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Relevant bibliographies by topics / Cerebral ischemia, neuroscience, demyelination

Academic literature on the topic 'Cerebral ischemia, neuroscience, demyelination'

Author: Grafiati

Published: 10 March 2023

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Journal articles on the topic "Cerebral ischemia, neuroscience, demyelination"

1

Bernstein, Hans-Gert, Gerburg Keilhoff, Henrik Dobrowolny, Paul C. Guest, and Johann Steiner. "Perineuronal oligodendrocytes in health and disease: the journey so far." Reviews in the Neurosciences 31, no. 1 (December 18, 2019): 89–99. http://dx.doi.org/10.1515/revneuro-2019-0020.

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Abstract Perineuronal oligodendrocytes (pn-Ols) are located in the cerebral gray matter in close proximity to neuronal perikarya and less frequently near dendrites and neurites. Although their morphology is indistinguishable from that of other oligodendrocytes, it is not known if pn-Ols have a similar or different cell signature from that of typical myelinating oligodendroglial cells. In this review, we discussed the potential roles of these cells in myelination under normal and pathophysiologic conditions as functional and nutritional supporters of neurons, as restrainers of neuronal firing, and as possible players in glutamate-glutamine homeostasis. We also highlighted the occurrences in which perineuronal oligodendroglia are altered, such as in experimental demyelination, multiple sclerosis, cerebral ischemia, epilepsy, Alzheimer’s disease, schizophrenia, major depression, and bipolar disorder.

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Coppi, Elisabetta, Ilaria Dettori, Federica Cherchi, Irene Bulli, Martina Venturini, Daniele Lana, Maria Grazia Giovannini, Felicita Pedata, and Anna Maria Pugliese. "A2B Adenosine Receptors: When Outsiders May Become an Attractive Target to Treat Brain Ischemia or Demyelination." International Journal of Molecular Sciences 21, no. 24 (December 18, 2020): 9697. http://dx.doi.org/10.3390/ijms21249697.

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Adenosine is a signaling molecule, which, by activating its receptors, acts as an important player after cerebral ischemia. Here, we review data in the literature describing A2BR-mediated effects in models of cerebral ischemia obtained in vivo by the occlusion of the middle cerebral artery (MCAo) or in vitro by oxygen-glucose deprivation (OGD) in hippocampal slices. Adenosine plays an apparently contradictory role in this receptor subtype depending on whether it is activated on neuro-glial cells or peripheral blood vessels and/or inflammatory cells after ischemia. Indeed, A2BRs participate in the early glutamate-mediated excitotoxicity responsible for neuronal and synaptic loss in the CA1 hippocampus. On the contrary, later after ischemia, the same receptors have a protective role in tissue damage and functional impairments, reducing inflammatory cell infiltration and neuroinflammation by central and/or peripheral mechanisms. Of note, demyelination following brain ischemia, or autoimmune neuroinflammatory reactions, are also profoundly affected by A2BRs since they are expressed by oligodendroglia where their activation inhibits cell maturation and expression of myelin-related proteins. In conclusion, data in the literature indicate the A2BRs as putative therapeutic targets for the still unmet treatment of stroke or demyelinating diseases.

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Lin, HungWen, ReggieH C. Lee, MichelleH H. Lee, CelesteY C. Wu, Alexandre Couto e Silva, HarleeE Possoit, Tsung-Han Hsieh, and Alireza Minagar. "Cerebral ischemia and neuroregeneration." Neural Regeneration Research 13, no. 3 (2018): 373. http://dx.doi.org/10.4103/1673-5374.228711.

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Zhou, Yu‐Xi, Xin Wang, Dan Tang, Yan Li, Ying‐Fu Jiao, Yu Gan, Xiao‐Ming Hu, et al. "IL‐2mAb reduces demyelination after focal cerebral ischemia by suppressing CD8 + T cells." CNS Neuroscience & Therapeutics 25, no. 4 (November 15, 2018): 532–43. http://dx.doi.org/10.1111/cns.13084.

