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Journal articles on the topic 'Cerebral cortex'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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1

Cowey, A. "Cerebral cortex, functional properties of the cerebral cortex." Neuroscience 17, no. 4 (April 1986): 1297–98. http://dx.doi.org/10.1016/0306-4522(86)90096-5.

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2

Kaufman, K. J. "The Cerebral Cortex: Visual Cortex." Archives of Ophthalmology 104, no. 8 (August 1, 1986): 1141. http://dx.doi.org/10.1001/archopht.1986.01050200047040.

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3

Innocenti, Giorgio M. "Cerebral Cortex, Vol. 7. Development and Maturation of Cerebral Cortex." Trends in Neurosciences 13, no. 1 (January 1990): 36–37. http://dx.doi.org/10.1016/0166-2236(90)90061-e.

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4

Cowey, A. "Cerebral cortex, vol. 1 cellular components of the cerebral cortex." Neuroscience 15, no. 1 (May 1985): 309. http://dx.doi.org/10.1016/0306-4522(85)90137-x.

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5

Cowey, A. "Cerebral Cortex, Vol. 3, Visual Cortex." Neuroscience 19, no. 3 (November 1986): 1023. http://dx.doi.org/10.1016/0306-4522(86)90314-3.

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6

Hughes, John R. "Cerebral cortex. Vol. 3. Visual cortex." Electroencephalography and Clinical Neurophysiology 63, no. 4 (April 1986): 392. http://dx.doi.org/10.1016/0013-4694(86)90029-5.

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7

Molnár, Zoltán, and Gavin Clowry. "Human cerebral cortex development." Journal of Anatomy 235, no. 3 (August 21, 2019): 431. http://dx.doi.org/10.1111/joa.13000.

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8

Anderson, Mark. "A more cerebral cortex." IEEE Spectrum 47, no. 1 (January 2010): 58–63. http://dx.doi.org/10.1109/mspec.2010.5372504.

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9

Carlson, Chad, and Orrin Devinsky. "The excitable cerebral cortex." Epilepsy & Behavior 15, no. 2 (June 2009): 131–32. http://dx.doi.org/10.1016/j.yebeh.2009.03.002.

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10

Schneider, Julie A. "The cerebral cortex in cerebral amyloid angiopathy." Lancet Neurology 15, no. 8 (July 2016): 778–79. http://dx.doi.org/10.1016/s1474-4422(16)30100-4.

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11

Huxlin, Krystel R. "Cerebral Cortex: Extrastriate Cortex in Primates (Vol. 12)." Trends in Neurosciences 21, no. 11 (November 1998): 499. http://dx.doi.org/10.1016/s0166-2236(98)01321-6.

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12

Yokote, Hideyoshi, Toru Itakura, Kunio Nakai, Ichiro Kamei, Harumichi Imai, and Norihiko Komai. "A role of the central catecholamine neuron in cerebral circulation." Journal of Neurosurgery 65, no. 3 (September 1986): 370–75. http://dx.doi.org/10.3171/jns.1986.65.3.0370.

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✓ The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 ± 2.8 ml/100 gm/min; control cortex 38.5 ± 3.5 ml/100 gm/min; p < 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10−5 M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% ± 0.67%/mm Hg; control cortex 3.53% ± 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.
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13

Snyder, L. R., R. Cruz-Aguado, M. Sadilek, D. Galasko, C. A. Shaw, and T. J. Montine. "LACK OF CEREBRAL BMAA IN HUMAN CEREBRAL CORTEX." Neurology 72, no. 15 (April 13, 2009): 1360–61. http://dx.doi.org/10.1212/wnl.0b013e3181a0fed1.

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14

Van Essen, David C., Chad J. Donahue, and Matthew F. Glasser. "Development and Evolution of Cerebral and Cerebellar Cortex." Brain, Behavior and Evolution 91, no. 3 (2018): 158–69. http://dx.doi.org/10.1159/000489943.

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Cerebral cortex and cerebellar cortex both vary enormously across species in their size and complexity of convolutions. We discuss the development and evolution of cortical structures in terms of anatomy and functional organization. We propose that the distinctive shapes of cerebral and cerebellar cortex can be explained by relatively few developmental processes, notably including mechanical tension along axons and dendrites. Regarding functional organization, we show how maps of myelin content in cerebral cortex are evolutionarily conserved across primates but differ in the proportion of cortex devoted to sensory, cognitive, and other functions. We summarize recent progress and challenges in (i) parcellating cerebral cortex into a mosaic of distinct areas, (ii) distinguishing cortical areas that correspond across species from those that are present in one species but not another, and (iii) using this information along with surface-based interspecies registration to gain deeper insights into cortical evolution. We also comment on the methodological challenges imposed by the differences in anatomical and functional organization of cerebellar cortex relative to cerebral cortex.
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15

Berger, Mitchel S., and Costas G. Hadjipanayis. "SURGERY OF INTRINSIC CEREBRAL TUMORS." Neurosurgery 61, suppl_1 (July 1, 2007): SHC—279—SHC—305. http://dx.doi.org/10.1227/01.neu.0000255489.88321.18.

