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Increased Cell Fusion in Cerebral Cortex May Contribute to Poststroke Regeneration  [PDF]
Alexander Paltsyn,Svetlana Komissarova,Ivan Dubrovin,Aslan Kubatiev
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/869327
Abstract: In this study, we used a model of a hemorrhagic stroke in a motor zone of the cortex in rats at the age of 3 months The report shows that cortical neurons can fuse with oligodendrocytes. In formed binuclear cells, the nucleus of an oligodendrocyte undergoes neuron specific reprogramming. It can be confirmed by changes in chromatin structure and in size of the second nucleus, by expression of specific neuronal markers and increasing total transcription rate. The nucleus of an oligodendrocyte likely transforms into a second neuronal nucleus. The number of binuclear neurons was validated with quantitative analysis. Fusion of neurons with oligodendrocytes might be a regenerative process in general and specifically following a stroke. The appearance of additional neuronal nuclei increases the functional outcome of the population of neurons. Participation of a certain number of binuclear cells in neuronal function might compensate for a functional deficit that arises from the death of a subset of neurons. After a stroke, the number of binuclear neurons increased in cortex around the lesion zone. In this case, the rate of recovery of stroke-damaged locomotor behavior also increased, which indicates the regenerative role of fusion. 1. Introduction Protection, rehabilitation, and stroke outcome are determined by the extent of the preserved neuronal tissue. Thus, the maintenance and regeneration of stroke-injured neurons is a prominent topic on which there are many publications, all of which represent neuronal regeneration exclusively as a result of neurogenesis. This tendency can be justified only in one case, when a stroke occurs in the dentate gyrus (fascia dentata hippocampus) or in the olfactory bulb. These two zones are reasonably considered neurogenic because they are sites of the replacement of granular neurons. Granular neurons are formed in two other neurogenic zones: the subgranular layer of the dentate gyrus [1–5] and the subventricular layer of the cerebral ventricles [6–8]. Neuroblasts migrate from these zones to the granular layer of the dentate gyrus [9–11] and to the olfactory bulbs [8, 12], where they differentiate into granular neurons. Reports of neurogenesis in other brain regions, as in the review of Gould [13], contradict other experiments [14–17]. Therefore, scientific consensus purports that, in other brain regions, neurogenesis does not occur. According to one hypothesis, neurogenesis does not normally occur in the cortex but appears after stroke [18, 19]. However, some publications do not confirm this point of view [20]. These issues
Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats
Rahmy, T.R.;Hassona, I.A.;
Journal of Venomous Animals and Toxins including Tropical Diseases , 2004, DOI: 10.1590/S1678-91992004000100005
Abstract: the immunohistochemical expression of neuron-specific enolase, nse (a cytoplasmic glycolytic enzyme of the neurons), synaptophysin, syn (a major membrane glycoprotein of synaptic vesicles), and bcl-2 (anti-apoptotic protein) were determined in cerebral cortex of rats envenomed with neurotoxic venom from egyptian cobra. male rats were intramuscularly (im) injected with a single injection of either physiological saline solution or ? ld50 or ld50 of cobra venom and sacrificed 24, 48, or 72 hr after envenoming. formalin-fixed paraffin sections were immunohistochemically studied by avidin-biotin-peroxidase complex method. neuron histological structure and isolation of genomic dna were also detected. the results showed a dose and time-dependent increase in nse and syn immunoreactivity in cerebral cortex of envenomed rats except in 72 hr high dose envenoming, where decreased syn was observed. on the other hand, low dose venom induced high bcl-2 expression 24 hr after envenoming, while the high dose decreased bcl-2 protein expression. temporal and spatial bcl-2 expression was accompanied by dna fragmentation in cerebral cortex of all envenomed rats, although no serious histological alterations were noticed. these results suggest that cobra venom may lead to neuronal injury and impairment of axonal transport as ascertained by alterations in nse and syn immunoreactivity. it could also indicate that venom alters the molecular machinery of apoptosis by inhibiting bcl-2 expression; however, some vulnerable cells have the ability to overcome this by increasing bcl-2 protein. these immunohistochemical investigations can be used as tools for detecting neuronal abnormalities even before the occurrence of any histological alterations in case of cerebral cortex neurotoxicity.
