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Journal articles on the topic 'Brain cytoarchitecture'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Swindler, Daris R. "The primate brain from cytoarchitecture to endocasts." Reviews in Anthropology 13, no. 1 (1986): 14–19. http://dx.doi.org/10.1080/00988157.1986.9977755.

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Majocha, Ronald E., Charles A. Marotta, and Francine M. Benes. "Immunostaining of neurofilament protein in human postmortem cortex: A sensitive and specific approach to the pattern analysis of human cortical cytoarchitecture." Canadian Journal of Biochemistry and Cell Biology 63, no. 6 (1985): 577–84. http://dx.doi.org/10.1139/o85-076.

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Antibodies raised against the 200 000 neurofilament protein (NFP) of rat brain have been successfully applied to the staining of human postmortem cortex using a modified immunoperoxidase procedure. Human anterior cingulate cortex which has been in formaldehyde fixative for as long as 4 years shows extensive and reliable staining of axons and, to a lesser degree, apical dendrites of cortical neurons. The immunostaining of 200 000 NFP in human cortex has revealed cytoarchitectural details not generally visible with other more conventional neuroanatomical stains, particularly when counterstaining with cresyl violet is employed. Potential applications of this approach to the pattern analysis of human cortical cytoarchitecture in both health and disease are discussed.

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Amunts, Katrin, Hartmut Mohlberg, Sebastian Bludau, and Karl Zilles. "Julich-Brain: A 3D probabilistic atlas of the human brain’s cytoarchitecture." Science 369, no. 6506 (2020): 988–92. http://dx.doi.org/10.1126/science.abb4588.

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Cytoarchitecture is a basic principle of microstructural brain parcellation. We introduce Julich-Brain, a three-dimensional atlas containing cytoarchitectonic maps of cortical areas and subcortical nuclei. The atlas is probabilistic, which enables it to account for variations between individual brains. Building such an atlas was highly data- and labor-intensive and required the development of nested, interdependent workflows for detecting borders between brain areas, data processing, provenance tracking, and flexible execution of processing chains to handle large amounts of data at different spatial scales. Full cortical coverage was achieved by the inclusion of gap maps to complement cortical maps. The atlas is dynamic and will be adapted as mapping progresses; it is openly available to support neuroimaging studies as well as modeling and simulation; and it is interoperable, enabling connection to other atlases and resources.

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Rapuano, Kristina M., Jennifer S. Laurent, Donald J. Hagler, et al. "Nucleus accumbens cytoarchitecture predicts weight gain in children." Proceedings of the National Academy of Sciences 117, no. 43 (2020): 26977–84. http://dx.doi.org/10.1073/pnas.2007918117.

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The prevalence of obesity in children and adolescents worldwide has quadrupled since 1975 and is a key predictor of obesity later in life. Previous work has consistently observed relationships between macroscale measures of reward-related brain regions (e.g., the nucleus accumbens [NAcc]) and unhealthy eating behaviors and outcomes; however, the mechanisms underlying these associations remain unclear. Recent work has highlighted a potential role of neuroinflammation in the NAcc in animal models of diet-induced obesity. Here, we leverage a diffusion MRI technique, restriction spectrum imaging, to probe the microstructure (cellular density) of subcortical brain regions. More specifically, we test the hypothesis that the cell density of reward-related regions is associated with obesity-related metrics and early weight gain. In a large cohort of nine- and ten-year-olds enrolled in the Adolescent Brain Cognitive Development (ABCD) study, we demonstrate that cellular density in the NAcc is related to individual differences in waist circumference at baseline and is predictive of increases in waist circumference after 1 y. These findings suggest a neurobiological mechanism for pediatric obesity consistent with rodent work showing that high saturated fat diets increase gliosis and neuroinflammation in reward-related brain regions, which in turn lead to further unhealthy eating and obesity.

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Babovic, Sinisa, Dejan Ivanov, Ljilja Mijatov-Ukropina, Takashi Toyonaga, Ivan Dimitrijevic, and Milena Djordjevic. "Cytoarchitecture of the human paraventricular hypothalamic nucleus." Medical review 62, no. 9-10 (2009): 417–20. http://dx.doi.org/10.2298/mpns0910417b.

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Introduction. The significance of this research in terms of structure and biochemical processes in PVN contributes to further understanding of vital physiological processes from delivery and stress to delicate chemical processes that keep the hypothalamo-hypophysial axis in balance. Conclusion. Comparative studies of the human hypothalamus with the hypothalamus of other mammals enable further research, especially pharmacological and physiological ones. These are made possible with the aid of highly sophisticated equipment for examination of neurophysiological features of the brain.

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Park, JiSoo, Bo Kyeong Lee, Gi Seok Jeong, Jung Keun Hyun, C. Justin Lee, and Sang-Hoon Lee. "Three-dimensional brain-on-a-chip with an interstitial level of flow and its application as an in vitro model of Alzheimer's disease." Lab on a Chip 15, no. 1 (2015): 141–50. http://dx.doi.org/10.1039/c4lc00962b.

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In this paper, we developed a three-dimensional brain-on-a-chip with an interstitial level of flow. The chip contains an osmotic micropump system for providing interstitial flow and a concave microwell array for mimicking the brain's 3D cytoarchitecture.

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Lin, Tiffany V., Lawrence Hsieh, Tomoki Kimura, Taylor J. Malone, and Angélique Bordey. "Normalizing translation through 4E-BP prevents mTOR-driven cortical mislamination and ameliorates aberrant neuron integration." Proceedings of the National Academy of Sciences 113, no. 40 (2016): 11330–35. http://dx.doi.org/10.1073/pnas.1605740113.

