[Carbon Dioxide Mitigation Co-effect Analysis of Structural Adjustment Measures in the "2+26" Cities in the Jing-Jin-Ji Region and Its Surroundings].

The Three-Year Action Plan for Winning the Blue Sky Defense Battle states that structural adjustments of industrial, energy, transportation, and land use are important to significantly reduce CO2 and air pollutant emissions. This co-effect is evident but has not been quantified at the city-cluster level. This study developed an emission inventory for the "2+26" cities of the Jing-Jin-Ji region and its surroundings and quantitatively analyzed the impacts of measures in the Three-Year Action Plan for Winning the Blue Sky Defense Battle on the emissions of CO2 and major air pollutants using Greenhouse Gas and Air Pollution Interactions and Synergies in the "2+26" cities model (GAINS-JJJ). The results showed that in the "2+26" cities, the emission reductions in CO2, primary PM2.5, SO2, NOx, and NH3 under policy scenario 2020 were 29.1 Mt (equivalent to 2% of the emissions in 2017), 203.8 (21%), 281.8 (27%), 485.5 (17%), and 34.3 kt (3%), respectively, relative to 2017. In terms of the cities or sectors, the higher the pollutant emissions, the higher the reduction achieved. The CO2 mitigation co-effect results showed that industrial adjustment measures, such as eliminating backward production capacity, upgrades on industrial boilers, and phasing out small and polluting factories, contributed the most to the co-effect of CO2 emission reduction, whereas NOx presented the highest co-effects, with CO2 among the different air pollutants.

Reduced astrocytic mGluR5 in the hippocampus is associated with stress-induced depressive-like behaviors in mice.

Major depressive disorder (MDD) is one of the most common and disabling mental disorders that characterized by profound disturbances in emotional regulation, motivation, cognition, and the physiology of affected individuals. Although MDD was initially thought to be primarily triggered through neuronal dysfunction, the pathological alterations in astrocytic function have been previously reported in MDD. We report that chronic restraint stress (CRS) induces astrocyte activation and decreases expression of astrocytic mGluR5 in the hippocampal CA1 of susceptible mice exhibited depressive-like behaviors. Reducing expression of astrocytic mGluR5 in dorsal CA1 simulates CRS-induced depressive-like behaviors and impairs excitatory synaptic function in mice, while overexpression of astrocytic mGluR5 in dorsal CA1 rescues CRS-induced depressive-like traits and excitatory synaptic dysfunction. Thus, we provide direct evidence for an important role of astrocytic mGluR5 in producing the behavioral phenotypes of MDD, supporting astrocytic mGluR5 may serve as an effective therapeutic target for MDD.

Increasing astrogenesis in the developing hippocampus induces autistic-like behavior in mice via enhancing inhibitory synaptic transmission.

Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental disorder characterized primarily by impaired social communication and rigid, repetitive, and stereotyped behaviors. Many studies implicate abnormal synapse development and the resultant abnormalities in synaptic excitatory-inhibitory (E/I) balance may underlie many features of the disease, suggesting aberrant neuronal connections and networks are prone to occur in the developing autistic brain. Astrocytes are crucial for synaptic formation and function, and defects in astrocytic activation and function during a critical developmental period may also contribute to the pathogenesis of ASD. Here, we report that increasing hippocampal astrogenesis during development induces autistic-like behavior in mice and a concurrent decreased E/I ratio in the hippocampus that results from enhanced GABAergic transmission in CA1 pyramidal neurons. Suppressing the aberrantly elevated GABAergic synaptic transmission in hippocampal CA1 area rescues autistic-like behavior and restores the E/I balance. Thus, we provide direct evidence for a developmental role of astrocytes in driving the behavioral phenotypes of ASD, and our results support that targeting the altered GABAergic neurotransmission may represent a promising therapeutic strategy for ASD.