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1. Beyond the symptom: the biology of fatigue.

Author

Raizen, David, Mullington, Janet, Anaclet, Christelle, Clarke, Gerard, Critchley, Hugo, Dantzer, Robert, Davis, Ronald, Drew, Kelly, Fessel, Josh, Fuller, Patrick, Gibson, Erin, Harrington, Mary, Ian Lipkin, W, Klerman, Elizabeth, Klimas, Nancy, Komaroff, Anthony, Koroshetz, Walter, Krupp, Lauren, Kuppuswamy, Anna, Lasselin, Julie, Lewis, Laura, Magistretti, Pierre, Matos, Heidi, Miaskowski, Christine, Miller, Andrew, Nath, Avindra, Nedergaard, Maiken, Opp, Mark, Ritchie, Marylyn, Rogulja, Dragana, Rolls, Asya, Salamone, John, Saper, Clifford, Whittemore, Vicky, Wylie, Glenn, Younger, Jarred, Zee, Phyllis, and Craig Heller, H

Subjects
Humans, Fatigue, Motivation, Biology
Abstract

A workshop titled Beyond the Symptom: The Biology of Fatigue was held virtually September 27-28, 2021. It was jointly organized by the Sleep Research Society and the Neurobiology of Fatigue Working Group of the NIH Blueprint Neuroscience Research Program. For access to the presentations and video recordings, see: https://neuroscienceblueprint.nih.gov/about/event/beyond-symptom-biology-fatigue. The goals of this workshop were to bring together clinicians and scientists who use a variety of research approaches to understand fatigue in multiple conditions and to identify key gaps in our understanding of the biology of fatigue. This workshop summary distills key issues discussed in this workshop and provides a list of promising directions for future research on this topic. We do not attempt to provide a comprehensive review of the state of our understanding of fatigue, nor to provide a comprehensive reprise of the many excellent presentations. Rather, our goal is to highlight key advances and to focus on questions and future approaches to answering them.

Published
2023

5. Lactate biosensors for spectrally and spatially multiplexed fluorescence imaging

Author

Nasu, Yusuke, Aggarwal, Abhi, Le, Giang N. T., Vo, Camilla Trang, Kambe, Yuki, Wang, Xinxing, Beinlich, Felix R. M., Lee, Ashley Bomin, Ram, Tina R., Wang, Fangying, Gorzo, Kelsea A., Kamijo, Yuki, Boisvert, Marc, Nishinami, Suguru, Kawamura, Genki, Ozawa, Takeaki, Toda, Hirofumi, Gordon, Grant R., Ge, Shaoyu, Hirase, Hajime, Nedergaard, Maiken, Paquet, Marie-Eve, Drobizhev, Mikhail, Podgorski, Kaspar, and Campbell, Robert E.

Published
2023
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12. A community-based transcriptomics classification and nomenclature of neocortical cell types

Author

Yuste, Rafael, Hawrylycz, Michael, Aalling, Nadia, Arendt, Detlev, Armananzas, Ruben, Ascoli, Giorgio, Bielza, Concha, Bokharaie, Vahid, Bergmann, Tobias, Bystron, Irina, Capogna, Marco, Chang, Yoonjeung, Clemens, Ann, de Kock, Christiaan, DeFelipe, Javier, Santos, Sandra Dos, Dunville, Keagan, Feldmeyer, Dirk, Fiath, Richard, Fishell, Gordon, Foggetti, Angelica, Gao, Xuefan, Ghaderi, Parviz, Gunturkun, Onur, Hall, Vanessa Jane, Helmstaedter, Moritz, Herculano-Houzel, Suzana, Hilscher, Markus, Hirase, Hajime, Hjerling-Leffler, Jens, Hodge, Rebecca, Huang, Z. Josh, Huda, Rafiq, Juan, Yuan, Khodosevich, Konstantin, Kiehn, Ole, Koch, Henner, Kuebler, Eric, Kuhnemund, Malte, Larranaga, Pedro, Lelieveldt, Boudewijn, Louth, Emma Louise, Lui, Jan, Mansvelder, Huibert, Marin, Oscar, Martínez-Trujillo, Julio, Moradi, Homeira, Goriounova, Natalia, Mohapatra, Alok, Nedergaard, Maiken, Němec, Pavel, Ofer, Netanel, Pfisterer, Ulrich, Pontes, Samuel, Redmond, William, Rossier, Jean, Sanes, Joshua, Scheuermann, Richard, Saiz, Esther Serrano, Somogyi, Peter, Tamás, Gábor, Tolias, Andreas, Tosches, Maria, Garcia, Miguel Turrero, Aguilar-Valles, Argel, Munguba, Hermany, Wozny, Christian, Wuttke, Thomas, Yong, Liu, Zeng, Hongkui, and Lein, Ed S.