Relating Neuronal Firing Patterns to Functional Differentiation of Cerebral Cortex  [PDF]
Shigeru Shinomoto ,Hideaki Kim ,Takeaki Shimokawa ,Nanae Matsuno,Shintaro Funahashi,Keisetsu Shima,Ichiro Fujita,Hiroshi Tamura,Taijiro Doi,Kenji Kawano,Naoko Inaba,Kikuro Fukushima,Sergei Kurkin,Kiyoshi Kurata,Masato Taira,Ken-Ichiro Tsutsui,Hidehiko Komatsu,Tadashi Ogawa,Kowa Koida,Jun Tanji,Keisuke Toyama
PLOS Computational Biology , 2009, DOI: 10.1371/journal.pcbi.1000433
Abstract: It has been empirically established that the cerebral cortical areas defined by Brodmann one hundred years ago solely on the basis of cellular organization are closely correlated to their function, such as sensation, association, and motion. Cytoarchitectonically distinct cortical areas have different densities and types of neurons. Thus, signaling patterns may also vary among cytoarchitectonically unique cortical areas. To examine how neuronal signaling patterns are related to innate cortical functions, we detected intrinsic features of cortical firing by devising a metric that efficiently isolates non-Poisson irregular characteristics, independent of spike rate fluctuations that are caused extrinsically by ever-changing behavioral conditions. Using the new metric, we analyzed spike trains from over 1,000 neurons in 15 cortical areas sampled by eight independent neurophysiological laboratories. Analysis of firing-pattern dissimilarities across cortical areas revealed a gradient of firing regularity that corresponded closely to the functional category of the cortical area; neuronal spiking patterns are regular in motor areas, random in the visual areas, and bursty in the prefrontal area. Thus, signaling patterns may play an important role in function-specific cerebral cortical computation.
Neuronal activity (c-Fos) delineating interactions of the cerebral cortex and basal ganglia  [PDF]
Mei-Hong Qiu,Michael C. Chen,Zhi-Li Huang,Jun Lu
Frontiers in Neuroanatomy , 2014, DOI: 10.3389/fnana.2014.00013
Abstract: The cerebral cortex and basal ganglia (BG) form a neural circuit that is disrupted in disorders such as Parkinson’s disease. We found that neuronal activity (c-Fos) in the BG followed cortical activity, i.e., high in arousal state and low in sleep state. To determine if cortical activity is necessary for BG activity, we administered atropine to rats to induce a dissociative state resulting in slow-wave electroencephalography but hyperactive motor behaviors. Atropine blocked c-Fos expression in the cortex and BG, despite high c-Fos expression in the sub-cortical arousal neuronal groups and thalamus, indicating that cortical activity is required for BG activation. To identify which glutamate receptors in the BG that mediate cortical inputs, we injected ketamine [N-methyl-D-aspartate (NMDA) receptor antagonist] and 6-cyano-nitroquinoxaline-2, 3-dione (CNQX, a non-NMDA receptor antagonist). Systemic ketamine and CNQX administration revealed that NMDA receptors mediated subthalamic nucleus (STN) input to internal globus pallidus (GPi) and substantia nigra pars reticulata (SNr), while non-NMDA receptor mediated cortical input to the STN. Both types of glutamate receptors were involved in mediating cortical input to the striatum. Dorsal striatal (caudoputamen, CPu) dopamine depletion by 6-hydroxydopamine resulted in reduced activity of the CPu, globus pallidus externa (GPe), and STN but increased activity of the GPi, SNr, and putative layer V neurons in the motor cortex. Our results reveal that the cortical activity is necessary for BG activity and clarifies the pathways and properties of the BG-cortical network and their putative role in the pathophysiology of BG disorders.