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Abstract TUMORS AND OTHER structural lesions located with and adjacent to the cerebral cortex present certain challenges in terms of the overall management and design of surgical strategies. This comprehensive analysis attempts to define the current understanding of cerebral localization and function and includes the latest advances in functional imaging, as well as surgical technique, including localization of tumors and neurophysiological mapping to maximize extent of resection while minimizing morbidity. Finally, it remains to be seen whether or not stimulation mapping will be the most useful way to identify function within the cortex in the future. Another potential paradigm would be to actually record baseline oscillatory rhythms within the cortex and, following presentation of a given task, determine if those rhythms are disturbed enough to identify eloquent cortex as a means of functional localization. This would be a paradigm shift away from stimulation mapping, which currently deactivates the cortex, as opposed to identifying an activation function which identifies functional cortex.
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16

Jones, Edward G. "Neurotransmitters in the cerebral cortex." Journal of Neurosurgery 65, no. 2 (August 1986): 135–53. http://dx.doi.org/10.3171/jns.1986.65.2.0135.

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✓ This article surveys the conventional neurotransmitters and modulatory neuropeptides that are found in the cerebral cortex and attempts to place them into the perspective of both intracortical circuitry and cortical disease. The distribution of these substances is related, where possible, to particular types of cortical neuron or to afferent or efferent fibers. Their physiological actions, where known, on cortical neurons are surveyed, and their potential roles in disease states such as the dementias, epilepsy, and stroke are assessed. Conventional transmitters that occur in afferent fibers to the cortex from brain-stem and basal forebrain sites are: serotonin, noradrenaline, dopamine, and acetylcholine. All of these except dopamine are distributed to all cortical areas: dopamine is distributed to frontal and cingulate areas only. The transmitter in thalamic afferent systems is unknown. Gamma aminobutyric acid (GABA) is the transmitter used by the majority of cortical interneurons and has a profound effect upon the shaping of receptive field properties. The vast majority of the known cortical peptides are found in GABAergic neurons, and the possibility exists that they may act as trophic substances for other neurons. Levels of certain neuropeptides decline in cases of dementia of cortical origin. Acetylcholine is the only other known transmitter of cortical neurons. It, too, is contained in neurons that also contain a neuropeptide. The transmitter(s) used by excitatory cortical interneurons and by the efferent pyramidal cells is unknown, but it may be glutamate or aspartate. It is possible that excitotoxins released in anoxic disease of the cortex may produce damage by acting on receptors for these or related transmitter agents.
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17

Hoshide, Reid, and Rahul Jandial. "Human Cerebral Cortex Map 2.0." Neurosurgery 79, no. 6 (December 2016): N16—N17. http://dx.doi.org/10.1227/01.neu.0000508603.53941.07.

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18

Morrison, John H. "Aging and Mammalian Cerebral Cortex." Alzheimer Disease & Associated Disorders 17, Sup 2 (April 2003): S51—S53. http://dx.doi.org/10.1097/00002093-200304002-00006.

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19

Xie, Yu-feng, Fu-quan Huo, and Jing-shi Tang. "Cerebral cortex modulation of pain." Acta Pharmacologica Sinica 30, no. 1 (December 15, 2008): 31–41. http://dx.doi.org/10.1038/aps.2008.14.

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20

Weber, John T., Kenneth Hayataka, Mary-Frances O'Connor, and Keith K. Parker. "Rabbit Cerebral Cortex 5HT1a Receptors." Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology 117, no. 1 (May 1997): 19–24. http://dx.doi.org/10.1016/s0742-8413(97)00614-2.

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21

Kötter, Rolf, Klaas E. Stephan, Nicola Palomero-Gallagher, Stefan Geyer, Axel Schleicher, and Karl Zilles. "Multivariate parcellation of cerebral cortex." NeuroImage 13, no. 6 (June 2001): 178. http://dx.doi.org/10.1016/s1053-8119(01)91521-6.

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22

FOSTER, JOAQUIN M. "Memory in the Cerebral Cortex." Journal of Nervous and Mental Disease 184, no. 6 (June 1996): 385–86. http://dx.doi.org/10.1097/00005053-199606000-00014.