Subjects
Quantitative Biology - Genomics, Quantitative Biology - Neurons and Cognition
Abstract

To understand the function of cortical circuits it is necessary to classify their underlying cellular diversity. Traditional attempts based on comparing anatomical or physiological features of neurons and glia, while productive, have not resulted in a unified taxonomy of neural cell types. The recent development of single-cell transcriptomics has enabled, for the first time, systematic high-throughput profiling of large numbers of cortical cells and the generation of datasets that hold the promise of being complete, accurate and permanent. Statistical analyses of these data have revealed the existence of clear clusters, many of which correspond to cell types defined by traditional criteria, and which are conserved across cortical areas and species. To capitalize on these innovations and advance the field, we, the Copenhagen Convention Group, propose the community adopts a transcriptome-based taxonomy of the cell types in the adult mammalian neocortex. This core classification should be ontological, hierarchical and use a standardized nomenclature. It should be configured to flexibly incorporate new data from multiple approaches, developmental stages and a growing number of species, enabling improvement and revision of the classification. This community-based strategy could serve as a common foundation for future detailed analysis and reverse engineering of cortical circuits and serve as an example for cell type classification in other parts of the nervous system and other organs., Comment: 21 pages, 3 figures

Published
2019

14. A community-based transcriptomics classification and nomenclature of neocortical cell types

Author

Yuste, Rafael, Hawrylycz, Michael, Aalling, Nadia, Aguilar-Valles, Argel, Arendt, Detlev, Armañanzas, Ruben, Ascoli, Giorgio A, Bielza, Concha, Bokharaie, Vahid, Bergmann, Tobias Borgtoft, Bystron, Irina, Capogna, Marco, Chang, YoonJeung, Clemens, Ann, de Kock, Christiaan PJ, DeFelipe, Javier, Dos Santos, Sandra Esmeralda, Dunville, Keagan, Feldmeyer, Dirk, Fiáth, Richárd, Fishell, Gordon James, Foggetti, Angelica, Gao, Xuefan, Ghaderi, Parviz, Goriounova, Natalia A, Güntürkün, Onur, Hagihara, Kenta, Hall, Vanessa Jane, Helmstaedter, Moritz, Herculano-Houzel, Suzana, Hilscher, Markus M, Hirase, Hajime, Hjerling-Leffler, Jens, Hodge, Rebecca, Huang, Josh, Huda, Rafiq, Khodosevich, Konstantin, Kiehn, Ole, Koch, Henner, Kuebler, Eric S, Kühnemund, Malte, Larrañaga, Pedro, Lelieveldt, Boudewijn, Louth, Emma Louise, Lui, Jan H, Mansvelder, Huibert D, Marin, Oscar, Martinez-Trujillo, Julio, Chameh, Homeira Moradi, Mohapatra, Alok Nath, Munguba, Hermany, Nedergaard, Maiken, Němec, Pavel, Ofer, Netanel, Pfisterer, Ulrich Gottfried, Pontes, Samuel, Redmond, William, Rossier, Jean, Sanes, Joshua R, Scheuermann, Richard H, Serrano-Saiz, Esther, Staiger, Jochen F, Somogyi, Peter, Tamás, Gábor, Tolias, Andreas Savas, Tosches, Maria Antonietta, García, Miguel Turrero, Wozny, Christian, Wuttke, Thomas V, Liu, Yong, Yuan, Juan, Zeng, Hongkui, and Lein, Ed

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Biotechnology, Genetics, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Animals, Cells, Computational Biology, Humans, Neocortex, Neuroglia, Neurons, Single-Cell Analysis, Terminology as Topic, Transcriptome, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