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Hyperactive mammalian target of rapamycin complex 1 (mTORC1) is a shared molecular hallmark in several neurodevelopmental disorders characterized by abnormal brain cytoarchitecture. The mechanisms downstream of mTORC1 that are responsible for these defects remain unclear. We show that focally increasing mTORC1 activity during late corticogenesis leads to ectopic placement of upper-layer cortical neurons that does not require altered signaling in radial glia and is accompanied by changes in layer-specific molecular identity. Importantly, we found that decreasing cap-dependent translation by expressing a constitutively active mutant of the translational repressor eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) prevents neuronal misplacement and soma enlargement, while partially rescuing dendritic hypertrophy induced by hyperactive mTORC1. Furthermore, overactivation of translation alone through knockdown of 4E-BP2 was sufficient to induce neuronal misplacement. These data show that many aspects of abnormal brain cytoarchitecture can be prevented by manipulating a single intracellular process downstream of mTORC1, cap-dependent translation.

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King, Jace B., Melissa P. Lopez-Larson, and Deborah A. Yurgelun-Todd. "Mean cortical curvature reflects cytoarchitecture restructuring in mild traumatic brain injury." NeuroImage: Clinical 11 (2016): 81–89. http://dx.doi.org/10.1016/j.nicl.2016.01.003.

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Echoru, Isaac, Edmund E. M. Bukenya, Godfrey Masilili, Elna Owembabazi, Ann Monima Lemuel, and James Ahimbisibwe. "Khat distorts the prefrontal cortex histology and function of adult Wistar rats." Anatomy Journal of Africa 7, no. 1 (2018): 1121–31. http://dx.doi.org/10.4314/aja.v7i1.169485.

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Khat is a psychoactive herbal drug of pronounced ethno-pharmacological significance often abused due to its unregulated use. It affects many brain centers including the prefrontal cortex which is the anterior most part of the frontal lobe. The prefrontal cortex modulates working memory, planning complex cognitive behaviors however; it is linked to many psychological disorders such as depression, schizophrenia and memory loss. We studied the effects exerted by khat on the PFC cytoarchitecture and functions since this part of the brain is highly interconnected with various cortical regions. This was an experimental study of 6 weeks. A total of 24 male adult wistar rats of 130g-155g were divided into four groups of 6 animals that received respective khat doses of 2000mg/kg, 1000mg/kg, 500mg/kg and 10ml/kg of distilled water for the controls. Brain to body weight ratio was determined at week 6 using an analytical balance (Fisher Science Education™, RS232C; USA). Histology of the brain was determined using H and E and Kulvers staining technique. Khat exhibited features of prefrontal cortex disorientation such as necrosis, vacuolations, chromatolysis, demyelination, cortical degeneration and hemorrhage in a dose dependent manner. Selective attention and working memory were impaired well as brain to body weight ratio was reduced significantly (P ≤ 0.05). Repeated exposure to khat distorts the prefrontal cortex cytoarchitecture and impairs selective attention and working memory accuracy due to ischemia and cell exhaustion by khat toxicity.Keywords: Khat, prefrontal cortex histology, working memory, selective attention

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Wang, Nian, Leonard E. White, Yi Qi, Gary Cofer, and G. Allan Johnson. "Cytoarchitecture of the mouse brain by high resolution diffusion magnetic resonance imaging." NeuroImage 216 (August 2020): 116876. http://dx.doi.org/10.1016/j.neuroimage.2020.116876.

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Wei, Hongjiang, Luke Xie, Russell Dibb, et al. "Imaging whole-brain cytoarchitecture of mouse with MRI-based quantitative susceptibility mapping." NeuroImage 137 (August 2016): 107–15. http://dx.doi.org/10.1016/j.neuroimage.2016.05.033.

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Ronen, Itamar. "Studying brain cytoarchitecture with MRI-Present, future and promises of high field." International Journal of Imaging Systems and Technology 20, no. 1 (2010): 57–61. http://dx.doi.org/10.1002/ima.20224.

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Huggenberger, Stefan. "The size and complexity of dolphin brains—a paradox?" Journal of the Marine Biological Association of the United Kingdom 88, no. 6 (2008): 1103–8. http://dx.doi.org/10.1017/s0025315408000738.

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Dolphin brain size with respect to body size ranks between that of apes and humans. The hypertrophic auditory structures, the large cerebrum with extended gyrification and the highly cognitive capabilities of toothed whales seem to be in paradoxical contrast to their thin neocortex with a plesiomorphic or paedomorphic cytoarchitecture. The total number of neurons in the delphinid neocortex is comparable to that of the chimpanzee (Primates), but, in relation to body weight, in the magnitude of the hedgehog (Insectivora) neocortex since cetaceans may be able to obtain larger body sizes than terrestrial mammals due to reduced gravitational effects in water. During evolution, dolphins may have increased the computational performance of their cytoarchitectonically ‘simple’ neocortex by a multiplication of relevant structures (resulting in a hypertrophic surface area) instead of increasing its complexity. Based on this hypothesis, I suggest that the evolution of the large dolphin brain was possible due to a combination of different prerequisites based on adaptations to the aquatic environment including the sonar system. The latter facilitated a successful feeding strategy to support an increased metabolic turnover of the brain and led to a hypertrophic auditory system. Moreover, the rudimentary pelvic girdle did not limit brain size at birth. These adaptations favoured the evolutionary size increase of the cerebral cortex in dolphins facilitating highly cognitive capabilities as well as precise and rapid sound processing using a ‘simple’ kind of neocortical cytoarchitecture.

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Aria, Francesca, Sara A. Bonini, Valentina Cattaneo, et al. "Brain Structural and Functional Alterations in Mice Prenatally Exposed to LPS Are Only Partially Rescued by Anti-Inflammatory Treatment." Brain Sciences 10, no. 9 (2020): 620. http://dx.doi.org/10.3390/brainsci10090620.

