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Neuroglia, Volume 1, Issue 1 (June 2018)

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Editorial

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Open AccessEditorial Neuroglia: A New Open-Access Journal Publishing All Aspects of Glial Research
Neuroglia 2018, 1(1), 1; doi:10.3390/neuroglia1010001
Received: 4 December 2017 / Revised: 4 December 2017 / Accepted: 5 December 2017 / Published: 15 December 2017
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Abstract
Today, we announce the new journal Neuroglia, which we see as an inclusive and innovative open-access forum for publishing all aspects of glial research.[...] Full article
Open AccessEditorial Remembering Ben Barres
Neuroglia 2018, 1(1), 2; doi:10.3390/neuroglia1010002
Received: 6 January 2018 / Revised: 10 January 2018 / Accepted: 10 January 2018 / Published: 11 January 2018
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Abstract
Ben Barres, who was at the heart of glial cell physiology for over 30 years, died aged 63 on December 27, 2017.[...] Full article

Research

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Open AccessArticle Cooperation between NMDA-Type Glutamate and P2 Receptors for Neuroprotection during Stroke: Combining Astrocyte and Neuronal Protection
Neuroglia 2018, 1(1), 5; doi:10.3390/neuroglia1010005
Received: 13 February 2018 / Revised: 6 March 2018 / Accepted: 8 March 2018 / Published: 14 March 2018
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Abstract
Excitotoxicity is the principle mechanism of acute injury during stroke. It is defined as the unregulated accumulation of excitatory neurotransmitters such as glutamate within the extracellular space, leading to over-activation of receptors, ionic disruption, cell swelling, cytotoxic Ca2+ elevation and a feed-forward
[...] Read more.
Excitotoxicity is the principle mechanism of acute injury during stroke. It is defined as the unregulated accumulation of excitatory neurotransmitters such as glutamate within the extracellular space, leading to over-activation of receptors, ionic disruption, cell swelling, cytotoxic Ca2+ elevation and a feed-forward loop where membrane depolarisation evokes further neurotransmitter release. Glutamate-mediated excitotoxicity is well documented in neurons and oligodendrocytes but drugs targeting glutamate excitotoxicity have failed clinically which may be due to their inability to protect astrocytes. Astrocytes make up ~50% of the brain volume and express high levels of P2 adenosine triphosphate (ATP)-receptors which have excitotoxic potential, suggesting that glutamate and ATP may mediate parallel excitotoxic cascades in neurons and astrocytes, respectively. Mono-cultures of astrocytes expressed an array of P2X and P2Y receptors can produce large rises in [Ca2+]i; mono-cultured neurons showed lower levels of functional P2 receptors. Using high-density 1:1 neuron:astrocyte co-cultures, ischemia (modelled as oxygen-glucose deprivation: OGD) evoked a rise in extracellular ATP, while P2 blockers were highly protective of both cell types. GluR blockers were only protective of neurons. Neither astrocyte nor neuronal mono-cultures showed significant ATP release during OGD, showing that cell type interactions are required for ischemic release. P2 blockers were also protective in normal-density co-cultures, while low doses of combined P2/GluR blockers where highly protective. These results highlight the potential of combined P2/GluR block for protection of neurons and glia. Full article
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Open AccessArticle l-Dopa and Fluoxetine Upregulate Astroglial 5-HT2B Receptors and Ameliorate Depression in Parkinson’s Disease Mice
Neuroglia 2018, 1(1), 6; doi:10.3390/neuroglia1010006
Received: 19 March 2018 / Revised: 13 April 2018 / Accepted: 13 April 2018 / Published: 23 April 2018
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Abstract
Here, we report the association between depressive behavior (anhedonia) and astroglial expression of 5-hydroxytryptamine receptor 2B (5-HT2B) in an animal model of Parkinson’s disease, induced by bilateral injection of 6-hydroxydopamine (6-OHDA) into the striatum. Expression of the 5-HT2B receptor at
[...] Read more.
Here, we report the association between depressive behavior (anhedonia) and astroglial expression of 5-hydroxytryptamine receptor 2B (5-HT2B) in an animal model of Parkinson’s disease, induced by bilateral injection of 6-hydroxydopamine (6-OHDA) into the striatum. Expression of the 5-HT2B receptor at the mRNA and protein level was decreased in the brain tissue of 6-OHDA-treated animals with anhedonia. Expression of the 5-HT2B receptor was corrected by four weeks treatment with either l-3,4-dihydroxyphenylalanine (l-dopa) or fluoxetine. Simultaneously, treatment with l-dopa abolished 6-OHDA effects on both depressive behavior and motor activity. In contrast, fluoxetine corrected 6-OHDA-induced depression but did not affect 6-OHDA-induced motor deficiency. In addition, 6-OHDA downregulated gene expression of the 5-HT2B receptor in astrocytes in purified cell culture and this downregulation was corrected by both l-dopa and fluoxetine. Our findings suggest that 6-OHDA-induced depressive behavior may be related to the downregulation of gene expression of the 5-HT2B receptor but 6-OHDA-induced motor deficiency reflects, arguably, dopamine depletion. Previously, we demonstrated that fluoxetine regulates gene expression in astrocytes by 5-HT2B receptor-mediated transactivation of epidermal growth factor receptor (EGFR). However, the underlying mechanism of l-dopa action remains unclear. The present work indicates that the decrease of gene expression of the astroglial 5-HT2B receptor may contribute to development of depressive behavior in Parkinson’s disease. Full article
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Other

