scholarly journals Subependymal Zone: Immunohistochemically Distinct Compartment in the Adult Mammalian Forebrain

2004 ◽  
Vol 47 (4) ◽  
pp. 235-242 ◽  
Author(s):  
Jaroslav Mokrý ◽  
Dana Čížková ◽  
Jan Österreicher
Keyword(s):  
Cell Types ◽  
Brain Parenchyma ◽  
Mammalian Brain ◽  
Histological Structure ◽  
Astroglial Cell ◽  
Neuronal Markers ◽  
Subependymal Zone ◽  
Rat Forebrain ◽  
The Brain ◽  
Migratory Stream

The subependymal zone (SEZ) lining lateral walls of the lateral cerebral ventricles represents the site of active neurogenesis in the brain of adult mammals. Peroxidase immunohistochemistry performed in paraffin-embedded sections reveals that structural organization of the SEZ differs from other regions in the brain. The SEZ is devoid of synapses that are abundant in the adjacent striatal neuropil. Therefore immunostaining of synaptophysin detects sharp borders of the SEZ. Using immunophenotypization, we identified cell types constituting the SEZ in the intact rat forebrain. The presence of neural progenitor/stem cells was confirmed by finding of nestin-immunopositive cells. Detection of the astroglial marker GFAP confirmed that astrocytes represented major supporting elements responsible for creating a unique microenvironment of the SEZ. One type of the astroglia participated in covering surfaces of the blood vessels and boundaries of the SEZ. The second astroglial cell type formed branched elongated tubes that enwrapped other SEZ cell types with their cytoplasmic extensions. The interior of astrocytic channels was occupied with small densely aggregated NCAM-immunoreactive neuroblasts. Bipolar morphology indicated that these cells probably underwent migration. Immunodetection of other neuronal markers like β-III tubulin, MAP-2 and Pan neurofilaments identified positive cells in the neighbouring brain parenchyma but not in the SEZ. The rostral migratory stream (RMS) linked with the anterior SEZ had a similar structural arrangement. It contained a large amount of nestin+and vimentin+cells. The RMS consisted of GFAP+astrocytic tubes ensheathing NCAM+neuroblasts. On the contrary to the SEZ, the RMS neuroblasts expressed β-III tubulin. However, markers of postmitotic neurons MAP-2, Pan neurofilaments and synaptophysin were not expressed in the RMS. Our study describes a complex histological structure of the rat SEZ, identifies its individual cell types and demonstrates a usefulness of immunohistochemical detection of cell-specific markers in a study of microenvironment forming neurogenic zones in the mammalian brain.

Age-related changes in microglial physiology: the role for healthy brain ageing and neurodegenerative disorders

e-Neuroforum ◽  
2017 ◽  
Vol 23 (4) ◽  
Author(s):  
Olga Garaschuk
Keyword(s):  
Neurodegenerative Disorders ◽  
Healthy Aging ◽  
Molecular Mechanisms ◽  
Brain Parenchyma ◽  
Immune Defense ◽  
Synaptic Activity ◽  
Mammalian Brain ◽  
Age Related ◽  
Brain Ageing ◽  
The Brain

AbstractMicroglia are the main immune cells of the brain contributing, however, not only to brain’s immune defense but also to many basic housekeeping functions such as development and maintenance of functional neural networks, provision of trophic support for surrounding neurons, monitoring and modulating the levels of synaptic activity, cleaning of accumulating extracellular debris and repairing microdamages of the brain parenchyma. As a consequence, age-related alterations in microglial function likely have a manifold impact on brain’s physiology. In this review, I discuss the recent data about physiological properties of microglia in the adult mammalian brain; changes observed in the brain innate immune system during healthy aging and the probable biological mechanisms responsible for them as well as changes occurring in humans and mice during age-related neurodegenerative disorders along with underlying cellular/molecular mechanisms. Together these data provide a new conceptual framework for thinking about the role of microglia in the context of age-mediated brain dysfunction.

scholarly journals The Neurobiology of Selenium: Looking Back and to the Future

2021 ◽  
Vol 15 ◽  
Author(s):  
Ulrich Schweizer ◽  
Simon Bohleber ◽  
Wenchao Zhao ◽  
Noelia Fradejas-Villar
Keyword(s):  
Cell Biology ◽  
Molecular Mechanisms ◽  
Human Genetics ◽  
Epileptic Seizures ◽  
Cell Types ◽  
Mammalian Brain ◽  
The Individual ◽  
The Brain ◽  
Looking Back

