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The development of photocatalysts must be meticulous, especially when they are designed to degrade hazardous dyes that cause mutagenesis and carcinogenesis. In this meticulous approach, Ni-based metal–organic frameworks with different ligands, including terephthalic acid (NTP), 2-aminoterephthalic acid (NATP), and their composite with g-C3N4 (NTP/GCN, and NATP/GCN) have been synthesized using hydrothermal method. Structural analysis by XRD and ATR-IR revealed synergistic properties due to robust chemical interactions between the NATP-MOFs and GCN systems. A flower-like morphology was observed for both NTP and NATP, while their composites showed mixed-particulate structures mimicking the morphology of GCN. Optical analyses indicated visible-light driven properties with modulated recombination resistance in the system. Among the synthesized bare and composite systems, NATP/GCN exhibited the highest photocatalytic degradation efficiency for the cationic rhodamine B dye (~ 93% in 120 min), while it was relatively less efficient for the anionic Congo red dye, (~ 64% in 120 min). The insights gained from the fundamental characterizations including Mott–Schottky, scavenger, and electrochemical impedance analysis revealed that the amino-groups in NATP/GCN composite offered the band edge potentials suitable for the effective generation of energetic radical species with the improved carrier delocalization, recombination resistance, and charge transfer properties in the composite system through Z-scheme formation. Parametric investigations by varying the concentration of catalyst, dye, and pH along with recycle studies, demonstrated the excellent stability of the developed composites for sustainable photocatalytic applications. [ABSTRACT FROM AUTHOR]

Ca2+ entry into nigrostriatal dopamine (DA) neurons and axons via L‐type voltage‐gated Ca2+ channels (LTCCs) contributes, respectively, to pacemaker activity and DA release and has long been thought to contribute to vulnerability to degeneration in Parkinson's disease. LTCC function is greater in DA axons and neurons from substantia nigra pars compacta than from ventral tegmental area, but this is not explained by channel expression level. We tested the hypothesis that LTCC control of DA release is governed rather by local mechanisms, focussing on candidate biological factors known to operate differently between types of DA neurons and/or be associated with their differing vulnerability to parkinsonism, including biological sex, α‐synuclein, DA transporters (DATs) and calbindin‐D28k (Calb1). We detected evoked DA release ex vivo in mouse striatal slices using fast‐scan cyclic voltammetry and assessed LTCC support of DA release by detecting the inhibition of DA release by the LTCC inhibitors isradipine or CP8. Using genetic knockouts or pharmacological manipulations, we identified that striatal LTCC support of DA release depended on multiple intersecting factors, in a regionally and sexually divergent manner. LTCC function was promoted by factors associated with Parkinsonian risk, including male sex, α‐synuclein, DAT and a dorsolateral co‐ordinate, but limited by factors associated with protection, that is, female sex, glucocerebrosidase activity, Calb1 and ventromedial co‐ordinate. Together, these data show that LTCC function in DA axons and isradipine effect are locally governed and suggest they vary in a manner that in turn might impact on, or reflect, the cellular stress that leads to parkinsonian degeneration. [ABSTRACT FROM AUTHOR]

We characterize a new experimental model for inducing retinal ganglion cell (RGC) dysfunction and degeneration in mice. C57BL/6J mice were subjected to two acute periods of intraocular pressure (IOP) elevation (50 mmHg for 30 min) by cannulation of the anterior chamber. We used full-field electroretinography and visual evoked potentials (VEPs) to measure subsequent changes in retina and optic nerve function, and histochemical techniques to assess RGC survival and optic nerve structure. In 12 month old mice, a single IOP challenge caused loss and subsequent recovery of RGC function over the following 28 days with minimal cell death and no observed axonal damage. A second identical IOP challenge resulted in persistent RGC dysfunction and significant (36%) loss of RGC somas. This was accompanied by a 16.7% delay in the latency and a 27.6% decrease in the amplitude of the VEP. Severe axonal damage was seen histologically with enlargement of axons, myelin disruption, reduced axon density, and the presence of glial scarring. In contrast, younger 3 month old mice when exposed to a single or repeat IOP challenge showed quicker RGC functional recovery after a single challenge and full functional recovery after a repeat challenge with no detectable optic nerve dysfunction. These data demonstrate a highly reproducible and minimally invasive method for inducing RGC degeneration and axonal damage in mice. Resilience of the optic nerve to damage is highly dependent on animal age. The time-defined nature of functional versus structural loss seen in this model stands to facilitate investigation of neuroglial responses in the retina after IOP injury and the associated evaluation of neuroprotective treatment strategies. Further, the model may be used to investigate the impact of aging and the cellular switch between neurorecovery and neurodegeneration. • Repeat intraocular pressure challenge causes axonal degeneration in older mice. • An initial neurorecovery phase is followed by a neurodegeneration phase. • Younger mice are resilient to the effects of a repeat intraocular pressure challenge. • This model may be used to investigate glaucoma pathogenesis and treatment strategies. [ABSTRACT FROM AUTHOR]