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23

Ragsdale, Clifton W., and Elizabeth A. Grove. "Patterning the mammalian cerebral cortex." Current Opinion in Neurobiology 11, no. 1 (February 2001): 50–58. http://dx.doi.org/10.1016/s0959-4388(00)00173-2.

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24

Grove, Elizabeth A. "Patterning the developing cerebral cortex." Current Biology 2, no. 3 (March 1992): 142–44. http://dx.doi.org/10.1016/0960-9822(92)90259-d.

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25

Sur, Mriganka, and Alan Cowey. "Cerebral cortex: Function and development." Neuron 15, no. 3 (September 1995): 497–505. http://dx.doi.org/10.1016/0896-6273(95)90139-6.

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26

Swindale, N. V. "Is the cerebral cortex modular?" Trends in Neurosciences 13, no. 12 (December 1990): 487–92. http://dx.doi.org/10.1016/0166-2236(90)90082-l.

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27

Miller, Kenneth D. "Canonical computations of cerebral cortex." Current Opinion in Neurobiology 37 (April 2016): 75–84. http://dx.doi.org/10.1016/j.conb.2016.01.008.

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28

Jones, E. G. "Microcolumns in the cerebral cortex." Proceedings of the National Academy of Sciences 97, no. 10 (May 9, 2000): 5019–21. http://dx.doi.org/10.1073/pnas.97.10.5019.

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29

Bourouis, Sami. "Local Analysis of Cerebral Cortex." International Journal of Computer Applications 47, no. 11 (June 30, 2012): 10–16. http://dx.doi.org/10.5120/7230-0116.

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30

Szentágothai, J. "Cajal on the cerebral cortex." Neuroscience 36, no. 2 (January 1990): 569–70. http://dx.doi.org/10.1016/0306-4522(90)90446-b.

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31

Kenshalo, Dan R. "The cerebral cortex and pain." Pain 30 (1987): S331. http://dx.doi.org/10.1016/0304-3959(87)91723-4.

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32

Luján, Rafael. "Acetylcholine in the Cerebral Cortex." Journal of Chemical Neuroanatomy 27, no. 4 (July 2004): 283. http://dx.doi.org/10.1016/j.jchemneu.2004.04.002.

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33

Diamond, Marian Cleeves. "Sex and the cerebral cortex." Biological Psychiatry 25, no. 7 (April 1989): 823–25. http://dx.doi.org/10.1016/0006-3223(89)90261-8.

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34

Takao, Hidemasa, Osamu Abe, and Kuni Ohtomo. "Computational analysis of cerebral cortex." Neuroradiology 52, no. 8 (May 18, 2010): 691–98. http://dx.doi.org/10.1007/s00234-010-0715-4.

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35

Swindale, Nicholas V. "Cerebral Cortex: The Singular Precision of Visual Cortex Maps." Current Biology 16, no. 23 (December 2006): R991—R994. http://dx.doi.org/10.1016/j.cub.2006.10.039.

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36

Hamdy, Shaheen, John C. Rothwell, David J. Brooks, Dale Bailey, Qasim Aziz, and David G. Thompson. "Identification of the Cerebral Loci Processing Human Swallowing With H2 15O PET Activation." Journal of Neurophysiology 81, no. 4 (April 1, 1999): 1917–26. http://dx.doi.org/10.1152/jn.1999.81.4.1917.

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Identification of the cerebral loci processing human swallowing with H2 15O PET activation. Lesional and electrophysiological data implicate a role for the cerebral cortex in the initiation and modulation of human swallowing, and yet its functional neuroanatomy remains undefined. We therefore conducted a functional study of the cerebral loci processing human volitional swallowing with 15O-labeled water positron emission tomography (PET) activation imaging. Regional cerebral activation was investigated in 8 healthy right handed male volunteers with a randomized 12-scan paradigm of rest and water swallows (5 ml/bolus, continuous infusion) at increasing frequencies of 0.1, 0.2, and 0.3 Hz, which were visually cued and monitored with submental electromyogram (EMG). Group and individual linear covariate analyses were performed with SPM96. In five of eight subjects, the cortical motor representation of pharynx was subsequently mapped with transcranial magnetic stimulation (TMS) in a posthoc manner to substantiate findings of hemispheric differences in sensorimotor cortex activation seen with PET. During swallowing, group PET analysis identified increased regional cerebral blood flow (rCBF) ( P < 0.001) within bilateral caudolateral sensorimotor cortex [Brodmann’s area (BA) 3, 4, and 6], right anterior insula (BA 16), right orbitofrontal and temporopolar cortex (BA 11 and 38), left mesial premotor cortex (BA 6 and 24), left temporopolar cortex and amygdala (BA 38 and 34), left superiomedial cerebellum, and dorsal brain stem. Decreased rCBF ( P < 0.001) was also observed within bilateral posterior parietal cortex (BA 7), right anterior occipital cortex (BA 19), left superior frontal cortex (BA 8), right prefrontal cortex (BA 9), and bilateral superiomedial temporal cortex (BA 41 and 42). Individual PET analysis revealed asymmetric representation within sensorimotor cortex in six of eight subjects, four lateralizing to right hemisphere and two to left hemisphere. TMS mapping in the five subjects identified condordant interhemisphere asymmetries in the motor representation for pharynx, consistent with the PET findings. We conclude that volitional swallowing recruits multiple cerebral regions, in particular sensorimotor cortex, insula, temporopolar cortex, cerebellum, and brain stem, the sensorimotor cortex displaying strong degrees of interhemispheric asymmetry, further substantiated with TMS. Such findings may help explain the variable nature of swallowing disorders after stroke and other focal lesions to the cerebral cortex.
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37