Eighteen years ago, unexpected epileptic seizures in Selenop-knockout mice pointed to a potentially novel, possibly underestimated, and previously difficult to study role of selenium (Se) in the mammalian brain. This mouse model was the key to open the field of molecular mechanisms, i.e., to delineate the roles of selenium and individual selenoproteins in the brain, and answer specific questions like: how does Se enter the brain; which processes and which cell types are dependent on selenoproteins; and, what are the individual roles of selenoproteins in the brain? Many of these questions have been answered and much progress is being made to fill remaining gaps. Mouse and human genetics have together boosted the field tremendously, in addition to traditional biochemistry and cell biology. As always, new questions have become apparent or more pressing with solving older questions. We will briefly summarize what we know about selenoproteins in the human brain, glance over to the mouse as a useful model, and then discuss new questions and directions the field might take in the next 18 years.

scholarly journals Immovable Object Meets Unstoppable Force? Dialogue Between Resident and Peripheral Myeloid Cells in the Inflamed Brain

2020 ◽  
Vol 11 ◽  
Author(s):  
Alanna G. Spiteri ◽  
Claire L. Wishart ◽  
Nicholas J. C. King
Keyword(s):  
Myeloid Cells ◽  
Cell Types ◽  
Brain Parenchyma ◽  
Specific Cell ◽  
Novel Treatments ◽  
Experimental Systems ◽  
Immune Mediated ◽  
Recent Developments ◽  
The Central Nervous System ◽  
The Brain

Inflammation of the brain parenchyma is characteristic of neurodegenerative, autoimmune, and neuroinflammatory diseases. During this process, microglia, which populate the embryonic brain and become a permanent sentinel myeloid population, are inexorably joined by peripherally derived monocytes, recruited by the central nervous system. These cells can quickly adopt a morphology and immunophenotype similar to microglia. Both microglia and monocytes have been implicated in inducing, enhancing, and/or maintaining immune-mediated pathology and thus disease progression in a number of neuropathologies. For many years, experimental and analytical systems have failed to differentiate resident microglia from peripherally derived myeloid cells accurately. This has impeded our understanding of their precise functions in, and contributions to, these diseases, and hampered the development of novel treatments that could target specific cell subsets. Over the past decade, microglia have been investigated more intensively in the context of neuroimmunological research, fostering the development of more precise experimental systems. In light of our rapidly growing understanding of these cells, we discuss the differential origins of microglia and peripherally derived myeloid cells in the inflamed brain, with an analysis of the problems resolving these cell types phenotypically and morphologically, and highlight recent developments enabling more precise identification.

scholarly journals Cloning of DNA corresponding to rare transcripts of rat brain: evidence of transcriptional and post-transcriptional control and of the existence of nonpolyadenylated transcripts.

1984 ◽  
Vol 4 (10) ◽  
pp. 2187-2197 ◽  
Author(s):  
M H Brilliant ◽  
N Sueoka ◽  
D M Chikaraishi
Keyword(s):  
Rat Brain ◽  
Transcriptional Control ◽  
Cultured Cells ◽  
Cell Clone ◽  
Cell Types ◽  
Mammalian Brain ◽  
Neural Cells ◽  
Genes Encoding ◽  
Liver And Kidney ◽  
The Brain

To examine the expression of genes encoding rare transcripts in the rat brain, we have characterized genomic DNA clones corresponding to this class. In brain cells, as in all cell types, rare transcripts constitute the majority of different sequences transcribed. Moreover, when compared with other tissues or cultured cells, brain tissue may be expected to have an even larger set of rare transcripts, some of which could be restricted to subpopulations of neural cells. We have identified seven clones whose transcripts are nonabundant, averaging less than three copies per cell. Clone rg13 (rat genomic 13) RNA was detected only in the brain, whereas RNA of a second clone, rg40, was also detected in the brain and in a melanoma. Transcripts of rg13 were found in cerebellum, cerebral cortex, and regions underlying the cortex, whereas rg40 transcripts were not detected in the cerebellum. Transcripts of both rg13 and rg40 were found in pelleted polysomal RNA. RNA of another clone, rg34, was found in the brain, liver, and kidney but was found in pelleted polysomal RNA only in the brain, suggesting that its expression may be post-transcriptionally controlled. The remaining four clones represent rare transcripts that are common to the brain, liver, and kidney; rg18 RNA is restricted to the nucleus, whereas rg3, rg26, and rg36 transcripts are found in the cytoplasm of all three tissues. Transcripts of the brain-specific clone, rg13, and the commonly expressed clone, rg3, are nonpolyadenylated, presumably belonging to the high-complexity, nonpolyadenylated class of transcripts in the mammalian brain.

