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Finding new catalysts and improving the characteristics of existing catalysts are major research issues for boosting dye degradation efficiency. For this purpose, iron vanadates have been prepared by the solution combustion method using oxalyldihydrazide (ODH) and glycine (GLY) as fuel. The surface properties of catalysts were altered, and the degradation efficiency of methylene blue (MB) was improved, depending on the synthesis process and fuel type. When the ODH-assisted FeVO4 has irregular morphology, the GLY-assisted FeVO4 has 100–200-nm uniform nanoparticles with a surface area of 21.96 g/m2 and it is performed as an excellent heterogeneous nanocatalyst for Fenton-like degradation of MB using H2O2 under sunlight. The narrow bandgap allows the adsorption of light and enhances photocatalytic activity. After the optimization of the catalyst amount, H2O2 concentration, and degradation time, the degradation efficiency of MB was found to be nearly 100% with high reusability. The process has a high-rate constant of 0.0304 min−1 and the possible reaction mechanism has been proposed using GC–MS. The GLY-assisted FeVO4 can be a potentially powerful and reusable heterogeneous catalyst for the other contaminants.

Recent studies suggest that stimulus-evoked and spontaneous neurotransmitter release processes are mechanistically distinct. Here we targeted the non-canonical synaptic vesicle SNAREs Vps10p-tail-interactor-1a (vti1a) and vesicle-associated membrane protein 7 (VAMP7) to specifically inhibit spontaneous release events and probe whether these events signal independently of evoked release to the postsynaptic neuron. We found that loss of vti1a and VAMP7 impairs spontaneous high-frequency glutamate release and augments unitary event amplitudes by reducing postsynaptic eukaryotic elongation factor 2 kinase (eEF2K) activity subsequent to the reduction in N-methyl-D-aspartate receptor (NMDAR) activity. Presynaptic, but not postsynaptic, loss of vti1a and VAMP7 occludes NMDAR antagonist-induced synaptic potentiation in an intact circuit, confirming the role of these vesicular SNAREs in setting synaptic strength. Collectively, these results demonstrate that spontaneous neurotransmission signals independently of stimulus-evoked release and highlight its role as a key regulator of postsynaptic efficacy., Emerging evidence suggests that spontaneous neurotransmitter release contributes to the maintenance of synaptic efficacy. Here the authors selectively reduce spontaneous glutamatergic transmission while leaving the stimulus-evoked responses intact and show that this leads to homeostatic scaling at the postsynaptic side in cultured neurons and alters synaptic plasticity in acute brain slices.

Fast synaptic communication in the brain requires synchronous vesicle fusion that is evoked by action potential-induced Ca(2+) influx. However, synaptic terminals also release neurotransmitters by spontaneous vesicle fusion, which is independent of presynaptic action potentials. A functional role for spontaneous neurotransmitter release events in the regulation of synaptic plasticity and homeostasis, as well as the regulation of certain behaviours, has been reported. In addition, there is evidence that the presynaptic mechanisms underlying spontaneous release of neurotransmitters and their postsynaptic targets are segregated from those of evoked neurotransmission. These findings challenge current assumptions about neuronal signalling and neurotransmission, as they indicate that spontaneous neurotransmission has an autonomous role in interneuronal communication that is distinct from that of evoked release.

Synaptic communication in the nervous system is initiated by the fusion of synaptic vesicles with the presynaptic plasma membrane and subsequent neurotransmitter release. In the 1980s, this process was characterized by electron microscopy, albeit without the ability to follow processes in living cells. In the last two decades, fluorescence imaging methods have been developed that report synaptic vesicle fusion, endocytosis and recycling. These probes have provided unprecedented insight into synaptic vesicle trafficking in individual synaptic terminals and revealed heterogeneity in recycling pathways as well as synaptic vesicle populations. These methods either take advantage of uptake of fluorescent probes into recycling vesicles or exogenous expression of synaptic vesicle proteins tagged with a pH-sensitive fluorescent marker at regions facing the vesicle lumen. We provide an overview of these methods, with particular emphasis on the challenges associated with their use and the opportunities for future investigations.

Methyl-CpG-binding protein 2 (MeCP2) is a transcriptional regulator of gene expression that is an important epigenetic factor in the maintenance and development of the central nervous system. The neurodevelopmental disorders Rett syndrome and MECP2 duplication syndrome arise from loss-of-function and gain-of-function alterations in MeCP2 expression, respectively. Several animal models have been developed to recapitulate the symptoms of Rett syndrome and MECP2 duplication syndrome. Cell morphology, neurotransmission, and cellular processes that support learning and memory are compromised as a result of MeCP2 loss- or gain-of-function. Interestingly, loss-of-MeCP2 function and MeCP2 overexpression trigger diametrically opposite changes in synaptic transmission. These findings indicate that the precise regulation of MeCP2 expression is a key requirement for the maintenance of synaptic and neuronal homeostasis and underscore its importance in central nervous system function. This review highlights the functional role of MeCP2 in the brain as a regulator of synaptic and neuronal plasticity as well as its etiological role in the development of Rett syndrome and MECP2 duplication syndrome.

Clinical studies consistently demonstrate that a single sub-psychomimetic dose of ketamine, an ionotropic glutamatergic NMDAR (N-methyl-D-aspartate receptor) antagonist, produces fast-acting antidepressant responses in patients suffering from major depressive disorder, although the underlying mechanism is unclear. Depressed patients report the alleviation of major depressive disorder symptoms within two hours of a single, low-dose intravenous infusion of ketamine, with effects lasting up to two weeks, unlike traditional antidepressants (serotonin re-uptake inhibitors), which take weeks to reach efficacy. This delay is a major drawback to current therapies for major depressive disorder and faster-acting antidepressants are needed, particularly for suicide-risk patients. The ability of ketamine to produce rapidly acting, long-lasting antidepressant responses in depressed patients provides a unique opportunity to investigate underlying cellular mechanisms. Here we show that ketamine and other NMDAR antagonists produce fast-acting behavioural antidepressant-like effects in mouse models, and that these effects depend on the rapid synthesis of brain-derived neurotrophic factor. We find that the ketamine-mediated blockade of NMDAR at rest deactivates eukaryotic elongation factor 2 (eEF2) kinase (also called CaMKIII), resulting in reduced eEF2 phosphorylation and de-suppression of translation of brain-derived neurotrophic factor. Furthermore, we find that inhibitors of eEF2 kinase induce fast-acting behavioural antidepressant-like effects. Our findings indicate that the regulation of protein synthesis by spontaneous neurotransmission may serve as a viable therapeutic target for the development of fast-acting antidepressants.

Exposure to abnormal light–dark cycles causes depression-like behaviour and learning deficits in mice. The defects seem to occur independently of disturbances to sleep and other processes regulated by the biological clock. See Letter p.594 Disruption of the body's circadian clock by exposure to irregular light cycles can affect sleep–wake patterns and cause sleep deprivation, both of which are often associated with mood alterations and cognitive disruptions. This study in mice shows that irregular light schedules can directly affect mood and cognitive function, independent of sleep and circadian rhythms. The aberrant light effects are dependent on melanopsin-containing retinal ganglion cells, and administration of antidepressant drugs restores learning ability, suggesting that the depressive effect precedes learning impairment.

A recent study proposes that the random and spontaneous, NMDA receptor–dependent miniature postsynaptic currents at hippocampal synapses serve to regulate local postsynaptic protein synthesis, thereby stabilizing synaptic function.