ADAM17 Is Critical for Multipolar Exit and Radial Migration of Neuronal Intermediate Progenitor Cells in Mice Cerebral Cortex  [PDF]
Qingyu Li, Zhengyu Zhang, Zengmin Li, Mei Zhou, Bin Liu, Le Pan, Zhixing Ma, Yufang Zheng
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0065703
Abstract: The radial migration of neuronal progenitor cells is critical for the development of cerebral cortex layers. They go through a critical step transforming from multipolar to bipolar before outward migration. A Disintegrin and Metalloprotease 17 (ADAM17) is a transmembrane protease which can process many substrates involved in cell-cell interaction, including Notch, ligands of EGFR, and some cell adhesion molecules. In this study, we used in utero electroporation to knock down or overexpress ADAM17 at embryonic day 14.5 (E14.5) in neuronal progenitor cells to examine the role of ADAM17 in cortical embryonic neurogenesis. Our results showed that the radial migration of ADAM17-knocked down cells were normal till E16.5 and reached the intermediate zone (IZ). Then most transfected cells stopped migration and stayed at the IZ to inner cortical plate (CP) layer at E18.5, and there was higher percentage of multipolar cells at IZ layer in the ADAM17-knocked down group compared to the cells in control group. Marker staining revealed that those ADAM17-knocked down cells differentiated normally from neural stem cells (NSCs) to neuronal intermediate progenitor cells (nIPCs) but did not differentiate into mature neurons. The migration and multipolar exit defects caused by ADAM17 knockdown could be partially rescued by over-expressing an shRNA resistant ADAM17, while overexpressing ADAM17 alone did not affect the radial migration. Taken together, our results showed for the first time that, ADAM17 is critical in regulating the multipolar-stage exit and radial migration of the nIPCs during telencephalon cortex development in mice.
Diffusion Tensor Imaging Detects Early Cerebral Cortex Abnormalities in Neuronal Architecture Induced by Bilateral Neonatal Enucleation: An Experimental Model in the Ferret  [PDF]
Andrew S. Bock,Jaime F. Olavarria,Lindsey A. Leigland,Erin N. Taber,Sune N?rh?j Jespersen,Christopher D. Kroenke
Frontiers in Systems Neuroscience , 2010, DOI: 10.3389/fnsys.2010.00149
Abstract: Diffusion tensor imaging (DTI) is a technique that non-invasively provides quantitative measures of water translational diffusion, including fractional anisotropy (FA), that are sensitive to the shape and orientation of cellular elements, such as axons, dendrites and cell somas. For several neurodevelopmental disorders, histopathological investigations have identified abnormalities in the architecture of pyramidal neurons at early stages of cerebral cortex development. To assess the potential capability of DTI to detect neuromorphological abnormalities within the developing cerebral cortex, we compare changes in cortical FA with changes in neuronal architecture and connectivity induced by bilateral enucleation at postnatal day 7 (BEP7) in ferrets. We show here that the visual callosal pattern in BEP7 ferrets is more irregular and occupies a significantly greater cortical area compared to controls at adulthood. To determine whether development of the cerebral cortex is altered in BEP7 ferrets in a manner detectable by DTI, cortical FA was compared in control and BEP7 animals on postnatal day 31. Visual cortex, but not rostrally adjacent non-visual cortex, exhibits higher FA than control animals, consistent with BEP7 animals possessing axonal and dendritic arbors of reduced complexity than age-matched controls. Subsequent to DTI, Golgi-staining and analysis methods were used to identify regions, restricted to visual areas, in which the orientation distribution of neuronal processes is significantly more concentrated than in control ferrets. Together, these findings suggest that DTI can be of utility for detecting abnormalities associated with neurodevelopmental disorders at early stages of cerebral cortical development, and that the neonatally enucleated ferret is a useful animal model system for systematically assessing the potential of this new diagnostic strategy.
