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4. 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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19. 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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21. The Ocular Glymphatic System—Current Understanding and Future Perspectives.

Author

Delle, Christine, Wang, Xiaowei, and Nedergaard, Maiken

Subjects
MACULAR degeneration, AXONAL transport, DIABETIC retinopathy, CEREBROSPINAL fluid, OPTIC nerve, RETINA
Abstract

The ocular glymphatic system subserves the bidirectional polarized fluid transport in the optic nerve, whereby cerebrospinal fluid from the brain is directed along periarterial spaces towards the eye, and fluid from the retina is directed along perivenous spaces following upon its axonal transport across the glial lamina. Fluid homeostasis and waste removal are vital for retinal function, making the ocular glymphatic fluid pathway a potential route for targeted manipulation to combat blinding ocular diseases such as age-related macular degeneration, diabetic retinopathy, and glaucoma. Several lines of work investigating the bidirectional ocular glymphatic transport with varying methodologies have developed diverging mechanistic models, which has created some confusion about how ocular glymphatic transport should be defined. In this review, we provide a comprehensive summary of the current understanding of the ocular glymphatic system, aiming to address misconceptions and foster a cohesive understanding of the topic. [ABSTRACT FROM AUTHOR]

Published
2024
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27. 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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29. 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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42. Local extracellular K+ in cortex regulates norepinephrine levels, network state, and behavioral output.

Author

Dietz, Andrea Grostøl, Pia Weikop, Hauglund, Natalie, Andersen, Mie, Petersen, Nicolas Caesar, Rose, Laura, Hirase, Hajime, and Nedergaard, Maiken

Subjects
NORADRENALINE, SLEEP-wake cycle, DOPAMINE, SEROTONIN, ELECTROENCEPHALOGRAPHY
Abstract

Extracellular potassium concentration ([K+]e) is known to increase as a function of arousal. [K+]e is also a potent modulator of transmitter release. Yet, it is not known whether [K+]e is involved in the neuromodulator release associated with behavioral transitions. We here show that manipulating [K+]e controls the local release of monoaminergic neuromodulators, including norepinephrine (NE), serotonin, and dopamine. Imposing a [K+]e increase is adequate to boost local NE levels, and conversely, lowering [K+]e can attenuate local NE. Electroencephalography analysis and behavioral assays revealed that manipulation of cortical [K+]e was sufficient to alter the sleep-wake cycle and behavior of mice. These observations point to the concept that NE levels in the cortex are not solely determined by subcortical release, but that local [K+]e dynamics have a strong impact on cortical NE. Thus, cortical [K+]e is an underappreciated regulator of behavioral transitions. [ABSTRACT FROM AUTHOR]

Published
2023
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43. Astrocytic GPCR-Induced Ca 2+ Signaling Is Not Causally Related to Local Cerebral Blood Flow Changes.

Author

Ozawa, Katsuya, Nagao, Masaki, Konno, Ayumu, Iwai, Youichi, Vittani, Marta, Kusk, Peter, Mishima, Tsuneko, Hirai, Hirokazu, Nedergaard, Maiken, and Hirase, Hajime

Subjects
CALCIUM ions, CEREBRAL circulation, SOMATOSENSORY cortex, G protein coupled receptors, BLOOD plasma, BLOOD vessels, TRANSGENIC mice
Abstract

Activation of Gq-type G protein-coupled receptors (GPCRs) gives rise to large cytosolic Ca2+ elevations in astrocytes. Previous in vitro and in vivo studies have indicated that astrocytic Ca2+ elevations are closely associated with diameter changes in the nearby blood vessels, which astrocytes enwrap with their endfeet. However, the causal relationship between astrocytic Ca2+ elevations and blood vessel diameter changes has been questioned, as mice with diminished astrocytic Ca2+ signaling show normal sensory hyperemia. We addressed this controversy by imaging cortical vasculature while optogenetically elevating astrocyte Ca2+ in a novel transgenic mouse line, expressing Opto-Gq-type GPCR Optoα1AR (Astro-Optoα1AR) in astrocytes. Blue light illumination on the surface of the somatosensory cortex induced Ca2+ elevations in cortical astrocytes and their endfeet in mice under anesthesia. Blood vessel diameter did not change significantly with Optoα1AR-induced Ca2+ elevations in astrocytes, while it was increased by forelimb stimulation. Next, we labeled blood plasma with red fluorescence using AAV8-P3-Alb-mScarlet in Astro-Optoα1AR mice. We were able to identify arterioles that display diameter changes in superficial areas of the somatosensory cortex through the thinned skull. Photo-stimulation of astrocytes in the cortical area did not result in noticeable changes in the arteriole diameters compared with their background strain C57BL/6. Together, compelling evidence for astrocytic Gq pathway-induced vasodiameter changes was not observed. Our results support the notion that short-term (<10 s) hyperemia is not mediated by GPCR-induced astrocytic Ca2+ signaling. [ABSTRACT FROM AUTHOR]