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Hayashi, Takeshi, Kentaro Deguchi, Shoko Nagotani, Hanzhe Zhang, Yoshihide Sehara, Atsushi Tsuchiya, and Koji Abe. "Cerebral Ischemia and Angiogenesis." Current Neurovascular Research 3, no. 2 (May 1, 2006): 119–29. http://dx.doi.org/10.2174/156720206776875902.

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Borlongan, Cesario V., Yasuo Tajima, John Q. Trojanowski, Virginia M. Y. Lee, and Paul R. Sanberg. "Cerebral ischemia and CNS transplantation." NeuroReport 9, no. 16 (November 1998): 3703–9. http://dx.doi.org/10.1097/00001756-199811160-00025.

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Krnjević, Krešimir. "Electrophysiology of cerebral ischemia." Neuropharmacology 55, no. 3 (September 2008): 319–33. http://dx.doi.org/10.1016/j.neuropharm.2008.01.002.

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Haun, Steven E. "Pharmacology of cerebral ischemia." Molecular and Chemical Neuropathology 16, no. 1-2 (February 1992): 203. http://dx.doi.org/10.1007/bf03159970.

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9

Hua, Y., G. Xi, G. M. de Courten-Myers, K. R. Wagner, and R. E. Myers. "FOCAL CEREBRAL ISCHEMIA." Journal of Neuropathology and Experimental Neurology 55, no. 5 (May 1996): 663. http://dx.doi.org/10.1097/00005072-199605000-00240.

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10

Zhao, Hanshu, Rachel Nepomuceno, Xin Gao, Lesley M. Foley, Shaoxia Wang, Gulnaz Begum, Wen Zhu, et al. "Deletion of the WNK3-SPAK kinase complex in mice improves radiographic and clinical outcomes in malignant cerebral edema after ischemic stroke." Journal of Cerebral Blood Flow & Metabolism 37, no. 2 (July 20, 2016): 550–63. http://dx.doi.org/10.1177/0271678x16631561.

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The WNK-SPAK kinase signaling pathway controls renal NaCl reabsorption and systemic blood pressure by regulating ion transporters and channels. A WNK3-SPAK complex is highly expressed in brain, but its function in this organ remains unclear. Here, we investigated the role of this kinase complex in brain edema and white matter injury after ischemic stroke. Wild-type, WNK3 knockout, and SPAK heterozygous or knockout mice underwent transient middle cerebral artery occlusion. One cohort of mice underwent magnetic resonance imaging. Ex-vivo brains three days post-ischemia were imaged by slice-selective spin-echo diffusion tensor imaging magnetic resonance imaging, after which the same brain tissues were subjected to immunofluorescence staining. A second cohort of mice underwent neurological deficit analysis up to 14 days post-transient middle cerebral artery occlusion. Relative to wild-type mice, WNK3 knockout, SPAK heterozygous, and SPAK knockout mice each exhibited a >50% reduction in infarct size and associated cerebral edema, significantly less demyelination, and improved neurological outcomes. We conclude that WNK3-SPAK signaling regulates brain swelling, gray matter injury, and demyelination after ischemic stroke, and that WNK3-SPAK inhibition has therapeutic potential for treating malignant cerebral edema in the setting of middle cerebral artery stroke.

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Dissertations / Theses on the topic "Cerebral ischemia, neuroscience, demyelination"

1

Manrique-Castaño, Daniel [Verfasser], Dirk Matthias [Gutachter] Hermann, Patrik [Gutachter] Krieger, and Tracy D. [Gutachter] Farr. "Influence of the extracellular matrix protein Tenascin-C in the immune response, glial scar formation and ECM reorganization following cerebral ischemia in mice / Daniel Manrique-Castaño ; Gutachter: Dirk Matthias Hermann, Patrik Krieger, Tracy D. Farr ; International Graduate School of Neuroscience." Bochum : Ruhr-Universität Bochum, 2020. http://d-nb.info/1223176096/34.

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Gaviano, Lisa. "Adenosine a2b receptors and carbonic anhydrase: new therapeutic targets for cerebral ischemia and demyelination." Doctoral thesis, 2020. http://hdl.handle.net/2158/1188740.