scholarly journals The neutrophil enzyme myeloperoxidase directly modulates neuronal response after subarachnoid hemorrhage, a sterile injury model

2019 ◽  
Author(s):  
Aminata P. Coulibaly ◽  
Pinar Pezuk ◽  
Paul Varghese ◽  
William Gartman ◽  
Danielle Triebwasser ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cognitive Deficits ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neuronal Response ◽  
Neutrophil Infiltration ◽  
Cell Types ◽  
Brain Parenchyma ◽  
Cerebral Injury ◽  
Biologically Active ◽  
The Brain

AbstractNeutrophil infiltration into the central nervous system (CNS) after injury is associated with cognitive deficits. Using a murine model of aneurysmal subarachnoid hemorrhage (SAH), we elucidate the location and mode of action of neutrophils in the CNS. Following SAH, neutrophils infiltrate the meninges, and not the brain parenchyma. Mice lacking functional myeloperoxidase (MPO KO), a neutrophil enzyme, lack both the meningeal neutrophil infiltration and the cognitive deficits associated with delayed cerebral injury from SAH. The re-introduction of biologically active MPO, and its substrate hydrogen peroxide, to the cerebrospinal fluid of MPO KO mice at the time of hemorrhage restores the spatial memory deficit observed after SAH. This implicates MPO as a mediator of neuronal dysfunction in SAH. Using primary neuronal and astrocyte cultures, we demonstrate that MPO directly affects the function of both cell types. Neurons exposed to MPO and its substrate show decreased calcium activity at baseline and after stimulation with potassium chloride. In addition, MPO and its substrate lead to significant astrocyte loss in culture, a result observed in the brain after SAH as well. These results show that, in SAH, the activity of innate immune cells in the meninges modulates the activity and function of the underlying brain tissue.

scholarly journals Establishment and Preliminary Characterization of Three Astrocytic Cells Lines Obtained from Primary Rat Astrocytes by Sub-Cloning

Genes ◽  
2020 ◽  
Vol 11 (12) ◽  
pp. 1502
Author(s):  
Fabio Caradonna ◽  
Gabriella Schiera ◽  
Carlo Maria Di Liegro ◽  
Vincenzo Vitale ◽  
Ilenia Cruciata ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cell Types ◽  
Brain Parenchyma ◽  
Brain Cell ◽  
The Other ◽  
Cellular Events ◽  
Rat Astrocytes ◽  
The Brain ◽  
Brain Cell Types

Gliomas are complex and heterogeneous tumors that originate from the glial cells of the brain. The malignant cells undergo deep modifications of their metabolism, and acquire the capacity to invade the brain parenchyma and to induce epigenetic modifications in the other brain cell types. In spite of the efforts made to define the pathology at the molecular level, and to set novel approaches to reach the infiltrating cells, gliomas are still fatal. In order to gain a better knowledge of the cellular events that accompany astrocyte transformation, we developed three increasingly transformed astrocyte cell lines, starting from primary rat cortical astrocytes, and analyzed them at the cytogenetic and epigenetic level. In parallel, we also studied the expression of the differentiation-related H1.0 linker histone variant to evaluate its possible modification in relation with transformation. We found that the most modified astrocytes (A-FC6) have epigenetic and chromosomal alterations typical of cancer, and that the other two clones (A-GS1 and A-VV5) have intermediate properties. Surprisingly, the differentiation-specific somatic histone H1.0 steadily increases from the normal astrocytes to the most transformed ones. As a whole, our results suggest that these three cell lines, together with the starting primary cells, constitute a potential model for studying glioma development.