The Role of Neonatal Carnitine Palmitoyl Transferase Deficiency Type II on Proliferation of Neuronal Progenitor Cells and Layering of the Cerebral Cortex in the Developing Brain
Heepeel Chang,Phyllis Faust
Columbia Undergraduate Science Journal , 2007,
Abstract: Neonatal Carnitine Palmitoyl Transferase Deficiency Type II, characterized by the absence of CPT II enzyme, is one of the lethal disorders of mitochondrial fatty acid oxidation. CPT II regulates the conversion of long chain fatty acids, so that its product, acyl-CoA esters, can enter the Krebs cycle and generate energy. Neonatal mutations of CPT II lead to severe disruption of the metabolism of long-chain fatty acids and result in dysmorphic features, cystic renal dysplasia, and neuronal migration defects. Examination of the brain from an approximately 15-week gestation human fetus with CPT II deficiency revealed premature formation of cerebral cortical gyri and sulci and significantly lower levels of neuronal cell proliferation in the ventricular and subventricular zones as compared to the reference cases. We used immunohistochemical markers to further characterize the effect of CPT II deficiency on progenitor cell proliferation and layering of neurons. These studies demonstrated a premature generation of layer 5 cortical neurons. In addition, both the total number and percentage of progenitor cells proliferating in the ventricular zone were markedly reduced in the CPT II case in comparison to a reference case. Our results indicate that CPT II deficiency alters the normal program of cellular proliferation and differentiation in the cortex, with early differentiation of progenitor cells associated with premature cortical maturation.
Does brain activity stem from high-dimensional chaotic dynamics? Evidence from the human electroencephalogram, cat cerebral cortex and artificial neuronal networks  [PDF]
Sami El Boustani,Alain Destexhe
Physics , 2009,
Abstract: Nonlinear time series analyses have suggested that the human electroencephalogram (EEG) may share statistical and dynamical properties with chaotic systems. During slow-wave sleep or pathological states like epilepsy, correlation dimension measurements display low values, while in awake and attentive subjects, there is not such low dimensionality, and the EEG is more similar to a stochastic variable. We briefly review these results and contrast them with recordings in cat cerebral cortex, as well as with theoretical models. In awake or sleeping cats, recordings with microelectrodes inserted in cortex show that global variables such as local field potentials (local EEG) are similar to the human EEG. However, in both cases, neuronal discharges are highly irregular and exponentially distributed, similar to Poisson stochastic processes. To attempt reconcile these results, we investigate models of randomly-connected networks of integrate-and-fire neurons, and also contrast global (averaged) variables, with neuronal activity. The network displays different states, such as "synchronous regular" (SR) or "asynchronous irregular" (AI) states. In SR states, the global variables display coherent behavior with low dimensionality, while in AI states, the global activity is high-dimensionally chaotic with exponentially distributed neuronal discharges, similar to awake cats. Scale-dependent Lyapunov exponents and epsilon-entropies show that the seemingly stochastic nature at small scales (neurons) can coexist with more coherent behavior at larger scales (averages). Thus, we suggest that brain activity obeys similar scheme, with seemingly stochastic dynamics at small scales (neurons), while large scales (EEG) display more coherent behavior or high-dimensional chaos.