To understand the function of cortical circuits, it is necessary to catalog their cellular diversity. Past attempts to do so using anatomical, physiological or molecular features of cortical cells have not resulted in a unified taxonomy of neuronal or glial cell types, partly due to limited data. Single-cell transcriptomics is enabling, for the first time, systematic high-throughput measurements of cortical cells and generation of datasets that hold the promise of being complete, accurate and permanent. Statistical analyses of these data reveal clusters that often correspond to cell types previously defined by morphological or physiological criteria and that appear conserved across cortical areas and species. To capitalize on these new methods, we propose the adoption of a transcriptome-based taxonomy of cell types for mammalian neocortex. This classification should be hierarchical and use a standardized nomenclature. It should be based on a probabilistic definition of a cell type and incorporate data from different approaches, developmental stages and species. A community-based classification and data aggregation model, such as a knowledge graph, could provide a common foundation for the study of cortical circuits. This community-based classification, nomenclature and data aggregation could serve as an example for cell type atlases in other parts of the body.

Published
2020

16. An ocular glymphatic clearance system removes β-amyloid from the rodent eye

Author

Wang, Xiaowei, Lou, Nanhong, Eberhardt, Allison, Yang, Yujia, Kusk, Peter, Xu, Qiwu, Förstera, Benjamin, Peng, Sisi, Shi, Meng, Ladrón-de-Guevara, Antonio, Delle, Christine, Sigurdsson, Björn, Xavier, Anna LR, Ertürk, Ali, Libby, Richard T, Chen, Lu, Thrane, Alexander S, and Nedergaard, Maiken

Subjects
Neurosciences, Neurodegenerative, Eye Disease and Disorders of Vision, Aging, Eye, Amyloid beta-Peptides, Animals, Aquaporin 4, Glymphatic System, Intracranial Pressure, Mice, Optic Nerve, Retina, Vitreous Body, Biological Sciences, Medical and Health Sciences
Abstract

Despite high metabolic activity, the retina and optic nerve head lack traditional lymphatic drainage. We here identified an ocular glymphatic clearance route for fluid and wastes via the proximal optic nerve in rodents. β-amyloid (Aβ) was cleared from the retina and vitreous via a pathway dependent on glial water channel aquaporin-4 (AQP4) and driven by the ocular-cranial pressure difference. After traversing the lamina barrier, intra-axonal Aβ was cleared via the perivenous space and subsequently drained to lymphatic vessels. Light-induced pupil constriction enhanced efflux, whereas atropine or raising intracranial pressure blocked efflux. In two distinct murine models of glaucoma, Aβ leaked from the eye via defects in the lamina barrier instead of directional axonal efflux. The results suggest that, in rodents, the removal of fluid and metabolites from the intraocular space occurs through a glymphatic pathway that might be impaired in glaucoma.

Published
2020

18. Transient but not chronic hyperglycemia accelerates ocular glymphatic transport

Author

Delle, Christine, primary, Wang, Xiaowei, additional, Giannetto, Michael, additional, Newbold, Evan, additional, Peng, Weiguo, additional, Gomolka, Ryszard Stefan, additional, Ladrón-de-Guevara, Antonio, additional, Cankar, Neža, additional, Schiøler Nielsen, Elise, additional, Kjaerby, Celia, additional, Weikop, Pia, additional, Mori, Yuki, additional, and Nedergaard, Maiken, additional

Published
2024
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23. The glymphatic system: Current understanding and modeling

Author

Bohr, Tomas, Hjorth, Poul G., Holst, Sebastian C., Hrabětová, Sabina, Kiviniemi, Vesa, Lilius, Tuomas, Lundgaard, Iben, Mardal, Kent-Andre, Martens, Erik A., Mori, Yuki, Nägerl, U. Valentin, Nicholson, Charles, Tannenbaum, Allen, Thomas, John H., Tithof, Jeffrey, Benveniste, Helene, Iliff, Jeffrey J., Kelley, Douglas H., and Nedergaard, Maiken

Published
2022
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24. Oxygen tension-mediated erythrocyte membrane interactions regulate cerebral capillary hyperemia.