Nunes, Ana R., Marco G. Alves, Gonçalo D. Tomás, Vanessa R. Conde, Ana C. Cristóvão, Paula I. Moreira, Pedro F. Oliveira, and Branca M. Silva. "Daily consumption of white tea (Camellia sinensis (L.)) improves the cerebral cortex metabolic and oxidative profile in prediabetic Wistar rats." British Journal of Nutrition 113, no. 5 (February 26, 2015): 832–42. http://dx.doi.org/10.1017/s0007114514004395.

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Diabetes mellitus (DM) is a major public health problem and its incidence is rising dramatically. The brain, particularly the cerebral cortex, is very susceptible to glucose fluctuations and hyperglycaemia-induced oxidative stress. Tea (Camellia sinensis (L.)) is widely consumed; however, the antidiabetic properties of white tea remain largely unexplored. In the present study, we investigated the effects of daily consumption of white tea on the cerebral cortex of prediabetic rats. The cerebral cortex metabolic profile was evaluated, and the expression levels of GLUT, phosphofructokinase-1, lactate dehydrogenase (LDH) and monocarboxylate transporter 4 were assessed. LDH activity was also determined. The cerebral cortex oxidative profile was determined by evaluating its antioxidant power, lipid peroxidation and protein oxidation levels. Catalase, glutathione, glutamate, N-acetylaspartate, aspartate, choline, γ-aminobutyric acid, taurine and valine contents were determined. Daily consumption of white tea ameliorated glucose tolerance and insulin sensitivity. Moreover, white tea altered the cortex glycolytic profile, modulating GLUT expression and lactate and alanine contents. Finally, white tea consumption restored protein oxidation and lipid peroxidation levels and catalase expression, and improved antioxidant capacity. In conclusion, daily consumption of white tea improved the cerebral cortex metabolic and oxidative profile in prediabetic rats, suggesting it as a good, safe and inexpensive strategy to prevent DM-related effects in the cerebral cortex.
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38

Dedman, D. J., A. Treffry, J. M. Candy, G. A. A. Taylor, C. M. Morris, C. A. Bloxham, R. H. Perry, J. A. Edwardson, and P. M. Harrison. "Iron and aluminium in relation to brain ferritin in normal individuals and Alzheimer's-disease and chronic renal-dialysis patients." Biochemical Journal 287, no. 2 (October 15, 1992): 509–14. http://dx.doi.org/10.1042/bj2870509.

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Ferritin has been isolated and its subunit composition, iron and aluminium content determined in the cerebral cortex and cerebellum of normal individuals and in the cerebral cortex of Alzheimer's-disease and renal-dialysis patients. An e.l.i.s.a. for ferritin has been developed and the ferritin, non-haem iron and aluminium content of the parietal cortex were determined in normal individuals and Alzheimer's-disease patients. It was found that ferritin from the cerebral cortex and cerebellum of normal individuals had a high H-subunit content, similar to that of heart ferritin. The subunit composition of ferritin isolated from the cerebral cortex was not significantly altered in Alzheimer's-disease or renal-dialysis patients. Ferritin from the cerebral cortex of normal individuals had only approx. 1500 atoms of iron per molecule and the iron content of ferritin was not significantly changed in Alzheimer's-disease or renal-dialysis patients. Ferritin isolated from the cerebral cortex of normal, Alzheimer's-disease and renal-dialysis patients had less than 9 atoms of aluminium per molecule. The failure to find increased concentrations of aluminium associated with ferritin in dialysis patients, who had markedly increased concentrations of aluminium in the cerebral cortex, shows that aluminium does not accumulate in ferritin in vivo. This has important implications for the toxicity of aluminium, since it implies that cells are unable to detoxify aluminium by the same mechanism as that available for iron. Comparison of the concentrations of ferritin, aluminium and iron in the parietal cortex from normal and Alzheimer's-disease patients showed that, whereas the concentration of aluminium was not increased, both ferritin and iron were significantly increased in Alzheimer's disease.
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39