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Open AccessPerspective Interlaminar Glia and Other Glial Themes Revisited: Pending Answers Following Three Decades of Glial Research
Neuroglia 2018, 1(1), 3; doi:10.3390/neuroglia1010003
Received: 23 January 2018 / Revised: 20 February 2018 / Accepted: 22 February 2018 / Published: 1 March 2018
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Abstract
This review aims to highlight the various significant matters in glial research stemming from personal work by the author and associates at the Unit of Applied Neurobiology (UNA, CEMIC-CONICET), and some of the pending questions. A reassessment and further comments on interlaminar astrocytes—an
[...] Read more.
This review aims to highlight the various significant matters in glial research stemming from personal work by the author and associates at the Unit of Applied Neurobiology (UNA, CEMIC-CONICET), and some of the pending questions. A reassessment and further comments on interlaminar astrocytes—an astroglial cell type that is specific to humans and other non-human primates, and is not found in rodents, is presented. Tentative hypothesis regarding their function and future possible research lines that could contribute to further the analysis of their development and possible role(s), are suggested. The possibility that they function as a separate entity from the “territorial” astrocytes, is also considered. In addition, the potential significance of our observations on interspecies differences in in vitro glial cell dye coupling, on glial diffusible factors affecting the induction of this glial phenotype, and on their interference with the cellular toxic effects of cerebrospinal fluid obtained from l-DOPA treated patients with Parkinson´s disease, is also considered. The major differences oberved in the cerebral cortex glial layout between human and rodents—the main model for studying glial function and pathology—calls for a careful assessment of known and potential species differences in all aspects of glial cell biology. This is essential to provide a better understanding of the organization and function of human and non-human primate brain, and of the neurobiological basis of their behavior. Full article
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Open AccessCommentary The Special Case of Human Astrocytes
Neuroglia 2018, 1(1), 4; doi:10.3390/neuroglia1010004
Received: 19 February 2018 / Accepted: 19 February 2018 / Published: 1 March 2018
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Abstract
In this first issue of Neuroglia, it is highly appropriate that Professor Jorge A. Colombo at the Unit of Applied Neurobiology (UNA, CEMIC-CONICET) in Buenos Aires, Argentina, writes a perspective of idiosyncrasies of astrocytes in the human brain. Much of his work
[...] Read more.
In this first issue of Neuroglia, it is highly appropriate that Professor Jorge A. Colombo at the Unit of Applied Neurobiology (UNA, CEMIC-CONICET) in Buenos Aires, Argentina, writes a perspective of idiosyncrasies of astrocytes in the human brain. Much of his work has been focused on the special case of interlaminar astrocytes, so-named because of their long straight processes that traverse the layers of the human cerebral cortex. Notably, interlaminar astrocytes are primate-specific and their evolutionary development is directly related to that of the columnar organization of the cerebral cortex in higher primates. The human brain also contains varicose projection astrocytes or polarized astrocytes which are absent in lower animals. In addition, classical protoplasmic astrocytes dwelling in the brains of humans are ≈15-times larger and immensely more complex than their rodent counterparts. Human astrocytes retain their peculiar morphology even after grafting into rodent brains; that is, they replace the host astrocytes and confer certain cognitive advantages into so-called ‘humanised’ chimeric mice. Recently, a number of innovative studies have highlighted the major differences between human and rodent astrocytes. Nonetheless, these differences are not widely recognized, and we hope that Jorge Colombo’s Perspective and our associated Commentary will help stimulate appreciation of human astrocytes by neuroscientists and glial cell biologists alike. Full article
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