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Aberrant immune activity during neurodevelopment could participate in the generation of neurological dysfunctions characteristic of several neurodevelopmental disorders (NDDs). Numerous epidemiological studies have shown a link between maternal infections and NDDs risk; animal models of maternal immune activation (MIA) have confirmed this association. Activation of maternal immune system during pregnancy induces behavioral and functional alterations in offspring but the biological mechanisms at the basis of these effects are still poorly understood. In this study, we investigated the effects of prenatal lipopolysaccharide (LPS) exposure in peripheral and central inflammation, cortical cytoarchitecture and behavior of offspring (LPS-mice). LPS-mice reported a significant increase in interleukin-1β (IL-1β) serum level, glial fibrillary acidic protein (GFAP)- and ionized calcium-binding adapter molecule 1 (Iba1)-positive cells in the cortex. Furthermore, cytoarchitecture analysis in specific brain areas, showed aberrant alterations in minicolumns’ organization in LPS-mice adult brain. In addition, we demonstrated that LPS-mice presented behavioral alterations throughout life. In order to better understand biological mechanisms whereby LPS induced these alterations, dams were treated with meloxicam. We demonstrated for the first time that exposure to LPS throughout pregnancy induces structural permanent alterations in offspring brain. LPS-mice also present severe behavioral impairments. Preventive treatment with meloxicam reduced inflammation in offspring but did not rescue them from structural and behavioral alterations.

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Fulcher, Ben D. "Discovering Conserved Properties of Brain Organization Through Multimodal Integration and Interspecies Comparison." Journal of Experimental Neuroscience 13 (January 2019): 117906951986204. http://dx.doi.org/10.1177/1179069519862047.

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The primate cerebral cortex is broadly organized along hierarchical processing streams underpinned by corresponding variation in the brain’s microstructure and interareal connectivity patterns. Fulcher et al. recently demonstrated that a similar organization exists in the mouse cortex by combining independent datasets of cytoarchitecture, gene expression, cell densities, and long-range axonal connectivity. Using the T1w:T2w magnetic resonance imaging map as a common spatial reference for data-driven comparison of cortical gradients between mouse and human, we highlighted a common hierarchical expression pattern of numerous brain-related genes, providing new understanding of how systematic structural variation shapes functional specialization in mammalian brains. Reflecting on these findings, here we discuss how open neuroscience datasets, combined with advanced neuroinformatics approaches, will be crucial in the ongoing search for organization principles of brain structure. We explore the promises and challenges of integrative studies and argue that a tighter collaboration between experimental, statistical, and theoretical neuroscientists is needed to drive progress further.

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Mariappan, Aruljothi, Gladiola Goranci-Buzhala, Lucia Ricci-Vitiani, Roberto Pallini, and Jay Gopalakrishnan. "Trends and challenges in modeling glioma using 3D human brain organoids." Cell Death & Differentiation 28, no. 1 (2020): 15–23. http://dx.doi.org/10.1038/s41418-020-00679-7.

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AbstractThe human brain organoids derived from pluripotent cells are a new class of three-dimensional tissue systems that recapitulates several neural epithelial aspects. Brain organoids have already helped efficient modeling of crucial elements of brain development and disorders. Brain organoids’ suitability in modeling glioma has started to emerge, offering another usefulness of brain organoids in disease modeling. Although the current state-of-the organoids mostly reflect the immature state of the brain, with their vast cell diversity, human brain-like cytoarchitecture, feasibility in culturing, handling, imaging, and tractability can offer enormous potential in reflecting the glioma invasion, integration, and interaction with different neuronal cell types. Here, we summarize the current trend of employing brain organoids in glioma modeling and discuss the immediate challenges. Solving them might lay a foundation for using brain organoids as a pre-clinical 3D substrate to dissect the glioma invasion mechanisms in detail.

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Simões-Henriques, Carla, Miguel Mateus‐Pinheiro, Rita Gaspar, et al. "Microglia cytoarchitecture in the brain of adenosine A 2A receptor knockout mice: Brain region and sex specificities." European Journal of Neuroscience 51, no. 6 (2020): 1377–87. http://dx.doi.org/10.1111/ejn.14561.

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Morecraft, R. J., C. Geula, and M. M. Mesulam. "Cytoarchitecture and neural afferents of orbitofrontal cortex in the brain of the monkey." Journal of Comparative Neurology 323, no. 3 (1992): 341–58. http://dx.doi.org/10.1002/cne.903230304.

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Swain, Gary P., Joseph A. Snedeker, Joseph Ayers, and Michael E. Selzer. "Cytoarchitecture of spinal-projecting neurons in the brain of the larval sea lamprey." Journal of Comparative Neurology 336, no. 2 (1993): 194–210. http://dx.doi.org/10.1002/cne.903360204.

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Chen, Xiao, Xiaoyu Zhang, Qiuyuan Zhong, et al. "Simultaneous acquisition of neuronal morphology and cytoarchitecture in the same Golgi-stained brain." Biomedical Optics Express 9, no. 1 (2017): 230. http://dx.doi.org/10.1364/boe.9.000230.

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Baker, K. G., G. M. Halliday, P. Halasz, et al. "Cytoarchitecture of serotonin-synthesizing neurons in the pontine tegmentum of the human brain." Synapse 7, no. 4 (1991): 301–20. http://dx.doi.org/10.1002/syn.890070407.

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Bogolepova, I. N., L. I. Malofeeva, P. A. Agapov, and I. G. Malofeeva. "Cytoarchitecture Changes in the Prefrontal Brain Cortex of Adult and Aged Men and Women." Journal of Anatomy and Histopathology 6, no. 3 (2017): 13–18. http://dx.doi.org/10.18499/2225-7357-2017-6-3-13-18.

