Mice Lacking NMDA Receptors in Parvalbumin Neurons Display Normal Depression-Related Behavior and Response to Antidepressant Action of NMDAR Antagonists

The underlying circuit imbalance in major depression remains unknown and current therapies remain inadequate for a large group of patients. Discovery of the rapid antidepressant effects of ketamine - an NMDA receptor (NMDAR) antagonist – has linked the glutamatergic system to depression. Interestingly, dysfunction in the inhibitory GABAergic system has also been proposed to underlie depression and deficits linked to GABAergic neurons have been found with human imaging and in post-mortem material from depressed patients. Parvalbumin-expressing (PV) GABAergic interneurons regulate local circuit function through perisomatic inhibition and their activity is NMDAR-dependent, providing a possible link between NMDAR and the inhibitory system in the antidepressant effect of ketamine. We have therefore investigated the role of the NMDAR-dependent activity of PV interneurons for the development of depression-like behavior as well as for the response to rapid antidepressant effects of NMDAR antagonists. We used mutant mice lacking NMDA neurotransmission specifically in PV neurons (PV-Cre+/NR1f/f) and analyzed depression-like behavior and anhedonia. To study the acute and sustained effects of a single NMDAR antagonist administration, we established a behavioral paradigm of repeated exposure to forced swimming test (FST). We did not observe altered behavioral responses in the repeated FST or in a sucrose preference test in mutant mice. In addition, the behavioral response to administration of NMDAR antagonists was not significantly altered in mutant PV-Cre+/NR1f/f mice. Our results show that NMDA-dependent neurotransmission in PV neurons is not necessary to regulate depression-like behaviors, and in addition that NMDARs on PV neurons are not a direct target for the NMDAR-induced antidepressant effects of ketamine and MK801

Gas entrapment and microbial N2O reduction reduce N2O emissions from a biochar-amended sandy clay loam soil

Nitrous oxide (N(2)O) is a potent greenhouse gas that is produced during microbial nitrogen transformation processes such as nitrification and denitrification. Soils represent the largest sources of N(2)O emissions with nitrogen fertilizer application being the main driver of rising atmospheric N(2)O concentrations. Soil biochar amendment has been proposed as a promising tool to mitigate N(2)O emissions from soils. However, the underlying processes that cause N(2)O emission suppression in biochar-amended soils are still poorly understood. We set up microcosm experiments with fertilized, wet soil in which we used (15)N tracing techniques and quantitative polymerase chain reaction (qPCR) to investigate the impact of biochar on mineral and gaseous nitrogen dynamics and denitrification-specific functional marker gene abundance and expression. In accordance with previous studies our results showed that biochar addition can lead to a significant decrease in N(2)O emissions. Furthermore, we determined significantly higher quantities of soil-entrapped N(2)O and N(2) in biochar microcosms and a biochar-induced increase in typical and atypical nosZ transcript copy numbers. Our findings suggest that biochar-induced N(2)O emission mitigation is based on the entrapment of N(2)O in water-saturated pores of the soil matrix and concurrent stimulation of microbial N(2)O reduction resulting in an overall decrease of the N(2)O/(N(2)O + N(2)) ratio