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Cerebral ischemia is a multifactorial pathology characterized by different events evolving in time. The acute injury, characterized by a massive increase of extracellular glutamate levels, is followed by activation of resident immune cells and production or activation of inflammation mediators. Although after ischemia precocious activation of immune cells may be neuroprotective and supportive for regeneration, protracted neuroinflammation is now recognized as the predominant mechanism of secondary brain injury progression. In this thesis, I investigated on the putative protective effects of the agonists at adenosine A2B receptor subtype and of the carbonic anhydrase inhibitors in a rat model of focal ischemia. Demyelination occurs in a variety of pathophysiological conditions of the Central Nervous System (CNS). The most serious demyelination occurs in multiple sclerosis but also following cerebral ischemia. Remyelination does occur but is limited especially in chronic disease stages. Therefore, strategies aimed at promoting remyelination, represent an attractive additional therapy in demyelinating pathologies. The remyelination process is mediated by oligodendrocyte progenitor cells (OPCs), a population of cycling cells which persists in the adult CNS, where they can differentiate into mature myelinating oligodendrocytes (OLs). Oligodendrocytes at all maturational stages, express each of the different adenosine receptor subtypes (A1R, A2AR, A2BR and A3R). A number of pathways have been identified that may contribute to ameliorate/impaired remyelination among them, the adenosinergic signaling and sphingosine kinase/sphingosine 1-phosphate signaling axis (SphK/S1P). Therefore, a first aim of my work was to investigate the role of A2BR and of SphK/S1P signaling in modulating cell proliferation and maturation in cultured OPCs and the presence of a possible cross-talk between S1P/SphK and A2BR signaling. We used two A2BR agonists: BAY60-6583 (BAY) and the newly synthesized drug P453, the S1P analog Fingolimod-phosphate (FTY720-P) and the inhibitors of SphK VPC96047 and VPC96091. In cultured OPCs, phosphorylation of the SphK1 (a SphK subtype), that is a hallmark of the activation state of the enzyme, was enhanced after 10 min treatment with BAY (10 µM). Chronic application (7 days) of BAY (1-10 µM) or of P453 (50-100 nM) in cultured medium reduced OPC differentiation, as indicated by the decrease of the two genes target MAG (myelin-associated glycoprotein) and Mbp3 (myelin basic protein 3), typically expressed by mature oligodendrocytes. FTY720-P (1 µM), mimicked the effect of 10 µM BAY on OPC maturation. On the contrary, VPC96047 (500 nM), a pan-SphK inhibitor, and VPC96091 (500 nM) a selective SphK1 inhibitor, increased MAG and Mbp3 levels. These effects were abolished in the presence of 10 µM BAY. After 48 hours A2BR silencing by RNA interference (RNAi), about 50% of the A2BR was downregulated. A2B downregulation increased OPC differentiation (as demonstrated by the CNPase increase). These data are support that A2BR inhibits OPC maturation. Moreover, cells transfected with A2B-siRNA showed a striking increase in S1P lyase levels, the enzyme responsible for of S1P catabolism. Our results demonstrated that the adenosine A2BR inhibit OPC differentiation in cultured OPCs. Moreover, the A2BR agonist BAY increases the expression of phosphorylated SphK1, indicating an interaction between SphK1 and A2BR activation. To date this is the first characterization of the role of adenosine A2BR in oligodendrocyte maturation and of a cross-talk between A2BR and SphK/S1P signaling axis in inhibiting OPC maturation. Extracellular adenosine concentration dramatically increases during cerebral ischemia and a protective role is recognized to adenosine by acting on A1 receptors. However, the use of adenosine A1 agonists is hampered by peripheral and central side effects. Few studies are present in literature on the role of A2B receptors in brain ischemia. A2B receptors are present on endothelial cells, neurons