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Liu, X., D. Nemeth, D. McKim, et al. "Abstract # 2075 Structural and functional cytoarchitecture of IL-1R1-expressing system in the brain." Brain, Behavior, and Immunity 76 (February 2019): e10. http://dx.doi.org/10.1016/j.bbi.2018.11.201.

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Costantini, Irene, Giacomo Mazzamuto, Matteo Roffilli, et al. "Large-scale, cell-resolution volumetric mapping allows layer-specific investigation of human brain cytoarchitecture." Biomedical Optics Express 12, no. 6 (2021): 3684. http://dx.doi.org/10.1364/boe.415555.

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Ibe, C., S. Ojo, S. Salami, J. Ayo, U. Nlebedum, and E. Ikpegbu. "Cytoarchitecture and brain-derived neurotrophic factor immunolocalisation in the cerebellar cortex of African grasscutter (Thryonomys Swinderianus)." Journal of Morphological Sciences 33, no. 03 (2016): 146–54. http://dx.doi.org/10.4322/jms.100316.

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Abstract Introduction: The study described the lamina organization and immunolocalisation of brain-derived neurotrophic factor in the cerebellar cortex of the African grasscutter, at defined postnatal periods. Materials and Method: Brain samples extracted from African grasscutter neonates on postnatal day 3, juveniles on postnatal day 72 and adults on postnatal day 450 were prepared for routine histology and immunohistochemistry, using antibody specific to brain-derived neurotrophic factor. Results: On postnatal day 3, all the laminae typical of the concentric lamina organisation of the mammalian cerebellar cortex were evident, but, and external germinal layer was also observed. On postnatal day 72, and thereafter, the external germinal layer was no more evident. On postnatal day 3, the tree-like arrangement (Arbor vitae) of the cerebellum was not very striking, as the interlobular fissures were incomplete. On postnatal day 72, the Arbor vitae were better presented, as more lobules had been completely separated by interlobular fissures; although, there were some incompletely separated lobules, presented with interlobular fissural lines. On postnatal day 450, the lobules were distinct as the interlobular fissures separated all the vermal and hemispheric lobules. In all the postnatal periods, the granule cell layer was the most populated, while the Purkinje layer was a single cell line of Purkinje neurones. At all postnatal periods, strong immunoreactivity to brain-derived neurotrophic factor was observed in the Purkinje layer; the cell bodies and dendrites of all Purkinje neurones were immunoreactive; while the nuclei in neonate Purkinje neurons where not immunoreactive, the nuclei in the adults were immunoreactive. The cerebellar granule cells were not brain-derived neurotrophic factor immunoreactive, suggestive of their non-synthesis or loss of the synthesized protein, by anterograde axonal transport, to paracrine function. Conclusion: These findings and others were related to some behaviours of the African grasscutter, and compared with similar report in other rodents.

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Behrens, T. E. J., and H. Johansen-Berg. "Relating connectional architecture to grey matter function using diffusion imaging." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1457 (2005): 903–11. http://dx.doi.org/10.1098/rstb.2005.1640.

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Understanding brain function in terms of connectional architecture is a major goal of neuroimaging. However, direct investigation of the influence of brain circuitry on function has been hindered by the lack of a technique for exploring anatomical connectivity in the in vivo brain. Recent advances in magnetic resonance diffusion imaging have given scientists access to data relating to local white matter architecture and, for the first time, have raised the possibility of in vivo investigations into brain circuitry. This review investigates whether diffusion imaging may be used to identify regions of grey matter that are distinct in their connectional architecture, and whether these connectional differences are reflected either in local cytoarchitecture or in local grey matter function. Establishing a direct relationship between regional boundaries based on diffusion imaging and borders between regions that perform different functions would not only be of great significance when interpreting functional results, but would also provide a first step towards the validation of diffusion-based anatomical connectivity studies.

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Dinopoulos, A., G. C. Papadopoulos, H. Michaloudi, J. G. Parnavelas, H. B. M. Uylings, and A. N. Karamanlidis. "Claustrum in the hedgehog (Erinaceus europaeus) brain: Cytoarchitecture and connections with cortical and subcortical structures." Journal of Comparative Neurology 316, no. 2 (1992): 187–205. http://dx.doi.org/10.1002/cne.903160205.

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Brooks, Tracy A., Nicole Nametz, Rachael Charles та Thomas P. Davis. "Diclofenac Attenuates the Regional Effect of λ-Carrageenan on Blood-Brain Barrier Function and Cytoarchitecture". Journal of Pharmacology and Experimental Therapeutics 325, № 2 (2008): 665–73. http://dx.doi.org/10.1124/jpet.107.135632.

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Jelsing, Jacob, Anders Hay-Schmidt, Tim Dyrby, Ralf Hemmingsen, Harry B. M. Uylings, and Bente Pakkenberg. "The prefrontal cortex in the Göttingen minipig brain defined by neural projection criteria and cytoarchitecture." Brain Research Bulletin 70, no. 4-6 (2006): 322–36. http://dx.doi.org/10.1016/j.brainresbull.2006.06.009.

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Wei, Yongbin, Lianne H. Scholtens, Elise Turk, and Martijn P. van den Heuvel. "Multiscale examination of cytoarchitectonic similarity and human brain connectivity." Network Neuroscience 3, no. 1 (2019): 124–37. http://dx.doi.org/10.1162/netn_a_00057.

