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Reactive astrocytes are astrocytes undergoing morphological, molecular, and functional remodeling in response to injury, disease, or infection of the CNS. Although this remodeling was first described over a century ago, uncertainties and controversies remain regarding the contribution of reactive astrocytes to CNS diseases, repair, and aging. It is also unclear whether fixed categories of reactive astrocytes exist and, if so, how to identify them. We point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic-vs-neuroprotective or A1-vs-A2. We advocate, instead, that research on reactive astrocytes include assessment of multiple molecular and functional parameters-preferably in vivo-plus multivariate statistics and determination of impact on pathological hallmarks in relevant models. These guidelines may spur the discovery of astrocyte-based biomarkers as well as astrocyte-targeting therapies that abrogate detrimental actions of reactive astrocytes, potentiate their neuro- and glioprotective actions, and restore or augment their homeostatic, modulatory, and defensive functions.

Functional neuroimaging using MRI relies on measurements of blood oxygen level-dependent (BOLD) signals from which inferences are made about the underlying neuronal activity. This is possible because neuronal activity elicits increases in blood flow via neurovascular coupling, which gives rise to the BOLD signal. Hence, an accurate interpretation of what BOLD signals mean in terms of neural activity depends on a full understanding of the mechanisms that underlie the measured signal, including neurovascular and neurometabolic coupling, the contribution of different cell types to local signalling, and regional differences in these mechanisms. Furthermore, the contributions of systemic functions to cerebral blood flow may vary with ageing, disease and arousal states, with regard to both neuronal and vascular function. In addition, recent developments in non-invasive imaging technology, such as high-field fMRI, and comparative inter-species analysis, allow connections between non-invasive data and mechanistic knowledge gained from invasive cellular-level studies. Considered together, these factors have immense potential to improve BOLD signal interpretation and bring us closer to the ultimate purpose of decoding the mechanisms of human cognition. This theme issue covers a range of recent advances in these topics, providing a multidisciplinary scientific and technical framework for future work in the neurovascular and cognitive sciences. This article is part of the theme issue 'Key relationships between non-invasive functional neuroimaging and the underlying neuronal activity'.

Increases in brain blood flow, evoked by neuronal activity, power neural computation and form the basis of BOLD (blood-oxygen-level-dependent) functional imaging. Whether blood flow is controlled solely by arteriole smooth muscle, or also by capillary pericytes, is controversial. We demonstrate that neuronal activity and the neurotransmitter glutamate evoke the release of messengers that dilate capillaries by actively relaxing pericytes. Dilation is mediated by prostaglandin E.sub.2, but requires nitric oxide release to suppress vasoconstricting 20-HETE synthesis. In vivo, when sensory input increases blood flow, capillaries dilate before arterioles and are estimated to produce 84% of the blood flow increase. In pathology, ischaemia evokes capillary constriction by pericytes. We show that this is followed by pericyte death in rigor, which may irreversibly constrict capillaries and damage the blood-brain barrier. Thus, pericytes are major regulators of cerebral blood flow and initiators of functional imaging signals. Prevention of pericyte constriction and death may reduce the long-lasting blood flow decrease that damages neurons after stroke. Neuronal activity relaxes pericytes, leading to capillary dilation and increased blood flow, before arterioles dilate, suggesting that pericytes initiate blood-oxygen-level-dependent (BOLD) functional imaging signals; pericytes constrict and die in rigor in ischaemia, which will cause a long-lasting blood flow decrease after stroke, and damage the blood-brain barrier. Blood flow response to neural activity Cerebral blood flow dynamics have long been linked to neural activity, and form the basis of BOLD (blood-oxygen-level-dependent) functional imaging. But how such blood flow changes are mediated has remained controversial. Here, David Attwell and colleagues reveal how neuronal activity can hyperpolarize pericytes, leading to their relaxation and capillary dilation. Capillary dilation is responsible for 84% of the blood increase linked to neural activity, so irreversible capillary closure due to pericyte death during ischaemia can injure the blood-brain barrier and exacerbate injury. Pericyte death under pathological conditions can be reduced if glutamate receptor signalling is inhibited. This work suggests that pericytes are major regulators of cerebral blood flow and may initiate BOLD imaging signals., Author(s): Catherine N. Hall [sup.1] , Clare Reynell [sup.1] , Bodil Gesslein [sup.2] , Nicola B. Hamilton [sup.1] , Anusha Mishra [sup.1] , Brad A. Sutherland [sup.3] , Fergus M. [...]

This study investigates the potential of a pin to plate atmospheric plasma on the microbial decontamination of oat milk along with the changes in the physicochemical, rheological, functional, and particle morphology. As cold plasma comprises reactive species, and free radicals tend to rupture the microbial cells, microbial reduction in the oat milk is expected. Extracted oat milk (14.03 ± 0.67% solids) is treated with plasma input voltages of 170–230 V for an exposure time of 5–15 min. The treated milk is analyzed for the effect of plasma treatment on microbial reduction, physicochemical properties (total soluble solids [TSS], pH, titratable acidity [TA], color, and total protein content), viscosity, sedimentation index (SI), and the particle morphology. The highest microbial log reduction of 2.18 and 1.47 in bacteria and yeast and molds, respectively, is obtained at the intensive plasma treatment of 230 V and 15 min. With plasma treatment, TSS, TA, and SI are increased, whereas pH, total protein content, and viscosity are reduced. The modifications in the oat constituents and aggregate formations are the major causes of the observed results. This proves that cold plasma is a prospective decontamination technique for a plant‐based milk analog. Novelty impact statement: Microbial decontamination of oat‐milk through nonthermal cold plasma technology has never been explored.The physicochemical alteration, color, and rheological parameters have been extensively studied in the current study.Microbial reduction of up to 2 logs was obtained at 230 V treatment of 15 min without changing the fluidity of the oat milk. [ABSTRACT FROM AUTHOR]