and astrocytes 24 hours after transient middle cerebral artery occlusion (tMCAo) in the rat. Data in the literature indicate that A2BR agonist BAY protect from endothelial leakage and blood brain barrier permeability 24 hours after focal ischemia To date there are no evidences in literature on the protective effects of A2B receptor agonists at more distant times from ischemia when a defined neuroinflammation develops. A further aim of my thesis was to investigate, in the model of focal transient cerebral ischemia (tMCAo) in the rat, the putative protective effects of the A2B receptor agonist, BAY 7 days after ischemia, when a clear inflammatory response has developed. Treatment with BAY, chronically administered (0.1 mg/kg i.p. for 7 days), improves the neurological deficit evaluated 1 and 5 and up to 7 days after tMCAo (p<0.0005-0.02). Seven days after ischemia, BAY has significantly reduced the infarct volume in cortex (p<0.001) and in striatum (p<0.05), has reconstituted the cortical and striatal cytoarchitecture and has reduced glial cell proliferation that was induced by the ischemic insult. BAY has significantly reverted the increase in number of damaged neurons (stained with the specific marker for neurons, NeuN+). Furthermore, BAY has reverted the strong pattern of microglia activation and reduced the loss of astrocyte. Seven days after ischemia, plasma inflammatory marker of brain damage TNF-α, is definitely increased while the levels of IL10 regulatory cytokine with anti-inflammatory action is decreased. Interestingly, BAY has reverted these modifications. Moreover, two days after ischemia, BAY has reduced granulocytes (evaluated as HIS-48+ cells) infiltration into brain ischemic areas. Our results demonstrated a protective effect of the chronic treatment of the A2BR agonist BAY 7 days after focal ischemia. The protective effects of BAY can be attributed to the stimulation of A2BR located both on central neural cells and on blood cells where A2BR are known to reduce activation and cytokine production thus attenuating neuroinflammation that develops days after ischemia. The evidence that hypoxic microenvironments elicit the expression of specific isoforms of carbonic anhydrase (CA), in particular CAIX and CAXII, through the hypoxia inducible factor, has allowed to hypothesize a possible CA relevance in ischemia. Recently it has been demonstrated that carbonic anhydrase inhibitors (CAIs), sulfonamide and coumarin, were able to improve neurological functionalities after cerebral ischemic insult. Preliminary data obtained in our laboratory in a model of in vitro ischemia demonstrated that two CAIs, acetazolamide and AN11-740 were able to prevent the appearance of anoxic depolarization (AD), a phenomenon strictly related to cell damage and death, 30 minutes after oxygen and glucose deprivation (OGD) condition in hippocampal slices. Based on this preliminary result, the aim of third study in my thesis was to investigate the putative protective effect of two CAIs, acetazolamide and AN11-740 in the in vivo model of permanent cerebral ischemia (pMCAo) in the rat. Sub-chronic treatment with acetazolamide and AN11-740 at the dose 4.4 mg/kg i.p. and 1.0 mg/kg i.p. significantly reduced the neurological deficit (p<0.0010.0001) and the infarct volume in cortex and striatum (p<0.001) 24 hours after ischemia. Treatment with the two CAIs, significantly reverted the decrease in the number of neurons (stained with the specific marker for neurons, NeuN+) induced by pMCAo. Twenty-four hours after focal ischemia, plasma inflammatory markers of brain damage TNF-α, is definitely increased while the levels of IL10 is decreased. The sub-chronic treatment with both carbonic anhydrase inhibitors, acetazolamide and AN11-740, didn’t modify significantly neither TNF-α or IL-10 plasma levels. Our results demonstrated a protective role of CA inhibitors at an early time (i.e. 24 hours) after in vivo ischemia. Likely protective effect of CAIs are attributable to a early direct effect of reduction of excitotoxicity in the first hours after brain ischemia.

