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Little is known about age‐dependent changes in structure and function of astrocytes and of the impact of these on the cognitive decline in the senescent brain. The prevalent view on the age‐dependent increase in reactive astrogliosis and astrocytic hypertrophy requires scrutiny and detailed analysis. Using two‐photon microscopy in conjunction with 3D reconstruction, Sholl and volume fraction analysis, we demonstrate a significant reduction in the number and the length of astrocytic processes, in astrocytic territorial domains and in astrocyte‐to‐astrocyte coupling in the aged brain. Probing physiology of astrocytes with patch clamp, and Ca2+ imaging revealed deficits in K+ and glutamate clearance and spatiotemporal reorganisation of Ca2+ events in old astrocytes. These changes paralleled impaired synaptic long‐term potentiation (LTP) in hippocampal CA1 in old mice. Our findings may explain the astroglial mechanisms of age‐dependent decline in learning and memory. Ageing reduces the number and the length of astrocytic processes, astrocytic territorial domains and astrocyte‐to‐astrocyte coupling in the hippocampus. Such dystrophy causes deficits in K+ and glutamate clearance by astrocytes. Enhanced glutamate spillover impairs synaptic long‐term potentiation (LTP) in hippocampal CA1, which may represent the astroglial mechanisms of age‐dependent decline in learning and memory.

Perceived social support has been hypothesized to protect against the pathogenic effects of stress. How such protection might be conferred, however, is not well understood. Using a sample of 404 healthy adults, we examined the roles of perceived social support and received hugs in buffering against interpersonal stress-induced susceptibility to infectious disease. Perceived support was assessed by questionnaire, and daily interpersonal conflict and receipt of hugs were assessed by telephone interviews on 14 consecutive evenings. Subsequently, participants were exposed to a virus that causes a common cold and were monitored in quarantine to assess infection and illness signs. Perceived support protected against the rise in infection risk associated with increasing frequency of conflict. A similar stress-buffering effect emerged for hugging, which explained 32% of the attenuating effect of support. Among infected participants, greater perceived support and more-frequent hugs each predicted less-severe illness signs. These data suggest that hugging may effectively convey social support.

Astrocytes are connected in a functional syncytium via gap junctions, which contribute to the maintenance of extracellular K + homeostasis. The prevailing hypothesis is that K + released during neuronal firing is taken up by astrocytes via K ir channels and then distributed among neighboring astrocytes via gap junctions. Here, we tested the effect of blocking gap junctions and K ir channels, both independently and simultaneously, on field excitability of cortical slices in response to a stimulation train. Independently blocking either gap junctions or K ir channels increased the amplitude of the first fEPSC (field excitatory post-synaptic current) response, followed by suppression of both fiber volley (pre-synaptic action potentials) and fEPSCs during sustained stimulation. Surprisingly, simultaneous block of both gap junctions and K ir channels enhanced the suppression of neuronal activity, resulting in a ∼75% decrease in fiber volley amplitude in the first response, followed by a fast and strong suppression of fEPSCs during sustained stimulation. Genetic depletion of astrocyte gap junctions showed a reduction but not complete loss of Cx43, indicating partial syncytial decoupling, and, accordingly, had a weaker but similar effect on neuronal excitability as blocking gap junctions. Pharmacological K ir block in mice with reduced gap junction coupling suppressed sustained firing of the fiber volley but not fEPSCs. That this effect was milder than K ir block alone suggests that adaptive mechanisms may be recruited upon genetically induced astrocyte decoupling. We conclude that K + buffering via K ir and gap junctions in astrocytes together play a critical role in maintaining neuronal excitability, particularly during sustained activity, but that other mechanisms can be recruited to perform this function in their absence.

