex.
We have investigated the subtype of alpha2-adrenoceptor mediating prejunctional inhibition of neurotransmission in rat atrium in comparison with the alpha2-adrenoceptor mediating prejunctional inhibition in rat cerebral cortex. In rat atrium and cerebral cortex, prejunctional alpha2-adrenoceptors were investigated in terms of the ability of alpha2-adrenoceptor antagonists to increase the stimulation-evoked overflow of tritium in tissues pre-incubated with [3H]-noradrenaline. The relatively non-selective alpha2-adrenoceptor antagonist yohimbine and the alpha2D-adrenoceptor selective antagonist BRL 44408 had potencies in rat atrium which were similar to their potencies in rat cerebral cortex. The antagonists ARC 239, HV 723, WB 4101, prazosin, chlorpromazine and abanoquil, which have low affinity for alpha2D-adrenoceptors, significantly increased stimulation-evoked overflow at lower concentrations in rat atrium than rat cerebral cortex. Antagonist potency at prejunctional alpha2-adrenoceptors was correlated with antagonist affinity at alpha2-adrenoceptor ligand binding sites in membranes of rat kidney (alpha2B) and submandibular gland (alpha2D), and human recombinant alpha2C-adrenoceptors labelled with [3H]yohimbine. The correlation between ligand binding sites and the functional receptor in the rat cerebral cortex was significant only for the alpha2D-adrenoceptor ligand binding site (r=0.87, n=8, P<0.01) as compared to the alpha2B-adrenoceptor (r=0.32, n.s.) or alpha2C-adrenoceptor (r=0.12, n.s.) ligand binding sites. The correlation between ligand binding sites and the functional receptor in the rat atrium was not significant for any ligand binding site, with r=0.64, 0.68 and 0.67 for the alpha2D-, the alpha2B- and the alpha2C-adrenoceptor ligand binding sites, respectively. It is concluded that the functional prejunctional alpha2-adrenoceptor of rat cerebral cortex closely resembles the alpha2D-adrenoceptor ligand binding site of rat submandibular gland, but the rat atrium may contain two subypes of prejunctional alpha2-adrenoceptor, alpha2D and another subtype, possibly alpha2B or alpha2C.
Adrenergic alpha-2 Receptor Antagonists↗
A study of sensory projection from jaw muscles to the cerebral cortex in the rat.
The sensory projection from jaw muscles to the cerebral cortex have been studied in rats by electrophysiological and histochemical methods. Electrical stimulation of individual masticatory muscles elicited bilateral responses in the cortical areas 8, 10, 2, and 2a. The following pathway was postulated to mediate these cortical responses; impulses of muscle origin are conducted in turn to the trigeminal mesencephalic tract nucleus (TMT), the contralateral thalamic nucleus ventralis posteromedialis (VPM), the cerebral cortex and finally to the other cerebral cortex which is ipsilateral to the side of stimulation. The ipsilateral cortical response appeared about 5 msec later than the contralateral one and was abolished by sectioning the corpus callosum. By stimulating the cerebral cortex antidromically, the conduction time to the VPM was found to be as long as 6 msec. The conduction from the TMT to the contralateral VPM consumed a period of more than 10 msec. It was presumed to be multisynaptic, being based on the finding that horseradish peroxidase injected into the VPM could not be recovered in the contralateral TMT.
Afferent Pathways↗
[The effects of cholecystokinin octapeptide on PKC activity in rat cerebral cortex neurocytes].
OBJECTIVE: To investigate the effects of CCK8 on protein kinase C activity in rat cerebral cortex. METHODS: The cerebral cortex neurocytes were isolated and used as a model. The effects of CCK8, L-364, 718 and L-365, 260 on PKC activities were detected by using a non-radioactive method. RESULTS: CCK8 caused a detectable increase in PKC activity at 10(-11) mol/L, and a peak increase of PKC activity was observed at 10(-5) mol/L (about 4.5 U/mg protein). PKC activity was increased in dose-dependent manner by CCK8(10(-11)-10(-6) mol/L). The CCKB-selective receptor antagonist L-365, 260 with a higher efficiency, and the CCKA-selective receptor antagonist L-364, 718 with a lower efficiency were able to block a maximal effect of CCK8-induced PKC activation. CONCLUSIONS: CCK8 may regulate PKC activities in rat cerebral cortex through CCKB receptor.