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Books on the topic "Cerebral ischemia, neuroscience, demyelination"

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Capo Boi Conference on Neuroscience (6th 1989 Villasimius, Italy). Excitatory amino acids and brain ischemia: Pharmacological and clinical aspects : proceedings of the biannual Capo Boi Confernece on Neuroscience, June 1989, Villasimius, Italy. Edited by Biggio Giovanni. Oxford: Pergamon Press, 1990.

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2

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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3

Walz, Wolfgang. Cerebral Ischemia: Molecular and Cellular Pathophysiology (Contemporary Neuroscience). Humana Press, 1999.

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4

Lin, Rick C. S. New Concepts in Cerebral Ischemia (Methods and New Frontiers in Neuroscience). CRC, 2001.

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Lin, Rick C. S. New Concepts in Cerebral Ischemia. Methods and New Frontiers in Neuroscience. Taylor & Francis Group, 2002.

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6

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Book chapters on the topic "Cerebral ischemia, neuroscience, demyelination"

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Chan, P. H. "Oxygen Radical Mechanisms in Cerebral Ischemia and Reperfusion." In Monographs in Clinical Neuroscience, 14–27. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000061569.

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Zhang, Z. G., and M. Chopp. "Inflammatory Response and Adhesion Molecules in Focal Cerebral Ischemia." In Monographs in Clinical Neuroscience, 46–64. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000061571.

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Yenari, M. A., and H. S. Han. "Influence of Therapeutic Hypothermia on Regeneration after Cerebral Ischemia." In Frontiers of Neurology and Neuroscience, 122–28. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000346428.

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Takatsuru, Yusuke, Kayo Nakamura, and Junichi Nabekura. "Compensatory Contribution of the Contralateral Pyramidal Tract after Experimental Cerebral Ischemia." In Frontiers of Neurology and Neuroscience, 36–44. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000346409.

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Rajagopalan, Vanitha, Vasudha Singhal, and Charu Mahajan. "Translational research in delayed cerebral ischemia." In Perioperative Neuroscience, 189–202. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91003-3.00002-7.

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Fugate, Jennifer E. "Consequences of Anoxia and Ischemia to the Brain." In Mayo Clinic Critical and Neurocritical Care Board Review, edited by Eelco F. M. Wijdicks, James Y. Findlay, William D. Freeman, and Ayan Sen, 86–91. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190862923.003.0011.

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Systemic illness can have an abrupt and sometimes profound effect on the central nervous system. Organ failure and acute electrolyte disturbances may cause neurologic manifestations that are often accompanied by a decline in consciousness. Secondary injury is characterized by demyelination, cerebral edema, and anoxic-ischemic brain injury.

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Devarajan, Jagan, and Beth H. Minzter. "Ischemic Neuropathy." In Neuropathic Pain, edited by Jianguo Cheng, 123–36. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190298357.003.0015.

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This chapter discusses the subset of ischemic neuropathy which is due primarily to peripheral arterial disease. Peripheral arterial disease affects 5% of men and 2.5% of women and results in ischemic pain and claudication. Disease progression occurs in a small minority of patients to a stage of critical ischemia with rest pain and threatens limb survival. Ischemic neuropathy encompasses pain due to several stages of progression of tissue ischemia. Patients may have multiple comorbid conditions due to the same pathological process that affects coronary, cerebral, and other circulations. Diabetes mellitus is commonly associated with vascular ischemia and results in arterial occlusive diseases. Pathological changes involve demyelination, axonal loss, and disorderly remyelination. In addition to simple palpation of a pulse, Doppler flow estimation and angiography are used to determine the location and extent of the disease process. Ankle-brachial index, toe-brachial index, and digital flow estimations are more sensitive methods used for early identification. In addition to controlling risk factors and the management of comorbid conditions, medication and procedures to restore blood flow play a prominent role in management of ischemic neuropathy. Sympatholysis and spinal cord stimulation are effective methods to help manage chronic pain in advanced cases that are refractory to conventional treatment measures.

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Conference papers on the topic "Cerebral ischemia, neuroscience, demyelination"

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Ludmila, BELAYEV, and BAZAN Nicolas G. "Experimental models of cerebral ischemia: Implications for drug discovery." In I International Symposium in Neuroscience Meeting. Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/isnm-sine35.

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Loginova, Nadezhda, Nikola Panov, Nikolai Kositsyn, and Mikhail Svinov. "THE ROLE OF GAP JUNCTIONS IN THE CEREBRAL ISCHEMIA DEVELOPMENT." In XIV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2018. http://dx.doi.org/10.29003/m188.sudak.ns2018-14/305.