scholarly journals Brain Ultrastructure: Putting the Pieces Together

2021 ◽  
Vol 9 ◽  
Author(s):  
Patrick C. Nahirney ◽  
Marie-Eve Tremblay
Keyword(s):  
Three Dimensional ◽  
Cell Types ◽  
Brain Parenchyma ◽  
Electron Microscopic ◽  
Functional Relationships ◽  
Resolution Electron ◽  
The Central Nervous System ◽  
Cytoskeletal Elements ◽  
Different Cell Types ◽  
The Brain

Unraveling the fine structure of the brain is important to provide a better understanding of its normal and abnormal functioning. Application of high-resolution electron microscopic techniques gives us an unprecedented opportunity to discern details of the brain parenchyma at nanoscale resolution, although identifying different cell types and their unique features in two-dimensional, or three-dimensional images, remains a challenge even to experts in the field. This article provides insights into how to identify the different cell types in the central nervous system, based on nuclear and cytoplasmic features, amongst other unique characteristics. From the basic distinction between neurons and their supporting cells, the glia, to differences in their subcellular compartments, organelles and their interactions, ultrastructural analyses can provide unique insights into the changes in brain function during aging and disease conditions, such as stroke, neurodegeneration, infection and trauma. Brain parenchyma is composed of a dense mixture of neuronal and glial cell bodies, together with their intertwined processes. Intracellular components that vary between cells, and can become altered with aging or disease, relate to the cytoplasmic and nucleoplasmic density, nuclear heterochromatin pattern, mitochondria, endoplasmic reticulum and Golgi complex, lysosomes, neurosecretory vesicles, and cytoskeletal elements (actin, intermediate filaments, and microtubules). Applying immunolabeling techniques to visualize membrane-bound or intracellular proteins in neurons and glial cells gives an even better appreciation of the subtle differences unique to these cells across contexts of health and disease. Together, our observations reveal how simple ultrastructural features can be used to identify specific changes in cell types, their health status, and functional relationships in the brain.

scholarly journals Histone Methylations Define Neural Stem/Progenitor Cell Subtypes in the Mouse Subventricular Zone

2019 ◽  
Vol 57 (2) ◽  
pp. 997-1008 ◽  
Author(s):  
Zhichao Zhang ◽  
Adeel Manaf ◽  
Yanjiao Li ◽  
Sonia Peña Perez ◽  
Rajikala Suganthan ◽  
...  
Keyword(s):  
Subventricular Zone ◽  
Progenitor Cell ◽  
Individual Cell ◽  
Histone H3 ◽  
Cell Types ◽  
Mammalian Brain ◽  
Neural Stem Progenitor Cells ◽  
Neurologic Function ◽  
Novel Strategy ◽  
The Brain

Abstract Neural stem/progenitor cells (NSPCs) persist in the mammalian brain throughout life and can be activated in response to the physiological and pathophysiological stimuli. Epigenetic reprogramming of NPSC represents a novel strategy for enhancing the intrinsic potential of the brain to regenerate after brain injury. Therefore, defining the epigenetic features of NSPCs is important for developing epigenetic therapies for targeted reprogramming of NSPCs to rescue neurologic function after injury. In this study, we aimed at defining different subtypes of NSPCs by individual histone methylations. We found the three histone marks, histone H3 lysine 4 trimethylation (H3K4me3), histone H3 lysine 27 trimethylation (H3K27me3), and histone H3 lysine 36 trimethylation (H3K36me3), to nicely and dynamically portray individual cell types during neurodevelopment. First, we found all three marks co-stained with NSPC marker SOX2 in mouse subventricular zone. Then, CD133, Id1, Mash1, and DCX immunostaining were used to define NSPC subtypes. Type E/B, B/C, and C/A cells showed high levels of H3K27me3, H3K36me3, and H3K4me3, respectively. Our results reveal defined histone methylations of NSPC subtypes supporting that epigenetic regulation is critical for neurogenesis and for maintaining NSPCs.