The human cerebral cortex is neither one nor many: neuronal distribution reveals two quantitatively different zones in the gray matter, three in the white matter, and explains local variations in cortical folding  [PDF]
Pedro F. M. Ribeiro,Lissa Ventura-Antunes,Mariana Gabi,Bruno Mota,Lea T. Grinberg,José M. Farfel,Renata E. L. Ferretti-Rebustini,Renata E. P. Leite,Suzana Herculano-Houzel
Frontiers in Neuroanatomy , 2013, DOI: 10.3389/fnana.2013.00028
Abstract: The human prefrontal cortex has been considered different in several aspects and relatively enlarged compared to the rest of the cortical areas. Here we determine whether the white and gray matter of the prefrontal portion of the human cerebral cortex have similar or different cellular compositions relative to the rest of the cortical regions by applying the Isotropic Fractionator to analyze the distribution of neurons along the entire anteroposterior axis of the cortex, and its relationship with the degree of gyrification, number of neurons under the cortical surface, and other parameters. The prefrontal region shares with the remainder of the cerebral cortex (except for occipital cortex) the same relationship between cortical volume and number of neurons. In contrast, both occipital and prefrontal areas vary from other cortical areas in their connectivity through the white matter, with a systematic reduction of cortical connectivity through the white matter and an increase of the mean axon caliber along the anteroposterior axis. These two parameters explain local differences in the distribution of neurons underneath the cortical surface. We also show that local variations in cortical folding are neither a function of local numbers of neurons nor of cortical thickness, but correlate with properties of the white matter, and are best explained by the folding of the white matter surface. Our results suggest that the human cerebral cortex is divided in two zones (occipital and non-occipital) that differ in how neurons are distributed across their gray matter volume and in three zones (prefrontal, occipital, and non-occipital) that differ in how neurons are connected through the white matter. Thus, the human prefrontal cortex has the largest fraction of neuronal connectivity through the white matter and the smallest average axonal caliber in the white matter within the cortex, although its neuronal composition fits the pattern found for other, non-occipital areas.
Alteraciones de la morfología dendrítica neuronal en la corteza cerebral de ratones infectados con rabia: un estudio con la técnica de Golgi Neuronal dentritic morphology alterations in the cerebral cortex of rabies-infected mice: a Golgi study  [cached]
Orlando Torres-Fernández,Gloria E. Yepes,Javier E. Gómez
Biomédica , 2007,
Abstract: Introducción. Los signos neurológicos de la rabia son impresionantes; no obstante, el cerebro infectado sufre apenas cambios histológicos muy sutiles. Objetivo. Estudiar la morfología neuronal mediante la técnica de Golgi, en la corteza cerebral de ratones infectados con el virus de la rabia. Materiales y métodos. Se inocularon ratones con virus silvestre de la rabia (virus ‘calle') de origen canino o con virus adaptado (virus ‘fijo') de la cepa CVS (challenge virus standard). Los animales se sacrificaron en la fase terminal de la enfermedad y se fijaron por perfusión con paraformaldehído. Los cerebros se procesaron con la técnica de Golgi, se obtuvieron cortes coronales de la corteza, se contaron las neuronas impregnadas en un área de 1 mm2, se midió el tama o de sus cuerpos celulares y se tomaron fotografías en diferentes planos de profundidad. Resultados. Se observaron alteraciones morfológicas notables en el soma y las dendritas de neuronas piramidales, con pérdida acentuada de espinas, en 12,9% de neuronas corticales de animales infectados con virus ‘calle' por vía intracerebral; en 8,2% de neuronas de ratones inoculados con este mismo virus por la ruta intramuscular y en 31,8% de neuronas en los animales inoculados con virus ‘fijo' por vía intramuscular. Además, en las muestras de material infectado el número de neuronas impregnadas por la técnica de Golgi fue considerablemente menor al observado en las muestras no infectadas. Conclusiones. Estos resultados son evidencia de que el virus de la rabia sí puede inducir da o neuronal estructural. Además, esta infección aparentemente interfiere con los mecanismos de impregnación argéntica del método de Golgi. Introduction. The neurological signs of rabies are very dramatic. Nevertheless, the infected brain manifests only very subtle histological changes. Objective. The neuronal morphology in the cerebral cortex of rabies-infected mice was examined by means the Golgi technique for detection of neuropathy. Materials and methods. Two groups of mice were inoculated with rabies-one with street virus isolated from an infected dog and the second with fixed CVS (challenge virus standard) virus. At the terminal phase of illness, the animals were sacrificed and fixed for histological staining by perfusion with paraformaldehyde. Next, the brains were treated by the Golgi technique and coronal sections were obtained. Neurons enclosed within 1 mm2 frames of the frontal cortex sections were counted and the sizes of the cellular bodies were measured. Photographs of several depth levels from the sections were obtained.
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