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Urazov, Mark, Maria Vedunova, and Elena Mitroshina. "NEUROPROTECTIVE EFFECT OF BLOCKADE OF SRC AND RIPK1 KINASES IN MODELING CEREBRAL ISCHEMIA IN VIVO." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2359.sudak.ns2021-17/379-380.

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Denisova, Alina, Ivan Filippenkov, Vasily Stavchansky, Vadim Yuzhakov, Larisa Sevan’kaeva, Nikolai Myasoedov, Svetlana Limborska, Lyudmila Dergunova, and Leonid Gubsky. "PHARMACOTRANSCRIPTOME ANALYSIS OF THE PEPTIDE DRUGS ACTIONS UNDER EXPERIMENTAL MODEL CONDITION OF FOCAL CEREBRAL ISCHEMIA IN RATS." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2110.sudak.ns2021-17/133-134.

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Loginova, Nadezhda, Nikolay Panov, and Nikolay Kositsyn. "SPECIFIC BLOCKER OF ASTROCYTIC GAP JUNCTIONS INFLUENCES ON THE RECOVERY OF MOTOR FUNCTION AFTER THE CEREBRAL ISCHEMIA IN RATS." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m473.sudak.ns2019-15/276-277.

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Gainutdinov, Khalil, Vyacheslav Andrianov, Gusel Yafarova, Svetlana Pashkevich, Yuliya Stukach, Tatiana Bogodvid, Margarita Dosina, et al. "DYNAMICS OF NITRIC OXIDE CONTENT IN THE RAT DENTATE GYRUS (CA4 HIPPOCAMPAL REGION) OF RATS BEFORE AND AFTER MODELING OF CEREBRAL ISCHEMIA: EPR STUDY." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m353.sudak.ns2019-15/131-132.

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Cherkashova, Elvira, Veronika Burunova, Daria Namestnikova, Ilya Gubskiy, Tatiana Bukharova, Diasna Salikhova, Georgy Leonov, et al. "THE EFFECTIVENESS AND DISTRIBUTION OF INTRAVENOUS TRANSPLANTATION OF MESENCHYMAL STEM CELLS DERIVED FROM HUMAN PLACENTA AND NEURAL PROGENITOR CELLS DERIVED FROM INDUCED PLURIPOTENT STEM CELLS IN RATS WITH FOCAL CEREBRAL ISCHEMIA." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2398.sudak.ns2021-17/417-418.

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Zhou, Bingqian, Kuikui Fan, and Lingjie Kong. "A biocompatible hydrogel-coated fiber-optic probe for monitoring pH dynamics in brains of freely moving mice." In Optical Fiber Sensors. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/ofs.2022.w4.69.

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The pH dynamics in the brain microenvironment is related to a variety of brain diseases, so it is critical to develop pH probes with great efficiency for in vivo detection of brain. Here, we report a biocompatible hydrogel-coated fiber optic probe (HCFOP) for monitoring pH dynamics in the brains of freely-moving mice. The novel pH probe was prepared by combining hydrogel coated silica multimode fiber with pH-sensitive microspheres embedded in hydrogel fiber, and the pH calibration is based on fluorescence ratio detection. The sensor has a dynamic range of pH from 3.0 to 9.0, and a resolution of 0.0014 pH units with good reproducibility, reversibility, and time stability. We tested the capability of our proposed sensor in dynamically detecting pH in the brains of free moving mice, and the biocompatibility for long-term implantation. We implanted the fiber-optic probes into the striatum and hippocampus of mouse brains. During cerebral ischemia, we detected a decrease in pH of about 0.5 after ~15 mins. During epilepsy induced by kanic acid (KA), we found that pH in the hippocampus decreased by about 0.2 after ~80 mins, in relation to the dynamical concentrations of adenosine. This biofriendly and easy-to-manufacture HCFOP provides a unique solution for assessing small changes in the pH of the brain microenvironment, thus holds great promises in neuroscience study.

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