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The human brain comprises an efficient communication network, with its macroscale connectome organization argued to be directly associated with the underlying microscale organization of the cortex. Here, we further examine this link in the human brain cortex by using the ultrahigh-resolution BigBrain dataset; 11,660 BigBrain profiles of laminar cell structure were extracted from the BigBrain data and mapped to the MRI based Desikan–Killiany atlas used for macroscale connectome reconstruction. Macroscale brain connectivity was reconstructed based on the diffusion-weighted imaging dataset from the Human Connectome Project and cross-correlated to the similarity of laminar profiles. We showed that the BigBrain profile similarity between interconnected cortical regions was significantly higher than those between nonconnected regions. The pattern of BigBrain profile similarity across the entire cortex was also found to be strongly correlated with the pattern of cortico-cortical connectivity at the macroscale. Our findings suggest that cortical regions with higher similarity in the laminar cytoarchitectonic patterns have a higher chance of being connected, extending the evidence for the linkage between macroscale connectome organization and microscale cytoarchitecture.

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Murray, Robin M. "Neurodevelopmental Schizophrenia: The Rediscovery of Dementia Praecox." British Journal of Psychiatry 165, S25 (1994): 6–12. http://dx.doi.org/10.1192/s0007125000293148.

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Many people with severe schizophrenia have increased cerebral ventricular size and diffuse reduction in cortical volume; recent attention has focused on subtle malformations of the cytoarchitecture in the hippocampus and parahippocampal cortex. Sufferers also show an excess of dermatoglyphic and minor physical abnormalities, and a significant proportion had psychomotor deficits, cognitive or behavioural problems as children. Such findings suggest that the form of schizophrenia most akin to Kraepelin's original description of dementia praecox results from neurodevelopmental impairment. This may have its origin in genetic defects in the control of early brain growth, or in early environmental hazards such as prenatal exposure to maternal influenza or perinatal complications. How foetal or neonatal lesions produce hallucinations and delusions two or three decades later remains a mystery, but maturational changes in the brain may be important.

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Dean, Brian. "Signal Transmission, Rather Than Reception, is the Underlying Neurochemical Abnormality in Schizophrenia." Australian & New Zealand Journal of Psychiatry 34, no. 4 (2000): 560–69. http://dx.doi.org/10.1080/j.1440-1614.2000.00747.x.

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Objective: This review aims to summarise the outcome of studies on changes in the molecular architecture of the brain of subjects with schizophrenia and formulate a hypothesis on mechanisms involved in the pathology of the illness. Method: The outcomes from key studies using neuroimaging techniques and tissue obtained post-mortem that have been directed toward identifying abnormalities in the molecular architecture of the brain in subjects with schizophrenia were summarised. Using the results from these studies hypotheses were formulated on the underlying pathological process that precipitate schizophrenia. Results: Studies using neuroimaging techniques or tissue obtained post-mortem have revealed changes in the dopaminergic, serotoninergic, glutamatergic, GABAergic and cholinergic systems of the brain in schizophrenia. Some of these studies have identified abnormalities in presynaptic proteins or functioning that may be central to the pathology of schizophrenia. Conclusions: There appears to be diverse changes in the molecular cytoarchitecture of the brains from subjects with schizophrenia. It could be that it is by affecting these multiple systems that the atypical antipsychotic drugs produce their improved clinical outcomes. Abnormal functioning of presynaptic processes could be central to the pathology of schizophrenia. If the ‘presynaptic’ hypothesis is proven, future antipsychotic drug design should be directed away from post-synaptic receptor antagonism toward the modulating the functions of presynaptic neurones.

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Fotaki, Vassiliki, Mara Dierssen, Soledad Alcántara, et al. "Dyrk1A Haploinsufficiency Affects Viability and Causes Developmental Delay and Abnormal Brain Morphology in Mice." Molecular and Cellular Biology 22, no. 18 (2002): 6636–47. http://dx.doi.org/10.1128/mcb.22.18.6636-6647.2002.

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ABSTRACT DYRK1A is the human orthologue of the Drosophila minibrain (mnb) gene, which is involved in postembryonic neurogenesis in flies. Because of its mapping position on chromosome 21 and the neurobehavioral alterations shown by mice overexpressing this gene, involvement of DYRK1A in some of the neurological defects of Down syndrome patients has been suggested. To gain insight into its physiological role, we have generated mice deficient in Dyrk1A function by gene targeting. Dyrk1A−/− null mutants presented a general growth delay and died during midgestation. Mice heterozygous for the mutation (Dyrk1A+/−) showed decreased neonatal viability and a significant body size reduction from birth to adulthood. General neurobehavioral analysis revealed preweaning developmental delay of Dyrk1A+/− mice and specific alterations in adults. Brains of Dyrk1A+/− mice were decreased in size in a region-specific manner, although the cytoarchitecture and neuronal components in most areas were not altered. Cell counts showed increased neuronal densities in some brain regions and a specific decrease in the number of neurons in the superior colliculus, which exhibited a significant size reduction. These data provide evidence about the nonredundant, vital role of Dyrk1A and suggest a conserved mode of action that determines normal growth and brain size in both mice and flies.

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Мыцик, A. Mytsik, Акулинин, et al. "Modern problems of morphological studying of the human cortex cytoarchitecture in norm and during ischemia." Journal of New Medical Technologies. eJournal 8, no. 1 (2014): 1–9. http://dx.doi.org/10.12737/4789.

