RESUMEN
It is important to investigate the responses of greenhouse gases to climate change (temperature, precipitation) and anthropogenic factors in plateau wetland. Based on the DNDC model, we used meteorological, soil, and land cover data to simulate the soil CO2 emission pattern and its responses to climate change and anthropogenic factors in Guizhou, China. The results showed that the mean soil CO2 emission flux in the Caohai Karst Plateau Wetland was 5.89 ± 0.17 t·C·ha-1·yr-1 from 2000 to 2019, and the annual variation showed an increasing trend with the rate of 23.02 kg·C·ha-1·yr-1. The soil total annual mean CO2 emissions were 70.62 ± 2.04 Gg·C·yr-1 (annual growth rate was 0.28 Gg·C·yr-1). Caohai wetland has great spatial heterogeneity. The emissions around Caohai Lake were high (the areas with high, middle, and low values accounted for 3.07%, 70.96%, and 25.97%, respectively), and the emission pattern was characterized by a decrease in radiation from Caohai Lake to the periphery. In addition, the cropland and forest areas exhibited high intensities (7.21 ± 0.15 t·C·ha-1·yr-1 and 6.73 ± 0.58 t·C·ha-1·yr-1, respectively) and high total emissions (54.97 ± 1.16 Gg·C·yr-1 and 10.24 ± 0.88 Gg·C·yr-1, respectively). Croplands and forests were the major land cover types controlling soil CO2 emissions in the Caohai wetland, while anthropogenic factors (cultivation) significantly increased soil CO2 emissions. Results showed that the soil CO2 emissions were positively correlated with temperature and precipitation; and the temperature change had a greater impact on soil respiration than the change in precipitation. Our results indicated that future climate change (increased temperature and precipitation) may promote an increase in soil CO2 emissions in karst plateau wetlands, and reasonable control measures (e.g. returning cropland to lakes and reducing anthropogenic factors) are the keys to controlling CO2 emissions.
RESUMEN
Galantamine, a drug for Alzheimer's disease, is a novel cholinergic agent with a dual mode of action, which inhibits acetylcholinesterase and allosterically modulates nicotinic acetylcholine receptors (nAChRs), as a result stimulates catecholamine neurotransmission. In the present study, we investigated whether galantamine exerts cognitive improving effects through the allosteric modulation of nAChR in the intracerebroventricular beta amyloid (Abeta)(25-35)-injected animal model of Alzheimer's disease. Galantamine (3 mg/kg p.o.) significantly increased the extracellular dopamine release in the hippocampus of saline- and Abeta(25-35)-injected mice. The effects of nicotine on the extracellular dopamine release were potentiated by galantamine, but antagonized by mecamylamine, a nAChR antagonist. Abeta(25-35)-injected mice, compared with saline-injected mice, could not discriminate between new and familiar objects in the novel object recognition test and exhibited less freezing response in the fear-conditioning tasks, suggesting Abeta(25-35) induced cognitive impairment. Galantamine improved the Abeta(25-35)-induced cognitive impairment in the novel object recognition and fear-conditioning tasks. These improving effects of galantamine were blocked by the treatment with mecamylamine, SCH-23390, a dopamine-D1 receptor antagonist, and sulpiride, a dopamine-D2 receptor antagonist, but not by scopolamine, a muscarinic acetylcholine receptor antagonist. This study provides the first in vivo evidence that galantamine augments dopaminergic neurotransmission within the hippocampus through the allosteric potentiation of nAChRs. The improving-effects of galantamine on the Abeta(25-35)-induced cognitive impairment may be mediated through the activation of, at least in part, dopaminergic systems, and the enhancement of dopamine release may be one of multiple mechanisms underlying the therapeutic benefit of galantamine.