Guseinov, A. G., and Kh B. Mammadov. "The effect of hypoxia on the total electrical activity of the developing cerebral cortex." Azerbaijan Journal of Physiology, no. 1 (June 30, 2023): 57–64. http://dx.doi.org/10.59883/ajp.16.

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Hypoxia in the nervous system causes morphofunctional changes, which are reflected in the total activity of the cerebral cortex. Lack of oxygen leads to a change in all EEG indicators of the developing cerebral cortex, as well as the appearance of pathological activity in it. This review article summarizes and analyzes data on the effect of hypoxia in early ontogenesis on the total activity of the cerebral cortex.
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40

Kuznetsova, Tat'yana Ivanovna, Elena Vasil'evna Slesareva, Kirill Evgen'evich Nikishin, Malikat Magomedalievna Gadzhiarslanova, and Alina Alekseevna Vlasova. "CYTOMETRIC PARAMETERS OF CEREBRAL CORTEX NEURONS IN COVID-19." Ulyanovsk Medico-biological Journal, no. 3 (September 29, 2023): 122–30. http://dx.doi.org/10.34014/2227-1848-2023-3-122-130.

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COVID-19 has recently been one of the greatest challenges of public health services worldwide. SARS-CoV-19 affects not only the respiratory, but also other systems, including the brain. It causes strokes, meningitis, encephalopathy, encephalitis, etc. Due to the multifactorial nature and complexity of COVID-19 pathogenesis, studying its impact on brain tissue is relevant. The aim of the work is to study the cytometric parameters of neurons in the parietal-occipital lobe of the cerebral cortex in patients who died due to COVID-19. Materials and Methods. For histomorphological examination, autopsies of the parietal-occipital lobe of the cerebral cortex were fixed in 10 % neutral formalin and embedded in paraffin. Cross sections (5–6 μm) were stained with hematoxylin-eosin. Histologic specimens were studied under a light microscope. Morphometric measurements of the nucleus and cytoplasm area of neurons of the parietal-occipital lobe of the cerebral cortex were performed on the images. The nuclear-cytoplasmic ratio was calculated. The results of the histomorphological study were analyzed along with the medical history. For comparison, autopsies of the parietal-occipital lobe of the cerebral cortex from patients who died from cerebral infarction were used. Results. Nucleus and cytoplasm areas of neurons in the pyramidal and ganglionic layers of the cerebral cortex were measured. In the cerebral cortex, COVID-19 mainly affects the microvasculature vessels, disrupting their permeability and causing hemorrhages. Damage to the neurons of the cerebral cortex is less pronounced and does not have any specific pathomorphological picture, which corresponds to the pattern of long-term ischemic effects on the gray matter.
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41

L.I, Bon, Maksimovich N.Ye, Dremza I.K., and Lychkovskaya Maria A. "Stepwise Cerebral Ischemia Causes Disturbances in Mitochondrial Respiration of Neurons in the Cerebral Cortex of Rats." Biotechnology and Bioprocessing 3, no. 1 (January 5, 2022): 01–05. http://dx.doi.org/10.31579/2766-2314/063.