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Study of the human cortex morphology in norm and at the ischemia is due to the desire to identify common patterns and specific features of compensatory neural networks reorganization, seeking means of regulation of destructive and regenerative processes. The emergence of a large amount of information on the nervous tissue mor-phology is the need for increasing the accuracy of morphometric analysis. This requires an assessment of the overall methodological level of modern morphological studies of the human cortex. The authors analyzed the literature and their own data obtained from a morphological study of the human cortex. The main tendencies, current methodological issues and perspective directions of study the structural and functional state of neurons in norm and ischemia are presented. Great attention is paid to the immunohistochemical and morphometric methods of obtaining objective information. Currently there are methodological and methodical basis for further study of the human brain morphology. However, the total number of articles on the study of human brain morphology earned far less than the experimental works. For the fullest use of biopsy material is offered a comprehensive approach, including method of computer-aided analysis of images, immunohistochemistry, morphometry and statistical analysis.

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Crispino, Marianna, Floriana Volpicelli, and Carla Perrone-Capano. "Role of the Serotonin Receptor 7 in Brain Plasticity: From Development to Disease." International Journal of Molecular Sciences 21, no. 2 (2020): 505. http://dx.doi.org/10.3390/ijms21020505.

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Our knowledge on the plastic functions of the serotonin (5-HT) receptor subtype 7 (5-HT7R) in the brain physiology and pathology have advanced considerably in recent years. A wealth of data show that 5-HT7R is a key player in the establishment and remodeling of neuronal cytoarchitecture during development and in the mature brain, and its dysfunction is linked to neuropsychiatric and neurodevelopmental diseases. The involvement of this receptor in synaptic plasticity is further demonstrated by data showing that its activation allows the rescue of long-term potentiation (LTP) and long-term depression (LTD) deficits in various animal models of neurodevelopmental diseases. In addition, it is becoming clear that the 5-HT7R is involved in inflammatory intestinal diseases, modulates the function of immune cells, and is likely to play a role in the gut-brain axis. In this review, we will mainly focus on recent findings on this receptor’s role in the structural and synaptic plasticity of the mammalian brain, although we will also illustrate novel aspects highlighted in gastrointestinal (GI) tract and immune system.

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Mohamed, Hanan R. H., and Nahed A. Hussien. "Genotoxicity Studies of Titanium Dioxide Nanoparticles (TiO2NPs) in the Brain of Mice." Scientifica 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/6710840.

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Titanium dioxide nanoparticles (TiO2NPs) are excessively used and represent one of the top five most commonly used nanoparticles worldwide. Recently, various studies referred to their toxic potential on various organs using different treatment route. Male Swiss Webster mice were orally administrated TiO2NPs (500 mg/kg b.w.) daily for five consecutive days and then animals were sacrificed at 24 h, 7 days, or 14 days after the last treatment. The present results report that exposure to TiO2NPs produces mild to moderate changes in the cytoarchitecture of brain tissue in a time dependent manner. Moreover, Comet assay revealed the apoptotic DNA fragmentation, while PCR-SSCP pattern and direct sequencing showed point mutation of Presenilin 1 gene at exon 5, gene linked to inherited forms of the Alzheimer’s disease. Therefore, from these findings, the present study concluded that TiO2NPs is genotoxic and mutagenic to brain tissue which in turn might lead to Alzheimer’s disease incidence.

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Tararuk, Tatsiana, Nina Östman, Wenrui Li, et al. "JNK1 phosphorylation of SCG10 determines microtubule dynamics and axodendritic length." Journal of Cell Biology 173, no. 2 (2006): 265–77. http://dx.doi.org/10.1083/jcb.200511055.

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c-Jun NH2-terminal kinases (JNKs) are essential during brain development, when they regulate morphogenic changes involving cell movement and migration. In the adult, JNK determines neuronal cytoarchitecture. To help uncover the molecular effectors for JNKs in these events, we affinity purified JNK-interacting proteins from brain. This revealed that the stathmin family microtubule-destabilizing proteins SCG10, SCLIP, RB3, and RB3′ interact tightly with JNK. Furthermore, SCG10 is also phosphorylated by JNK in vivo on sites that regulate its microtubule depolymerizing activity, serines 62 and 73. SCG10-S73 phosphorylation is significantly decreased in JNK1−/− cortex, indicating that JNK1 phosphorylates SCG10 in developing forebrain. JNK phosphorylation of SCG10 determines axodendritic length in cerebrocortical cultures, and JNK site–phosphorylated SCG10 colocalizes with active JNK in embryonic brain regions undergoing neurite elongation and migration. We demonstrate that inhibition of cytoplasmic JNK and expression of SCG10-62A/73A both inhibited fluorescent tubulin recovery after photobleaching. These data suggest that JNK1 is responsible for regulation of SCG10 depolymerizing activity and neurite elongation during brain development.

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Sakai, Kenji, Mari Tada, Yosuke Yonemochi, et al. "Marinesco-Sjögren syndrome with atrophy of the brain stem tegmentum and dysplastic cytoarchitecture in the cerebral cortex." Neuropathology 28, no. 5 (2008): 541–46. http://dx.doi.org/10.1111/j.1440-1789.2008.00884.x.

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Watanabe-Sawaguchi, Kyoko, Kisou Kubota, and Tomio Arikuni. "Cytoarchitecture and intrafrontal connections of the frontal cortex of the brain of the hamadryas baboon (Papio hamadryas)." Journal of Comparative Neurology 311, no. 1 (1991): 108–33. http://dx.doi.org/10.1002/cne.903110109.

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Taufique, Sheikh Tahajjul, Abhilash Prabhat, and Vinod Kumar. "Light at night affects hippocampal and nidopallial cytoarchitecture: Implication for impairment of brain function in diurnal corvids." Journal of Experimental Zoology Part A: Ecological and Integrative Physiology 331, no. 2 (2018): 149–56. http://dx.doi.org/10.1002/jez.2238.

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ARNOLD, STEVEN E. "Neurodevelopmental abnormalities in schizophrenia: Insights from neuropathology." Development and Psychopathology 11, no. 3 (1999): 439–56. http://dx.doi.org/10.1017/s095457949900214x.