Published
2023
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45. Understanding the functions and relationships of the glymphatic system and meningeal lymphatics

Author

Louveau, Antoine, Plog, Benjamin A., Antila, Salli, Alitalo, Kari, Nedergaard, Maiken, and Kipnis, Jonathan

Subjects
Lymphatic system -- Physiological aspects, Health care industry
Abstract

Recent discoveries of the glymphatic system and of meningeal lymphatic vessels have generated a lot of excitement, along with some degree of skepticism. Here, we summarize the state of the field and point out the gaps of knowledge that should be filled through further research. We discuss the glymphatic system as a system that allows CNS perfusion by the cerebrospinal fluid (CSF) and interstitial fluid (ISF). We also describe the recently characterized meningeal lymphatic vessels and their role in drainage of the brain ISF, CSF, CNS-derived molecules, and immune cells from the CNS and meninges to the peripheral (CNS-draining) lymph nodes. We speculate on the relationship between the two systems and their malfunction that may underlie some neurological diseases. Although much remains to be investigated, these new discoveries have changed our understanding of mechanisms underlying CNS immune privilege and CNS drainage. Future studies should explore the communications between the glymphatic system and meningeal lymphatics in CNS disorders and develop new therapeutic modalities targeting these systems., Perivascular pathways: pseudolymphatic vessels of the brain? In peripheral organs, colloids are extravasated across a fenestrated capillary bed, and these proteins, as well as excess tissue fluid, are returned to [...]

Published
2017
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47. A sensitive and specific genetically-encoded potassium ion biosensor for in vivo applications across the tree of life

Author

Wu, Sheng-Yi, Wen, Yurong, Serre, Nelson B. C., Laursen, Cathrine Charlotte Heiede, Dietz, Andrea Grostøl, Taylor, Brian R., Drobizhev, Mikhail, Molina, Rosana S., Aggarwal, Abhi, Rancic, Vladimir, Becker, Michael, Ballanyi, Klaus, Podgorski, Kaspar, Hirase, Hajime, Nedergaard, Maiken, Fendrych, Matyáš, Lemieux, M. Joanne, Eberl, Daniel F., Kay, Alan R., Campbell, Robert E., and Shen, Yi

Subjects
Ions, Mice, Fluorescence Resonance Energy Transfer/methods, General Immunology and Microbiology, Biosensing Techniques/methods, General Neuroscience, Fluorescence Resonance Energy Transfer, Potassium, Animals, Biosensing Techniques, General Agricultural and Biological Sciences, General Biochemistry, Genetics and Molecular Biology
Abstract

Potassium ion (K+) plays a critical role as an essential electrolyte in all biological systems. Genetically-encoded fluorescent K+ biosensors are promising tools to further improve our understanding of K+-dependent processes under normal and pathological conditions. Here, we report the crystal structure of a previously reported genetically-encoded fluorescent K+ biosensor, GINKO1, in the K+-bound state. Using structure-guided optimization and directed evolution, we have engineered an improved K+ biosensor, designated GINKO2, with higher sensitivity and specificity. We have demonstrated the utility of GINKO2 for in vivo detection and imaging of K+ dynamics in multiple model organisms, including bacteria, plants, and mice.

Published
2023

48. Managing noradrenaline after traumatic brain injury.

Author

Hussain, Rashad and Nedergaard, Maiken

Subjects
*BRAIN injuries, *EPILEPSY, *NORADRENALINE, *SPASTICITY, *ALZHEIMER'S disease
Abstract

Traumatic brain injury (TBI) is a significant global health issue, causing death and disability in young adults. One of the complications of TBI is cerebral edema, which can lead to increased mortality and disability. Noradrenaline (NA) has been commonly used to treat TBI patients, but its role in cerebral edema was not well understood. A recent study using a mouse model found that blocking adrenergic receptors reduced cerebral edema and improved neurological function. The study also highlighted the importance of lymphatic drainage in TBI and suggested that noradrenergic inhibition could enhance glymphatic/lymphatic function. While more research is needed, these findings provide mechanistic insights into the benefits of pan-adrenergic blockage in TBI. [Extracted from the article]

Published
2024
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