Animals↗
Enhancement of [m-methoxy 3H]MDL100907 binding to 5HT2A receptors in cerebral cortex and brain stem of streptozotocin induced diabetic rats.
5-Hydroxytryptamine2A (5-HT2A) receptor kinetics was studied in cerebral cortex and brain stem of streptozotocin (STZ) induced diabetic rats. Scatchard analysis with [3H] (+/-) 2,3dimethoxyphenyl-1-[2-(4-piperidine)-methanol] ([3H]MDL100907) in cerebral cortex showed no significant change in maximal binding (Bmax) in diabetic rats compared to controls. Dissociation constant (Kd) of diabetic rats showed a significant decrease (p < 0.05) in cerebral cortex, which was reversed to normal by insulin treatment. Competition studies of [3H]MDL100907 binding in cerebral cortex with ketanserin showed the appearance of an additional low affinity site for 5-HT2A receptors in diabetic state, which was reversed to control pattern by insulin treatment. In brain stem, scatchard analysis showed a significant increase (p < 0.05) in Bmax accompanied by a significant increase (p < 0.05) in Kd. Competition analysis in brain stem also showed a shift in affinity towards a low affinity State for 5-HT2A receptors. All these parameters were reversed to control level by insulin treatment. These results show that in cerebral cortex there is an increase in affinity of 5-HT2A receptors without any change in its number and in the case of brain stem there is an increase in number of 5HT2A receptors accompanied by a decrease in its affinity during diabetes. Thus, from the results we suggest that the increase in affinity of 5-HT2A receptors in cerebral cortex and upregulation of 5-HT2A receptors in brain stem may lead to altered neuronal function in diabetes.
Animals↗
Redistribution of synaptic vesicle antigens is correlated with the disappearance of a transient synaptic zone in the developing cerebral cortex.
To examine the distribution of synaptic vesicle antigens during development of the cerebral cortex, antibodies against synapsin I and p65 were used on sections of cat cerebral cortex between E40 and adulthood. In the adult, the layers of the cerebral cortex are immunoreactive for each of these antigens, while the white matter is free of staining. In contrast, the fetal and neonatal pattern of immunostaining is reversed: the cortical plate (future cortical layers) is devoid of immunoreactivity, while the marginal (future layer 1) and the intermediate zones (future white matter) are stained. Electron microscopic immunohistochemistry shows that immunolabeling is associated with presynaptic nerve terminals in the adult and during development. These observations suggest that during development the white matter is a transient synaptic neuropil and that a global redistribution of synapses takes place as the mature pattern of connections within the cerebral cortex emerges.
Aging↗
A fibronectin-like molecule is present in the developing cat cerebral cortex and is correlated with subplate neurons.
The subplate is a transient zone of the developing cerebral cortex through which postmitotic neurons migrate and growing axons elongate en route to their adult positions within the cortical plate. To learn more about the cellular interactions that occur in this zone, we have examined whether fibronectins (FNs), a family of molecules known to promote migration and elongation in other systems, are present during the fetal and postnatal development of the cat's cerebral cortex. Three different anti-FN antisera recognized a single broad band with an apparent molecular mass of 200-250 kD in antigen-transfer analyses (reducing conditions) of plasma-depleted (perfused) whole fetal brain or synaptosome preparations, indicating that FNs are present at these ages. This band can be detected as early as 1 mo before birth at embryonic day 39. Immunohistochemical examination of the developing cerebral cortex from animals between embryonic day 46 and postnatal day 7 using any of the three antisera revealed that FN-like immunoreactivity is restricted to the subplate and the marginal zones, and is not found in the cortical plate. As these zones mature into their adult counterparts (the white matter and layer 1 of the cerebral cortex), immunostaining gradually disappears and is not detectable by postnatal day 70. Previous studies have shown that the subplate and marginal zones contain a special, transient population of neurons (Chun, J. J. M., M. J. Nakamura, and C. J. Shatz. 1987. Nature (Lond.). 325:617-620). The FN-like immunostaining in the subplate and marginal zone is closely associated with these neurons, and some of the immunostaining delineates them. Moreover, the postnatal disappearance of FN-like immunostaining from the subplate is correlated spatially and temporally with the disappearance of the subplate neurons. When subplate neurons are killed by neurotoxins, FN-like immunostaining is depleted in the lesioned area. These observations show that an FN-like molecule is present transiently in the subplate of the developing cerebral cortex and, further, is spatially and temporally correlated with the transient subplate neurons. The presence of FNs within this zone, but not in the cortical plate, suggests that the extracellular milieu of the subplate mediates a unique set of interactions required for the development of the cerebral cortex.