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Growing epidemiological, genetic, and clinical neurobiological evidence indicates that abnormalities in brain development play determining roles in the pathobiology of schizophrenia. Neuropathological research has made significant progress in delineating cellular and molecular abnormalities in schizophrenia that have relevance to neurodevelopment. This paper reviews the neurodevelopmental processes of neurogenesis, neuronal migration, differentiation, synaptogenesis, neuron and synaptic pruning, and myelination and the reported neuropathological findings in schizophrenia that may be a consequence of disturbances in these processes. While many neuropathological findings in schizophrenia are controversial or await confirmation, reported abnormalities in neuron density, number and morphology, cytoarchitecture, dendritic arbors and spines, synapse-related proteins, and the well-established absence of gliosis or any other evidence of neurodegeneration or neural injury all provide support for the neurodevelopmental model of schizophrenia.

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Fulcher, Ben D., John D. Murray, Valerio Zerbi, and Xiao-Jing Wang. "Multimodal gradients across mouse cortex." Proceedings of the National Academy of Sciences 116, no. 10 (2019): 4689–95. http://dx.doi.org/10.1073/pnas.1814144116.

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The primate cerebral cortex displays a hierarchy that extends from primary sensorimotor to association areas, supporting increasingly integrated function underpinned by a gradient of heterogeneity in the brain’s microcircuits. The extent to which these hierarchical gradients are unique to primate or may reflect a conserved mammalian principle of brain organization remains unknown. Here we report the topographic similarity of large-scale gradients in cytoarchitecture, gene expression, interneuron cell densities, and long-range axonal connectivity, which vary from primary sensory to prefrontal areas of mouse cortex, highlighting an underappreciated spatial dimension of mouse cortical specialization. Using the T1-weighted:T2-weighted (T1w:T2w) magnetic resonance imaging map as a common spatial reference for comparison across species, we report interspecies agreement in a range of large-scale cortical gradients, including a significant correspondence between gene transcriptional maps in mouse cortex with their human orthologs in human cortex, as well as notable interspecies differences. Our results support the view of systematic structural variation across cortical areas as a core organizational principle that may underlie hierarchical specialization in mammalian brains.

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Rosenfeld, Amy B., David J. Doobin, Audrey L. Warren, Vincent R. Racaniello, and Richard B. Vallee. "Replication of early and recent Zika virus isolates throughout mouse brain development." Proceedings of the National Academy of Sciences 114, no. 46 (2017): 12273–78. http://dx.doi.org/10.1073/pnas.1714624114.

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Fetal infection with Zika virus (ZIKV) can lead to congenital Zika virus syndrome (cZVS), which includes cortical malformations and microcephaly. The aspects of cortical development that are affected during virus infection are unknown. Using organotypic brain slice cultures generated from embryonic mice of various ages, sites of ZIKV replication including the neocortical proliferative zone and radial columns, as well as the developing midbrain, were identified. The infected radial units are surrounded by uninfected cells undergoing apoptosis, suggesting that programmed cell death may limit viral dissemination in the brain and may constrain virus-associated injury. Therefore, a critical aspect of ZIKV-induced neuropathology may be defined by death of uninfected cells. All ZIKV isolates assayed replicated efficiently in early and midgestation cultures, and two isolates examined replicated in late-gestation tissue. Alteration of neocortical cytoarchitecture, such as disruption of the highly elongated basal processes of the radial glial progenitor cells and impairment of postmitotic neuronal migration, were also observed. These data suggest that all lineages of ZIKV tested are neurotropic, and that ZIKV infection interferes with multiple aspects of neurodevelopment that contribute to the complexity of cZVS.

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Hilgetag, Claus C., Sarah F. Beul, Sacha J. van Albada, and Alexandros Goulas. "An architectonic type principle integrates macroscopic cortico-cortical connections with intrinsic cortical circuits of the primate brain." Network Neuroscience 3, no. 4 (2019): 905–23. http://dx.doi.org/10.1162/netn_a_00100.

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The connections linking neurons within and between cerebral cortical areas form a multiscale network for communication. We review recent work relating essential features of cortico-cortical connections, such as their existence and laminar origins and terminations, to fundamental structural parameters of cortical areas, such as their distance, similarity in cytoarchitecture, defined by lamination or neuronal density, and other macroscopic and microscopic structural features. These analyses demonstrate the presence of an architectonic type principle. Across species and cortices, the essential features of cortico-cortical connections vary consistently and strongly with the cytoarchitectonic similarity of cortical areas. By contrast, in multivariate analyses such relations were not found consistently for distance, similarity of cortical thickness, or cellular morphology. Gradients of laminar cortical differentiation, as reflected in overall neuronal density, also correspond to regional variations of cellular features, forming a spatially ordered natural axis of concerted architectonic and connectional changes across the cortical sheet. The robustness of findings across mammalian brains allows cross-species predictions of the existence and laminar patterns of projections, including estimates for the human brain that are not yet available experimentally. The architectonic type principle integrates cortical connectivity and architecture across scales, with implications for computational explorations of cortical physiology and developmental mechanisms.

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González-García, Ismael, and Cristina García-Cáceres. "Hypothalamic Astrocytes as a Specialized and Responsive Cell Population in Obesity." International Journal of Molecular Sciences 22, no. 12 (2021): 6176. http://dx.doi.org/10.3390/ijms22126176.