Author

Zhou, Sitong, Giannetto, Michael, DeCourcey, James, Kang, Hongyi, Kang, Ning, Li, Yizeng, Zheng, Suilan, Zhao, Hetince, Simmons, William R, Wei, Helen S, Bodine, David M, Low, Philip S, Nedergaard, Maiken, and Wan, Jiandi

Subjects
Brain, Erythrocyte Membrane, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Hyperemia, Oxygen, Anion Exchange Protein 1, Erythrocyte, Hemoglobins, Blood Flow Velocity, Cerebrovascular Circulation, Lab-On-A-Chip Devices, Clinical Research, Neurosciences, Aetiology, Underpinning research, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning
Abstract

The tight coupling between cerebral blood flow and neural activity is a key feature of normal brain function and forms the basis of functional hyperemia. The mechanisms coupling neural activity to vascular responses, however, remain elusive despite decades of research. Recent studies have shown that cerebral functional hyperemia begins in capillaries, and red blood cells (RBCs) act as autonomous regulators of brain capillary perfusion. RBCs then respond to local changes of oxygen tension (PO2) and regulate their capillary velocity. Using ex vivo microfluidics and in vivo two-photon microscopy, we examined RBC capillary velocity as a function of PO2 and showed that deoxygenated hemoglobin and band 3 interactions on RBC membrane are the molecular switch that responds to local PO2 changes and controls RBC capillary velocity. Capillary hyperemia can be controlled by manipulating RBC properties independent of the neurovascular unit, providing an effective strategy to treat or prevent impaired functional hyperemia.

Published
2019

25. Vascular dysfunction-The disregarded partner of Alzheimer's disease.

Author

Sweeney, Melanie D, Montagne, Axel, Sagare, Abhay P, Nation, Daniel A, Schneider, Lon S, Chui, Helena C, Harrington, Michael G, Pa, Judy, Law, Meng, Wang, Danny JJ, Jacobs, Russell E, Doubal, Fergus N, Ramirez, Joel, Black, Sandra E, Nedergaard, Maiken, Benveniste, Helene, Dichgans, Martin, Iadecola, Costantino, Love, Seth, Bath, Philip M, Markus, Hugh S, Salman, Rustam A, Allan, Stuart M, Quinn, Terence J, Kalaria, Rajesh N, Werring, David J, Carare, Roxana O, Touyz, Rhian M, Williams, Steve CR, Moskowitz, Michael A, Katusic, Zvonimir S, Lutz, Sarah E, Lazarov, Orly, Minshall, Richard D, Rehman, Jalees, Davis, Thomas P, Wellington, Cheryl L, González, Hector M, Yuan, Chun, Lockhart, Samuel N, Hughes, Timothy M, Chen, Christopher LH, Sachdev, Perminder, O'Brien, John T, Skoog, Ingmar, Pantoni, Leonardo, Gustafson, Deborah R, Biessels, Geert Jan, Wallin, Anders, Smith, Eric E, Mok, Vincent, Wong, Adrian, Passmore, Peter, Barkof, Frederick, Muller, Majon, Breteler, Monique MB, Román, Gustavo C, Hamel, Edith, Seshadri, Sudha, Gottesman, Rebecca F, van Buchem, Mark A, Arvanitakis, Zoe, Schneider, Julie A, Drewes, Lester R, Hachinski, Vladimir, Finch, Caleb E, Toga, Arthur W, Wardlaw, Joanna M, and Zlokovic, Berislav V

Subjects
Blood-Brain Barrier, Brain, Humans, Alzheimer Disease, Vascular Diseases, Cerebrovascular Circulation, United States, National Institute on Aging (U.S.), Amyloid beta-Peptides, White Matter, Biomarkers, Alzheimer's disease, Blood-brain barrier, Cerebral blood flow, MRI, Vascular, National Institute on Aging, Neurosciences, Clinical Sciences, Geriatrics
Abstract

Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. The recently updated AD Research Framework put forth by the National Institute on Aging-Alzheimer's Association describes a biomarker-based pathologic definition of AD focused on amyloid, tau, and neuronal injury. In response to this article, here we first discussed evidence that vascular dysfunction is an important early event in AD pathophysiology. Next, we examined various imaging sequences that could be easily implemented to evaluate different types of vascular dysfunction associated with, and/or contributing to, AD pathophysiology, including changes in blood-brain barrier integrity and cerebral blood flow. Vascular imaging biomarkers of small vessel disease of the brain, which is responsible for >50% of dementia worldwide, including AD, are already established, well characterized, and easy to recognize. We suggest that these vascular biomarkers should be incorporated into the AD Research Framework to gain a better understanding of AD pathophysiology and aid in treatment efforts.