Abstract WP115: Transplanted Induced Neural Stem Cells Differentiate and Integrate Into the Brain Parenchyma of Ischemic Stroke Pigs Leading to Improved Tissue Recovery

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Emily W Baker ◽  
Simon R Platt ◽  
Shannon P Holmes ◽  
Liya Wang ◽  
Vivian W Lau ◽  
...  
Keyword(s):  
Stem Cells ◽  
Ischemic Stroke ◽  
Neural Stem Cells ◽  
Brain Tissue ◽  
Cell Types ◽  
Brain Parenchyma ◽  
Neural Cell ◽  
Post Injection ◽  
Tissue Recovery ◽  
The Brain

Studies in rodents have provided evidence that induced pluripotent stem cell derived neural stem cells (iNSCs) have a multifunctional role in stroke recovery. iNSCs mitigate tissue loss due to secondary injury, promote tissue recovery through angiogenesis, and differentiate into mature neural cell types resulting in recovery and replacement of lost and damaged brain tissue. However, many stroke therapies developed in the rodent have failed in clinical trials, suggesting that iNSC therapy should be tested in a more translatable large animal model such as the pig. The objective of this study was to assess the ability of iNSCs to differentiate into mature neural cell types and characterize the effects of iNSCs on brain tissue recovery utilizing non-invasive magnetic resonance imaging (MRI) and spectroscopy approaches in a pig model. Eight male landrace pigs underwent middle cerebral artery occlusion stroke surgery. After 5 days, 4 pigs received iNSC intraparenchymal injections and 4 pigs received vehicle only injections. Pigs underwent MRI assessment at 24 hrs post-stroke and 1, 4, and 12 wks post-injection, and brain tissues were collected 12 wks post-injection. At 12 wks post-injection, iNSC treated pigs showed significant improvement in white matter integrity with recovery of fractional anisotropy being 4-fold higher in treated pigs relative to non-treated pigs. Perfusion weighted imaging demonstrated significant improvement in cerebral blood volume (13%), time to peak (36%), and mean transit time (41%) in treated pigs at 12 wks post-injection vs. non-treated pigs. In addition, treated pigs showed significant improvement in neurometabolites NAA, Cr, and Cho at 12 wks post-injection relative to non-treated pigs. Gene expression analysis established significant increases in neurotrophic and angiogenic factors including BDNF and ANG1, respectively, in brain tissue of treated pigs vs. non-treated pigs suggesting potential modes of action. iNSCs were located in the brain parenchyma 12 wks post-injection, and the majority were positive for the mature neuronal marker NeuN. These results demonstrated that iNSCs are capable of neuronal differentiation and long term integration while promoting tissue recovery in a preclinical pig ischemic stroke model.

Cloning of DNA corresponding to rare transcripts of rat brain: evidence of transcriptional and post-transcriptional control and of the existence of nonpolyadenylated transcripts

1984 ◽  
Vol 4 (10) ◽  
pp. 2187-2197
Author(s):  
M H Brilliant ◽  
N Sueoka ◽  
D M Chikaraishi
Keyword(s):  
Rat Brain ◽  
Transcriptional Control ◽  
Cultured Cells ◽  
Cell Clone ◽  
Cell Types ◽  
Mammalian Brain ◽  
Neural Cells ◽  
Genes Encoding ◽  
Liver And Kidney ◽  
The Brain

To examine the expression of genes encoding rare transcripts in the rat brain, we have characterized genomic DNA clones corresponding to this class. In brain cells, as in all cell types, rare transcripts constitute the majority of different sequences transcribed. Moreover, when compared with other tissues or cultured cells, brain tissue may be expected to have an even larger set of rare transcripts, some of which could be restricted to subpopulations of neural cells. We have identified seven clones whose transcripts are nonabundant, averaging less than three copies per cell. Clone rg13 (rat genomic 13) RNA was detected only in the brain, whereas RNA of a second clone, rg40, was also detected in the brain and in a melanoma. Transcripts of rg13 were found in cerebellum, cerebral cortex, and regions underlying the cortex, whereas rg40 transcripts were not detected in the cerebellum. Transcripts of both rg13 and rg40 were found in pelleted polysomal RNA. RNA of another clone, rg34, was found in the brain, liver, and kidney but was found in pelleted polysomal RNA only in the brain, suggesting that its expression may be post-transcriptionally controlled. The remaining four clones represent rare transcripts that are common to the brain, liver, and kidney; rg18 RNA is restricted to the nucleus, whereas rg3, rg26, and rg36 transcripts are found in the cytoplasm of all three tissues. Transcripts of the brain-specific clone, rg13, and the commonly expressed clone, rg3, are nonpolyadenylated, presumably belonging to the high-complexity, nonpolyadenylated class of transcripts in the mammalian brain.

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