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Astrocytes are a type of glial cell anatomically and functionally integrated into the neuronal regulatory circuits for the neuroendocrine control of metabolism. Being functional integral compounds of synapses, astrocytes are actively involved in the physiological regulatory aspects of metabolic control, but also in the pathological processes that link neuronal dysfunction and obesity. Between brain areas, the hypothalamus harbors specialized functional circuits that seem selectively vulnerable to metabolic damage, undergoing early cellular rearrangements which are thought to be at the core of the pathogenesis of diet-induced obesity. Such changes in the hypothalamic brain region consist of a rise in proinflammatory cytokines, the presence of a reactive phenotype in astrocytes and microglia, alterations in the cytoarchitecture and synaptology of hypothalamic circuits, and angiogenesis, a phenomenon that cannot be found elsewhere in the brain. Increasing evidence points to the direct involvement of hypothalamic astrocytes in such early metabolic disturbances, thus moving the study of these glial cells to the forefront of obesity research. Here we provide a comprehensive review of the most relevant findings of molecular and pathophysiological mechanisms by which hypothalamic astrocytes might be involved in the pathogenesis of obesity.

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Song, Liqing, Yuanwei Yan, Mark Marzano, and Yan Li. "Studying Heterotypic Cell–Cell Interactions in the Human Brain Using Pluripotent Stem Cell Models for Neurodegeneration." Cells 8, no. 4 (2019): 299. http://dx.doi.org/10.3390/cells8040299.

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Human cerebral organoids derived from induced pluripotent stem cells (iPSCs) provide novel tools for recapitulating the cytoarchitecture of the human brain and for studying biological mechanisms of neurological disorders. However, the heterotypic interactions of neurovascular units, composed of neurons, pericytes (i.e., the tissue resident mesenchymal stromal cells), astrocytes, and brain microvascular endothelial cells, in brain-like tissues are less investigated. In addition, most cortical organoids lack a microglia component, the resident immune cells in the brain. Impairment of the blood-brain barrier caused by improper crosstalk between neural cells and vascular cells is associated with many neurodegenerative disorders. Mesenchymal stem cells (MSCs), with a phenotype overlapping with pericytes, have promotion effects on neurogenesis and angiogenesis, which are mainly attributed to secreted growth factors and extracellular matrices. As the innate macrophages of the central nervous system, microglia regulate neuronal activities and promote neuronal differentiation by secreting neurotrophic factors and pro-/anti-inflammatory molecules. Neuronal-microglia interactions mediated by chemokines signaling can be modulated in vitro for recapitulating microglial activities during neurodegenerative disease progression. In this review, we discussed the cellular interactions and the physiological roles of neural cells with other cell types including endothelial cells and microglia based on iPSC models. The therapeutic roles of MSCs in treating neural degeneration and pathological roles of microglia in neurodegenerative disease progression were also discussed.

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Mehta, Suresh L., Anil K. Chokkalla, TaeHee Kim, et al. "Long Noncoding RNA Fos Downstream Transcript Is Developmentally Dispensable but Vital for Shaping the Poststroke Functional Outcome." Stroke 52, no. 7 (2021): 2381–92. http://dx.doi.org/10.1161/strokeaha.120.033547.

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Background and Purpose: Stroke induces the expression of several long noncoding RNAs in the brain. However, their functional significance in poststroke outcome is poorly understood. We recently observed that a brain-specific long noncoding RNA called Fos downstream transcript (FosDT) is induced rapidly in the rodent brain following focal ischemia. Using FosDT knockout rats, we presently evaluated the role of FosDT in poststroke brain damage. Methods: FosDT knockout rats were generated using CRISPR-Cas9 genome editing on a Sprague-Dawley background. Male and female FosDT −/− and FosDT +/+ cohorts were subjected to transient middle cerebral artery occlusion. Postischemic sensorimotor deficits were evaluated between days 1 and 7 and lesion volume on day 7 of reperfusion. The developmental expression profile of FosDT was determined with real-time polymerase chain reaction and mechanistic implications of FosDT in the ischemic brain were conducted with RNA-sequencing analysis and immunostaining of pathological markers. Results: FosDT expression is developmentally regulated, with the adult cerebral cortex showing significantly higher FosDT expression than neonates. FosDT −/− rats did not show any anomalies in growth and development, fertility, brain cytoarchitecture, and cerebral vasculature. However, when subjected to transient focal ischemia, FosDT −/− rats of both sexes showed enhanced sensorimotor recovery and reduced brain damage. RNA-sequencing analysis showed that improved poststroke functional outcome in FosDT −/− rats is partially associated with curtailed induction of inflammatory genes, reduced apoptosis, mitochondrial dysfunction, and oxidative stress. Conclusions: Our study shows that FosDT is developmentally dispensable, mechanistically important, and a functionally promising target to reduce ischemic brain damage and facilitate neurological recovery.

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Nie, Xingju, Eric D. Hamlett, Ann-Charlotte Granholm, et al. "Evidence of altered age-related brain cytoarchitecture in mouse models of down syndrome: a diffusional kurtosis imaging study." Magnetic Resonance Imaging 33, no. 4 (2015): 437–47. http://dx.doi.org/10.1016/j.mri.2014.12.008.

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Bakhshi, K., and S. A. Chance. "The neuropathology of schizophrenia: A selective review of past studies and emerging themes in brain structure and cytoarchitecture." Neuroscience 303 (September 2015): 82–102. http://dx.doi.org/10.1016/j.neuroscience.2015.06.028.

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Guerrero-Cázares, Hugo, Oscar Gonzalez-Perez, Mario Soriano-Navarro, Grettel Zamora-Berridi, José Manuel García-Verdugo, and Alfredo Quinoñes-Hinojosa. "Cytoarchitecture of the lateral ganglionic eminence and rostral extension of the lateral ventricle in the human fetal brain." Journal of Comparative Neurology 519, no. 6 (2011): 1165–80. http://dx.doi.org/10.1002/cne.22566.

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