Published
2019

29. “Small Blood Vessels: Big Health Problems?”: Scientific Recommendations of the National Institutes of Health Workshop

Author

Bosetti, Francesca, Galis, Zorina S, Bynoe, Margaret S, Charette, Marc, Cipolla, Marilyn J, del Zoppo, Gregory J, Gould, Douglas, Hatsukami, Thomas S, Jones, Teresa LZ, Koenig, James I, Lutty, Gerard A, Maric‐Bilkan, Christine, Stevens, Troy, Tolunay, H Eser, Koroshetz, Walter, Participants, the Small Blood Vessels Big Health Problems Workshop, Agalliu, Dritan, Antonetti, David A, Boehm, Manfred, Brooks, Claudette E, Caron, Kathleen M, Chilian, William, Daemen, Mat J, D'Amato, Robert, Davis, Thomas P, Ergul, Adviye, Faber, James E, Gomez, Ariel R, Grayson, Peter, Grumbach, Isabella, Grutzendler, Jaime, Gu, Chenghua, Gutterman, David, Hallenbeck, John, Herman, Ira, Humphrey, Jay, Iadecola, Costantino, Inscho, Edward W, Kleinfeld, David, Lo, Eng H, Lopez, Jose A, Macknik, Stephen, Malik, Asrar, Mayadas, Tanya N, McGavern, Dorian, Meininger, Gerald A, Miller, Virginia M, Nedergaard, Maiken, Nelson, Mark T, Peirce‐Cottler, Shayn, Ramadan, Ipolia, Rosenberg, Gary A, Schiffrin, Ernesto L, Searson, Peter, Stachenfeld, Nina, Stan, Radu V, Suarez, Yajaira, Ubogu, Eroboghene E, Vexler, Zinaida S, Weyand, Cornelia M, and Zlokovic, Berislav V

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Good Health and Well Being, Capillaries, Cardiovascular Diseases, Coronary Circulation, Health, Humans, Microcirculation, National Institutes of Health (U.S.), Practice Guidelines as Topic, United States, endothelium, hypertension, imaging, ischemia, microcirculation, remodeling, “Small Blood Vessels: Big Health Problems” Workshop Participants, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology
Published
2016

30. Erythrocytes Are Oxygen-Sensing Regulators of the Cerebral Microcirculation

Author

Wei, Helen Shinru, Kang, Hongyi, Rasheed, Izad-Yar Daniel, Zhou, Sitong, Lou, Nanhong, Gershteyn, Anna, McConnell, Evan Daniel, Wang, Yixuan, Richardson, Kristopher Emil, Palmer, Andre Francis, Xu, Chris, Wan, Jiandi, and Nedergaard, Maiken

Subjects
Neurosciences, 1.1 Normal biological development and functioning, Underpinning research, Neurological, Animals, Brain, Erythrocytes, Hyperemia, Mice, Microcirculation, Oxygen, Psychology, Cognitive Sciences, Neurology & Neurosurgery
Abstract

Energy production in the brain depends almost exclusively on oxidative metabolism. Neurons have small energy reserves and require a continuous supply of oxygen (O2). It is therefore not surprising that one of the hallmarks of normal brain function is the tight coupling between cerebral blood flow and neuronal activity. Since capillaries are embedded in the O2-consuming neuropil, we have here examined whether activity-dependent dips in O2 tension drive capillary hyperemia. In vivo analyses showed that transient dips in tissue O2 tension elicit capillary hyperemia. Ex vivo experiments revealed that red blood cells (RBCs) themselves act as O2 sensors that autonomously regulate their own deformability and thereby flow velocity through capillaries in response to physiological decreases in O2 tension. This observation has broad implications for understanding how local changes in blood flow are coupled to synaptic transmission.