Soil has the nature of acidity and alkalinity, mostly indicated by soil pH that could greatly affect soil ecological processes and functions. With exogenous inputs of acidic materials (such as acid rain), soils may more or less resist to maintain their pH levels within specific thresholds by various buffering processes. It has been well established that soil properties such as cation exchange capacity (CEC), soil organic matter (SOM), and clay content play important roles in mitigating the effects of acid inputs, but the factors varied across soils. This microcosm experiment was conducted to investigate changes in the soil pH and quantitatively estimate the critical pH threshold of simulated acid rain for three highly weathered soils (red soil, lateritic red soil, and latosol) that are typical soil types widely distributed across the world’s subtropical and tropical climatic zones, as well as important influential factors, after continuously adding different levels of simulated acid rain on the surface of soil cores. The results showed that the change in the soil pH was not significantly different among the three soils, although it was exponentially related to soil CEC and clay content. Resultantly, the latosol that had high soil CEC and clay content was more resistant to simulated acid rain, especially when relatively weak simulated acid rain treatments were applied. The lateritic red soil that contained the lowest soil CEC and clay content showed the greatest decline in the soil pH under the strongest simulated acid rain treatment of pH being 2.5. Furthermore, we estimated the critical pH threshold of simulated acid rain for the three soils and observed that it was considerably different among the soils. Surprisingly, the pH threshold of simulated acid rain was also positively related to the soil CEC and clay content, therefore making the highest pH threshold in the latosol. Our results imply that soil CEC and clay content may play critical roles in the soil acid-buffering processes from two aspects; it could not only contribute to the soil acid-buffering capacity, but also affect the threshold of acidity of acid rain below which abrupt soil acidification may occur.

Calreticulin (CALR) is an endoplasmic reticulum (ER)-resident protein involved in a spectrum of cellular processes. In healthy cells, CALR operates as a chaperone and Ca 2+ buffer to assist correct protein folding within the ER. Besides favoring the maintenance of cellular proteostasis, these cell-intrinsic CALR functions support Ca 2+ -dependent processes, such as adhesion and integrin signaling, and ensure normal antigen presentation on MHC Class I molecules. Moreover, cancer cells succumbing to immunogenic cell death (ICD) expose CALR on their surface, which promotes the uptake of cell corpses by professional phagocytes and ultimately supports the initiation of anticancer immunity. Thus, loss-of-function CALR mutations promote oncogenesis not only as they impair cellular homeostasis in healthy cells, but also as they compromise natural and therapy-driven immunosurveillance. However, the prognostic impact of total or membrane-exposed CALR levels appears to vary considerably with cancer type. For instance, while genetic CALR defects promote pre-neoplastic myeloproliferation, patients with myeloproliferative neoplasms bearing CALR mutations often experience improved overall survival as compared to patients bearing wild-type CALR . Here, we discuss the context-dependent impact of CALR on malignant transformation, tumor progression and response to cancer therapy.

TRPM8 is a cold temperature‐sensitive and non‐selective Ca2+‐channel. Previously we have observed that TRPM8 is endogenously expressed and affects T cell activation process. Now, we report that TRPM8 regulates functions of mitochondria and ER, two important sub‐cellular compartments. Pharmacological modulation of TRPM8 and/or due to TCR‐treatment regulates mitochondrial Ca2+, ATP, membrane potential, cardiolipin level and mitochondrial temperature in a context‐dependent manner. In addition, TRPM8 alters the relative temperature of mitochondria and ER, ER‐mitochondrial contact points, mainly at the immunological synapse (IS), and thus TRPM8 has the potential to affect the overall cellular functions. Our data suggests both, i.e., the presence and enrichment of TRPM8 in the IS of T cells. We suggest that TRPM8 is a crucial regulator of Ca2+‐signalling in T cells and significantly contributes to Ca2+‐buffering by modulating cellular and sub‐cellular organelle functions. These findings are useful to understand the functions of T cells in different pathological conditions.