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Objectives: To conduct a comparative analysis of respiration of mitochondria of brain homogenates of rats with stepwise subtotal cerebral ischemia with different duration between ligations of both common carotid arteries. Methods: The experiments were performed on 24 male mongrel white rats weighing 260 ±20 g. Cerebral ischemia (CI) was simulated under intravenous thiopental anesthesia (40-50 mg/kg). The control group consisted of falsely operated rats of similar sex and weight. To study mitochondrial respiration, the brain was extracted in the cold (0-4°C), dried with filter paper, weighed and homogenized in an isolation medium containing 0.32 M sucrose, 10 mM Tris-HCl, 1 mM EDTA, pH 7.4 (in a ratio of 1:10), using Potter-Evelheim homogenizer with Teflon pestle according to the modified method. To prevent systematic measurement errors, brain samples from the compared control and experimental groups of animals were studied under the same conditions. Results: Stepwise SCI with an interval of 1 and 3 days between bandages of both OCA leads to damage to the neurons of the parietal cortex and hippocampus of rats, which manifests itself in a decrease in their size, deformation of the pericaryons, an increase in the number of shrunken neurons and shadow cells. The most pronounced changes were observed in the subgroup with an interval between dressings of 1 day. These changes were similar to the changes in SCI (p>0.05), except for the absence of cells with pericellular edema in the hippocampus and a smaller number of them in the parietal cortex. SCI with an interval between WASP dressings of 7 days, on the contrary, it is manifested by less pronounced histological changes, especially in the hippocampus. Conclusion: In cerebral ischemia, damage to the inner mitochondrial membrane occurs due to activation of free radical oxidation processes. Damage to the inner mitochondrial membrane, in turn, leads to an increase in its permeability and a decrease in the level of the proton gradient due to the transition of protons along the concentration gradient through the resulting nonspecific pores into the mitochondrial matrix. As a result, the efficiency of ATP synthesis decreases, and more substrates and oxygen are required to maintain the intermembrane potential under these conditions.
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42

Kawasaki, H. "Mechanisms underlying the development and evolution of the mammalian cerebral cortex." Siberian Medical Review, no. 2 (2022): 105. http://dx.doi.org/10.20333/25000136-2022-2-105.

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43

Chernykh, Ivan V., Aleksey V. Shchul’kin, Natal'ya M. Popova, Mariya V. Gatsanoga, and Elena N. Yakusheva. "Regulation of ABCB1 Protein Function in the Cerebral Cortex with the Underlying Global Cerebral Ischemia." I.P. Pavlov Russian Medical Biological Herald 31, no. 4 (January 5, 2024): 613–22. http://dx.doi.org/10.17816/pavlovj111932.

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INTRODUCTION: ABCB1 is a membrane transporter protein responsible for efflux of a wide range of drugs from cells. The study of the mechanisms of regulation of the functioning of ABCB1 protein in the brain in its ischemia will permit to propose new approaches to pharmacotherapy of cerebral ischemic pathology. AIM: To study the regulation of ABCB1 protein function in the cerebral cortex of rats with global cerebral ischemia. MATERIALS AND METHODS: The experiment was performed on 30 male rats with global cerebral ischemia modeled by bilateral occlusion of the common carotid arteries. The amount of ABCB1 protein and Nrf2 and HIF-1α transcription factors in the cerebral cortex was determined by enzyme immunoassay. The free radical status of the cerebral cortex was assessed by the concentration of malondialdehyde, SH groups, and by glutathione peroxidase (G-per) activity. RESULTS: Bilateral occlusion of the common carotid arteries caused an increase in the level of ABCB1 protein in the cerebral cortex of rats by the 4th hour of ischemia; in 24 hours it remained elevated, and in 72 hours decreased to values that did not differ from those of falsely operated rats. The content of malondialdehyde in the cerebral cortex increased in 2 and 4 hours after occlusion and then gradually decreased to the initial values. In 30 minutes and 4 hours after ischemia modeling, G-per activity decreased compared to the control values. The content of Nrf2 in the cerebral cortex increased in 2 and 4 hours after occlusion, then slightly decreased on the next day, and reached the initial values on the 3rd day of the experiment. The amount of HIF-1α increased only in 24 and 72 hours after the surgery. CONCLUSION: The amount of ABCB1 protein in the cerebral cortex of rats with global cerebral ischemia depends on the severity of oxidative stress, with Nrf2 and HIF-1α transcription factors playing a role in its regulation. Reduction of the amount of the transporter in the blood-brain barrier through the influence on the lipid peroxidation processes or synthesis of the studied transcription factors expands the possibilities of using ABCB1 protein substrates for improving the effectiveness of pharmacotherapy of diseases of the central nervous system.
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44

Clark, C., H. Klonoff, and M. Hayden. "Regional Cerebral Glucose Metabolism in Turner Syndrome." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 2 (May 1990): 140–44. http://dx.doi.org/10.1017/s0317167100030341.

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ABSTRACT:Regional cerebral glucose metabolism was examined in females with Turner syndrome, a sex chromosome abnormality. Previous studies have found a visual/spatial cognitive anomaly in these women but, to date, no abnormalities in brain structure or function have been associated with the condition. In the present study, decreases in regional metabolism were found in the occipital and parietal cortex. The involvement of the occipital cortex, although consistent with the observed cognitive anomalies, has not been suggested previously as an area dysfunction. Because the occipital cortex is a primary sensory cortex, the reduction of glucose metabolism in the parietal cortex may reflect a lack of innervation from the occipital cortex. Besides insight into the functional specialization of the brain, these findings are also consistent with previous reports on animals regarding the effects of estrogen in brain maturation.
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45

Ilg, U. J., and K. P. Hoffmann. "Functional grouping of the cortico-pretectal projection." Journal of Neurophysiology 70, no. 2 (August 1, 1993): 867–69. http://dx.doi.org/10.1152/jn.1993.70.2.867.