Published
2016

37. Glial Biology in Learning and Cognition

Author

Fields, R Douglas, Araque, Alfonso, Johansen-Berg, Heidi, Lim, Soo-Siang, Lynch, Gary, Nave, Klaus-Armin, Nedergaard, Maiken, Perez, Ray, Sejnowski, Terrence, and Wake, Hiroaki

Subjects
Neurosciences, Basic Behavioral and Social Science, Behavioral and Social Science, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Animals, Brain, Cognition, Humans, Learning, Neurogenesis, Neuroglia, Space Perception, memory, astrocyte, microglia, oligodendrocyte, myelin, synaptic plasticity, neuron-glia interactions, neuron–glia interactions, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery
Abstract

Neurons are exquisitely specialized for rapid electrical transmission of signals, but some properties of glial cells, which do not communicate with electrical impulses, are well suited for participating in complex cognitive functions requiring broad spatial integration and long-term temporal regulation. Astrocytes, microglia, and oligodendrocytes all have biological properties that could influence learning and cognition. Myelination by oligodendrocytes increases conduction velocity, affecting spike timing and oscillations in neuronal activity. Astrocytes can modulate synaptic transmission and may couple multiple neurons and synapses into functional assemblies. Microglia can remove synapses in an activity-dependent manner altering neural networks. Incorporating glia into a bicellular mechanism of nervous system function may help answer long-standing questions concerning the cellular mechanisms of learning and cognition.

Published
2014

38. Vascular dysfunction—The disregarded partner of Alzheimer's disease

Author

Sweeney, Melanie D., Montagne, Axel, Sagare, Abhay P., Nation, Daniel A., Schneider, Lon S., Chui, Helena C., Harrington, Michael G., Pa, Judy, Law, Meng, Wang, Danny J.J., Jacobs, Russell E., Doubal, Fergus N., Ramirez, Joel, Black, Sandra E., Nedergaard, Maiken, Benveniste, Helene, Dichgans, Martin, Iadecola, Costantino, Love, Seth, Bath, Philip M., Markus, Hugh S., Salman, Rustam A., Allan, Stuart M., Quinn, Terence J., Kalaria, Rajesh N., Werring, David J., Carare, Roxana O., Touyz, Rhian M., Williams, Steve C.R., Moskowitz, Michael A., Katusic, Zvonimir S., Lutz, Sarah E., Lazarov, Orly, Minshall, Richard D., Rehman, Jalees, Davis, Thomas P., Wellington, Cheryl L., González, Hector M., Yuan, Chun, Lockhart, Samuel N., Hughes, Timothy M., Chen, Christopher L.H., Sachdev, Perminder, O'Brien, John T., Skoog, Ingmar, Pantoni, Leonardo, Gustafson, Deborah R., Biessels, Geert Jan, Wallin, Anders, Smith, Eric E., Mok, Vincent, Wong, Adrian, Passmore, Peter, Barkof, Frederick, Muller, Majon, Breteler, Monique M.B., Román, Gustavo C., Hamel, Edith, Seshadri, Sudha, Gottesman, Rebecca F., van Buchem, Mark A., Arvanitakis, Zoe, Schneider, Julie A., Drewes, Lester R., Hachinski, Vladimir, Finch, Caleb E., Toga, Arthur W., Wardlaw, Joanna M., and Zlokovic, Berislav V.

Published
2019
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39. Rapid manifestation of reactive astrogliosis in acute hippocampal brain slices

Author

Takano, Takahiro, He, Wei, Han, Xiaoning, Wang, Fushun, Xu, Qiwu, Wang, Xiaohai, Bush, Nancy Ann Oberheim, Cruz, Nancy, Dienel, Gerald A, and Nedergaard, Maiken

Subjects
Biomedical and Clinical Sciences, Neurosciences, 1.1 Normal biological development and functioning, Underpinning research, Neurological, Animals, Animals, Newborn, Aquaporin 4, Astrocytes, Calcium, Excitatory Postsynaptic Potentials, Female, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Gliosis, Glycogen, Green Fluorescent Proteins, Hippocampus, In Vitro Techniques, Lactic Acid, Male, Mice, NAD, Quaternary Ammonium Compounds, NADH, astrohcytes, electron microscopy, interstitial space, mitochondria, purinergic receptors, two-photon microscopy, Neurology & Neurosurgery
Abstract