Alzheimer’s disease (AD) is the most frequent cause of age-related neurodegeneration and cognitive impairment, and there are currently no broadly effective therapies. The underlying pathogenesis is complex, but a growing body of evidence implicates mitochondrial dysfunction as a common pathomechanism involved in many of the hallmark features of the AD brain, such as formation of amyloid-beta (Aβ) aggregates (amyloid plaques), neurofibrillary tangles, cholinergic system dysfunction, impaired synaptic transmission and plasticity, oxidative stress, and neuroinflammation, that lead to neurodegeneration and cognitive dysfunction. Indeed, mitochondrial dysfunction concomitant with progressive accumulation of mitochondrial Aβ is an early event in AD pathogenesis. Healthy mitochondria are critical for providing sufficient energy to maintain endogenous neuroprotective and reparative mechanisms, while disturbances in mitochondrial function, motility, fission, and fusion lead to neuronal malfunction and degeneration associated with excess free radical production and reduced intracellular calcium buffering. In addition, mitochondrial dysfunction can contribute to amyloid-β precursor protein (APP) expression and misprocessing to produce pathogenic fragments (e.g., Aβ1-40). Given this background, we present an overview of the importance of mitochondria for maintenance of neuronal function and how mitochondrial dysfunction acts as a driver of cognitive impairment in AD. Additionally, we provide a brief summary of possible treatments targeting mitochondrial dysfunction as therapeutic approaches for AD.

Synapses enable neurons to communicate with each other and are therefore a prerequisite for normal brain function. Presynaptically, this communication requires energy and generates large fluctuations in calcium concentrations. Mitochondria are optimized for supplying energy and buffering calcium, and they are actively recruited to presynapses. However, not all presynapses contain mitochondria; thus, how might synapses with and without mitochondria differ? Mitochondria are also increasingly recognized to serve additional functions at the presynapse. Here, we discuss the importance of presynaptic mitochondria in maintaining neuronal homeostasis and how dysfunctional presynaptic mitochondria might contribute to the development of disease.

Salinization of agricultural lands is a major threat to agriculture. Many different factors affect and determine plant salt tolerance. Nonetheless, there is a consensus on the relevance of maintaining an optimal cytosolic potassium : sodium ion (K⁺ : Na⁺) ratio for salinity tolerance in plants. This ratio depends on the operation of plasma membrane and tonoplast transporters. In the present review we focus on some aspects related to the energetic cost of maintaining that K⁺ : Na⁺ ratio. One of the factors that affect the cost of the first step of K⁺ acquisition – root K⁺ uptake through High Affinity K⁺ transporter and Arabidopsis K⁺ transport system 1 transport systems – is the value of the plasma membrane potential of root cells, a parameter that may differ amongst plant species. In addition to its role in nutrition, cytosolic K⁺ also is important for signalling, and K⁺ efflux through gated outward-rectifying K⁺ and nonselective cation channels can be regarded as a switch to redirect energy towards defence reactions. In maintaining cytosolic K⁺, the great buffer capacity of the vacuole should be considered. The possible role of high-affinity K⁺ transporters (HKT)2s in mediating K⁺ uptake under saline conditions and the importance of cycling of K⁺ throughout the plant also are discussed.

Nearly all families in the United States were exposed to varying degrees of stress related to the COVID-19 pandemic during the spring of 2020. Building on previous research documenting the pernicious effects of stress on youth mental health, we aimed to test the effects of exposure to COVID-19-related stress on youth symptomatology. Further, in light of evidence suggesting that parents play an important role in buffering children from environmental stress, we assessed how specific parental behaviors (i.e., parental emotion socialization, maintenance of home routines, and availability to discuss the pandemic with child) contributed to effective parental buffering of the impact of pandemic-related stress on children’s symptomatology. Conversely, we tested whether parental anxiety-related symptomatology and parenting stress exacerbated the effect of children’s exposure to pandemic-related stress on children’s symptomatology. Results suggest that parents who engaged in relatively higher levels of emotion coaching of children’s negative emotions and who maintained more stable home routines during the pandemic were more effectively able to buffer the effects of pandemic-related stress on children’s symptomatology. Parents who reported higher levels of parenting stress and anxiety-related symptomatology were less likely to effectively buffer stress. Though interpretation of the findings is limited due to sole reliance on parental report and the cross-sectional study design due to the constraints of collecting data during a global pandemic, findings underscore the importance of assessing family-level factors when considering the impact of stressors on children’s symptomatology and highlight the need to support parents during global events that place families under significant stress.