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The ascendency of the cerebral cortex in mammals naturally raises questions about the role of the archetypal subcortical centers we share in common with other phyla. Here we report a situation in which an ancient oculomotor control center, the nucleus of the optic tract, is not so much dominated by the cerebral cortex as served by it. We suggest that the organization of cortical output to subcortical centers may be helpful in understanding the function of the cerebral cortex.
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46

Tamad, Fatiha Sri Utami, Trianggoro Budisulistyo, Amin Husni, Retnaningsih Retnaningsih, Herlina Suryawati, and Suryadi Suryadi. "Wistar Rat Parietal Lobe Cell And Pain Perception Changes After Frequent Of Mobile Phone Electromagnetic Wave Expose." Medica Hospitalia : Journal of Clinical Medicine 10, no. 2 (July 31, 2023): 147–52. http://dx.doi.org/10.36408/mhjcm.v10i2.884.

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Background: The increasing number of mobile phone users raises concerns about the effects. Mobile phone electromagnetic wave radiation harms pain perception due to granular cell changes in the cerebral parietal cortex. Objective: To determine the effect of exposure to electromagnetic waves mobile phone on pain perception due to changes in the granular cells of the cerebral parietal cortex Wistar rats. Methods: Experimental research using randomized posttest with control group design. Samples were 28 rats divided into 4 groups. The control group was not exposed, the treatment group was exposed to 2100 MHz electromagnetic waves for 2 hours/day with a distance of 3 cm for 15 days in treatment group 1, for 30 days in treatment group 2, and 45 days in treatment group 3. Measurement of pain onset using the hot method. Changes in pain threshold were taken from the difference in pain onset after exposure to before exposure. Granular cell changes in the cerebral parietal cortex were assessed from the total score with the provisions of normal cells (sumx0), hydropic degenerated cells (sumx1), and necrotic cells (sumx2). Results: The longer the exposure to mobile phones, the higher the pain threshold and the cerebral parietal cortex granular cell damage score. There was a significant difference in pain threshold and changes in cerebral parietal cortex granular cells between groups (p=0.000). There was a significant relationship between changes in the parietal cerebral cortex granular cells and pain threshold in Wistar rats exposed to electromagnetic waves (p=0.000). Conclusion: Exposure to mobile phone electromagnetic waves affects pain perception due to changes in the granular cells of the cerebral parietal cortex in wistar rats.
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47

Yamamoto, Kazumi, Fumiharu Akai, Toshiki Yoshimine, and Takehiko Yanagihara. "Immunohistochemical investigation of cerebral ischemia after middle cerebral artery occlusion in gerbils." Journal of Neurosurgery 67, no. 3 (September 1987): 414–20. http://dx.doi.org/10.3171/jns.1987.67.3.0414.

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✓ Progression and recovery of ischemic and postischemic damage after occlusion of the middle cerebral artery and subsequent reperfusion were investigated in the gerbil. This study was performed by immunohistochemical reaction testing for tubulin and creatine kinase BB-isoenzyme to visualize the neuronal structure and by immunohistochemical reaction testing for astroprotein (an astrocyte-specific protein) to visualize reactive astrocytes. The earliest ischemic lesion became visible in the frontoparietal cortex after 7 minutes of ischemia as a laminar loss of the reaction for tubulin involving the neuropil, neuronal perikarya, and dendrites. The earliest lesion in the caudoputamen evolved after 30 minutes of ischemia. After reestablishment of cerebral circulation, the immunohistochemical ischemic lesions in the neuronal structure disappeared if the ischemic period was 10 minutes or less and partially disappeared even after ischemia for 15 minutes in the cerebral cortex, while the postischemic lesion in the caudoputamen disappeared even after ischemia for 15 minutes. Reactive astrocytes were detected in the cerebral cortex and caudoputamen as early as 24 hours after reperfusion, both in the areas with and without the neuronal lesions. No lesion was identified in the hippocampus or thalamus. This experimental model is suitable for investigation of rapidly progressive regional ischemia in the cerebral cortex and for comparison with other regional or global cerebral ischemia in the gerbil or other animal species.
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48

Chiang, Yung-Hsiao, Shinn-Zong Lin, Cesario V. Borlongan, Barry J. Hoffer, Marisela Morales, and Yun Wang. "Transplantation of Fetal Kidney Tissue Reduces Cerebral Infarction Induced by Middle Cerebral Artery Ligation." Journal of Cerebral Blood Flow & Metabolism 19, no. 12 (December 1999): 1329–35. http://dx.doi.org/10.1097/00004647-199912000-00006.