Animals↗
Structural organization of the human cerebral cortex prior to the appearance of the cortical plate.
The early development and the structural organization of the human cerebral cortex, prior to the appearance of the cortical plate (Carnegie stage 22, ca. 54 days), was studied in two embryos: 43 (stage 18) and 50 day old (stage 20), respectively. It has been shown that the human cerebral cortex begins its ontogenetic development around the sixth rather than around the eighth week of gestation as it has been previously assumed. The human cerebral cortex starts to develop soon after the cerebral vesicles have been formed (stage 15) and a primitive internal capsule has been established (stage 17, ca. 41 days). By stage 18 of human development fibres from this primitive internal capsule have reached and probably have penetrated into the developing cerebral vesicle, through its more superficial zone. Fibres from this primitive internal capsule have been traced backward through the ventral thalamus to the mesencephalic tegmentum. The possible existence of primitive ascending fibres from the mid-brain which terminate in the superficial zone of the developing cerebral cortex (tegmento-thalamostriato-cortical tract) is suggested. The arrival of these primitive corticipetal fibres establishes in the outer zone of the cerebral cortex a primordial plexiform lamina or an external white matter. Horizontal-bipolar cells (embryonic Cajal-Retzius neurons) begin to differentiate by stage 18 of human development (43 days in our case). By stage 20 (50 days in our case), the primordial plexiform lamina is well established, extends throughout the entire surface of the developing cerebral cortex, and is considered to be functionally active. It is, by this age, a superficial, 40 micrometers thick, complex fibrillar neuronal organization composed of numerous horizontal corticipetal fibres (demonstrable with silver methods), horizontal-bipolar Cajal-Retzius neurons and a few other, less defined, cellular elements. This primordial plexiform lamina is considered to represent a primitive "premammalian" cortical organization. The next event in cortical ontogenesis is the appearance of the cortical plate or the mammalian neocortical grey at stage 22 (ca. 54 days). Migrating neuroblasts attracted toward the preexisting primordial plexiform lamina and guided by glial fibres start to accumulate within it.(ABSTRACT TRUNCATED AT 400 WORDS)
Cell Movement↗
Rabbit cerebral cortex 5HT1a receptors.
Selective 5HT1a agonist binding to membranes from rabbit cerebral cortex was concentration-dependent and saturable; the Kd was 1.1 nM and Bmax of 480 fmols/mg protein. Scatchard as well as Hill plots were linear; the Hill coefficient was 0.96, suggesting a single, non-interacting binding site. Agonist binding was inhibited in a concentration-dependent fashion by gamma S GTP, a result consistent with the coupling of this binding site to the G protein signal transduction system. In competition experiments involving agonist and a series of agents with known affinities and specificities at 5HT1a receptors, a rank order relationship was found consistent with this binding site being a 5HT1a binding site. Direct comparisons of agonist and antagonist binding at rat cerebral cortex 5HT1a receptors and cloned human 5HT1a receptors also suggested that the rabbit binding site belongs to the 5HT1a class. The only rank order anomalies were with methiothepin in rabbit cerebral cortex, where a comparatively high Ki was observed and with buspirone in cloned human 5HT1a receptor, where a low Ki was determined; these anomalies bear further study in light of the comparative pharmacology of 5HT1a receptors. Finally, the natural product parthenolide was tested for affinity in the rabbit, rat, and human systems, where it uniformly was unable to displace agonist, suggesting that the 5HT1a receptor is not a target for this compound. Overall, these results suggest that a functional 5HT1a receptor exists in rabbit cerebral cortex.
8-Hydroxy-2-(di-n-propylamino)tetralin↗