A flurry of studies over the past decade has shown that astrocytes play a more active role in neural function than previously recognized. Hippocampal slices prepared from young rodent pups have served as a popular model for studying the pathways by which astrocytes participate in synaptic transmission. It is, however, not known how well astrocytes tolerate traumatic injury and hypoxia, which are unavoidable when preparing acute slices. We here showed that astrocytes exhibit striking changes in expression of several receptors and structural proteins, including re-expression of the developmental marker nestin within 90 min following preparation of live vibratome slices. Moreover, immunoelectron microscopy showed a 2.7-fold loss of astrocytic processes in acute hippocampal slices prepared from glial fibrillary acidic protein-green fluorescent protein reporter mice. A sharp decrease in the number of mitochondria was also noted in acute slices, concurrently with an increase in mitochondrial size. Glycogen content decreased 3-fold upon slice preparation and did not recover despite stable recordings of field excitatory postsynaptic current. Analysis of Ca(2+) signaling showed that astrocytic responses to purine receptor and mGluR5 agonists differed in slice versus in vivo. These observations suggest that the functional properties and the fine structure of astrocytes in slices may be reflective of early stages of reactive gliosis and should be confirmed in vivo when possible.

Published
2014

41. Effect of sleep deprivation and NREM sleep stage on physiological brain pulsations.

Author

Helakari, Heta, Järvelä, Matti, Väyrynen, Tommi, Tuunanen, Johanna, Piispala, Johanna, Kallio, Mika, Ebrahimi, Seyed Mohsen, Poltojainen, Valter, Kananen, Janne, Elabasy, Ahmed, Huotari, Niko, Raitamaa, Lauri, Tuovinen, Timo, Korhonen, Vesa, Nedergaard, Maiken, and Kiviniemi, Vesa

Subjects
SLEEP deprivation, SLEEP stages, FUNCTIONAL magnetic resonance imaging
Abstract

Introduction: Sleep increases brain fluid transport and the power of pulsations driving the fluids. We investigated how sleep deprivation or electrophysiologically different stages of non-rapid-eye-movement (NREM) sleep affect the human brain pulsations. Methods: Fast functional magnetic resonance imaging (fMRI) was performed in healthy subjects (n = 23) with synchronous electroencephalography (EEG), that was used to verify arousal states (awake, N1 and N2 sleep). Cardiorespiratory rates were verified with physiological monitoring. Spectral power analysis assessed the strength, and spectral entropy assessed the stability of the pulsations. Results: In N1 sleep, the power of vasomotor (VLF < 0.1 Hz), but not cardiorespiratory pulsations, intensified after sleep deprived vs. non-sleep deprived subjects. The power of all three pulsations increased as a function of arousal state (N2 > N1 > awake) encompassing brain tissue in both sleep stages, but extra-axial CSF spaces only in N2 sleep. Spectral entropy of full band and respiratory pulsations decreased most in N2 sleep stage, while cardiac spectral entropy increased in ventricles. Discussion: In summary, the sleep deprivation and sleep depth, both increase the power and harmonize the spectral content of human brain pulsations. [ABSTRACT FROM AUTHOR]

Published
2023
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46. Neurological diseases as primary gliopathies: a reassessment of neurocentrism.

Author

Verkhratsky, Alexei, Sofroniew, Michael V, Messing, Albee, deLanerolle, Nihal C, Rempe, David, Rodríguez, José Julio, and Nedergaard, Maiken

Subjects
Astrocytes, Neurons, Animals, Humans, Brain Ischemia, Neurodegenerative Diseases, Gliosis, Homeostasis, aging, astrocyte, brain, calcium, disease, supportive cell, transmitter, Neurosciences
Abstract

Diseases of the human brain are almost universally attributed to malfunction or loss of nerve cells. However, a considerable amount of work has, during the last decade, expanded our view on the role of astrocytes in CNS (central nervous system), and this analysis suggests that astrocytes contribute to both initiation and propagation of many (if not all) neurological diseases. Astrocytes provide metabolic and trophic support to neurons and oligodendrocytes. Here, we shall endeavour a broad overviewing of the progress in the field and forward the idea that loss of homoeostatic astroglial function leads to an acute loss of neurons in the setting of acute insults such as ischaemia, whereas more subtle dysfunction of astrocytes over periods of months to years contributes to epilepsy and to progressive loss of neurons in neurodegenerative diseases. The majority of therapeutic drugs currently in clinical use target neuronal receptors, channels or transporters. Future therapeutic efforts may benefit by a stronger focus on the supportive homoeostatic functions of astrocytes.

Published
2012

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