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The authors, and others, have recently reported that intracerebral administration of glial cell line-derived neurotrophic factor (GDNF) or osteogenic protein-1 protects against ischemia-induced injury in the cerebral cortex of adult rats. Because these trophic factors are highly expressed in the fetal, but not adult, kidney cortex, the possibility that transplantation of fetal kidney tissue could serve as a cellular reservoir for such molecules and protect against ischemic injury in cerebral cortex was examined. Fetal kidneys obtained from rat embryos at gestational day 16, and adult kidney cortex, were dissected and cut into small pieces. Adult male Sprague-Dawley rats were anesthetized with chloral hydrate and placed in a stereotactic apparatus. Kidney tissues were transplanted into three cortical areas adjacent to the right middle cerebral artery (MCA). Thirty minutes after grafting, the right MCA was transiently ligated for 90 minutes. Twenty-four hours after the onset of reperfusion, animals were evaluated behaviorally. It was found that the stroke animals that received adult kidney transplantation developed motor imbalance. However, animals that received fetal kidney grafts showed significant behavioral improvement. Animals were later sacrificed and brains were removed for triphenyltetrazolium chloride staining, Pax-2 immunostaining, and GDNF mRNA expression. It was noted that transplantation of fetal kidney but not adult kidney tissue greatly reduced the volume of infarction in the cerebral cortex. Fetal kidney grafts showed Pax-2 immunoreactivity and GDNF mRNA in the host cerebral cortex. In contrast, GDNF mRNA expression was not found in the adult kidney grafts. Taken together, our data indicate that fetal kidney transplantation reduces ischemia/reperfusion-induced cortical infarction and behavioral deficits in adult rats, and that such tissue grafts could serve as an unique cellular reservoir for trophic factor application to the brain.
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Stephan, Klaas E., Claus–C Hilgetag, Gully A. P. C. Burns, Marc A. O'Neill, Malcolm P. Young, and Rolf Kotter. "Computational analysis of functional connectivity between areas of primate cerebral cortex." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1393 (January 29, 2000): 111–26. http://dx.doi.org/10.1098/rstb.2000.0552.

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Recent analyses of association fibre networks in the primate cerebral cortex have revealed a small number of densely intra–connected and hierarchically organized structural systems. Corresponding analyses of data on functional connectivity are required to establish the significance of these structural systems. W e therefore built up a relational database by systematically collating published data on the spread of activity after strychnine–induced disinhibition in the macaque cerebral cortex in vivo . After mapping these data to two different parcellation schemes, we used three independent methods of analysis which demonstrate that the cortical network of functional interactions is not homogeneous, but shows a clear segregation into functional assemblies of mutually interacting areas. The assemblies suggest a principal division of the cortex into visual, somatomotor and orbito–temporo–insular systems, while motor and somatosensory areas are inseparably interrelated. These results are largely compatible with corresponding analyses of structural data of mammalian cerebral cortex, and deliver the first functional evidence for ‘small–world’ architecture of primate cerebral cortex.
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Viggiano, Meccariello, Santoro, Secondulfo, Operto, Monda, and Coppola. "A Calorie-Restricted Ketogenic Diet Reduces Cerebral Cortex Vascularization in Prepubertal Rats." Nutrients 11, no. 11 (November 5, 2019): 2681. http://dx.doi.org/10.3390/nu11112681.

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The antiepileptic effect of ketogenic diets is acknowledged but its mechanism of action is poorly understood. The present work aimed to evaluate possible effects of a calorie-restricted ketogenic diet (CRKD) on brain growth and angiogenesis in normal prepubertal rats. Two groups of prepubertal rats were fed with a standard diet (group 1) or a CRKD (group 2) for ten weeks. Then, rats were sacrificed and the thickness for the following structures was evaluated by histology: (1) cerebral cortex, (2) deep cerebral white matter, and (3) substantia nigra. The capillary density was also evaluated within: (1) cerebral cortex, (2) dentate gyrus of the hippocampus, (3) periaqueductal grey matter, and (4) substantia nigra. The results showed a smaller thickness of all the areas examined and a reduced capillary density within the cerebral cortex in the CRKD-treated group compared to the control group. These findings suggest an association between reduced angiogenesis within the cerebral cortex and the antiepileptic effects of CRKD.
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