ON and OFF pathways separately relay increment and decrement luminance signals from retinal bipolar cells to cortex. ON-OFF retinal ganglion cells (RGCs) are activated via synaptic inputs onto bistratified dendrites localized in the ON and OFF regions of the inner plexiform layer. Postnatal maturational processes convert bistratifying ON-OFF RGCs to monostratifying ON and OFF RGCs. Although visual deprivation influences refinement of higher visual centers, no previous studies suggest that light regulates either the development of the visual-evoked signaling in retinal ON and OFF pathways, nor pruning of bistratified RGC dendrites. We find that dark rearing blocks both the maturational loss of ON-OFF responsive RGCs and the pruning of dendrites. Thus, in retina, there is a previously unrecognized, pathway-specific maturation that is profoundly affected by visual deprivation.

Synucleins are a vertebrate-specific family of abundant neuronal proteins. They comprise three closely related members, α-, β-, and γ-synuclein. α-Synuclein has been the focus of intense attention since mutations in it were identified as a cause for familial Parkinson's disease. Despite their disease relevance, the normal physiological function of synucleins has remained elusive. To address this, we generated and characterized αβγ-synuclein knockout mice, which lack all members of this protein family. Deletion of synucleins causes alterations in synaptic structure and transmission, age-dependent neuronal dysfunction, as well as diminished survival. Abrogation of synuclein expression decreased excitatory synapse size by ∼30% both in vivo and in vitro, revealing that synucleins are important determinants of presynaptic terminal size. Young synuclein null mice show improved basic transmission, whereas older mice show a pronounced decrement. The late onset phenotypes in synuclein null mice were not due to a loss of synapses or neurons but rather reflect specific changes in synaptic protein composition and axonal structure. Our results demonstrate that synucleins contribute importantly to the long-term operation of the nervous system and that alterations in their physiological function could contribute to the development of Parkinson's disease.neurodegeneration | loss-of-function | Lewy bodies | ultrastructure | retina S ynucleins are a family of vertebrate-specific proteins with three closely related members, α-, β-, and γ-synuclein (1, 2). They are abundant neuronal proteins and are reported to account for 0.1% of total brain protein (3, 4). Synucleins have overlapping expression patterns and are enriched in presynaptic termini (5, 6). α-Synuclein has been the focus of intense attention since the identification of dominant mutations and gene multiplications that link it to familial Parkinson's disease (PD) (7). Recently, strong ties between the α-synuclein gene and sporadic PD have emerged in genomewide association studies, making α-synuclein the most broadly relevant PD gene (8, 9). Additionally, α-synuclein is the major component of Lewy bodies, the pathological hallmark of PD (10). The presynaptic localization and function of synucleins may also have a bearing on PD, as synapses are lost early in disease progression (11).Analysis of α-, β-, and γ-synuclein sequences reveals a shared, highly conserved N-terminal domain (∼80% identical) with a less conserved acidic C terminus (2). The N-terminal domain has seven imperfect repeats of 11 residues with the consensus sequence XKTKEGVXXXX that binds acidic phospholipid surfaces. Upon lipid binding, synucleins undergo a dramatic change to an α-helical conformation (12-14). α-Synuclein adopts either a conformation consisting of two anti-parallel, amphipathic α-helices with an unfolded C terminus (13-15) or a single extended α-helical structure (16, 17). Human β-and γ-synuclein also adopt the two-helix conformation upon folding (18,19). Together, the high sequence homolog...

SUMMARY Complex neural circuits in the mammalian brain develop through a combination of genetic instruction and activity-dependent refinement. The relative role of these factors and the form of neuronal activity responsible for circuit development is a matter of significant debate. In the mammalian visual system, retinal ganglion cell projections to the brain are mapped with respect to retinotopic location and eye of origin. We manipulated the pattern of spontaneous retinal waves present during development without changing overall activity levels through the transgenic expression of β2-nicotinic acetylcholine receptors in retinal ganglion cells of mice. We used this manipulation to demonstrate that spontaneous retinal activity is not just permissive, but instructive in the emergence of eye-specific segregation and retinotopic refinement in the mouse visual system. This suggests that specific patterns of spontaneous activity throughout the developing brain are essential in the emergence of specific and distinct patterns of neuronal connectivity.

Vesicular transporters regulate the amount and type of neurotransmitter sequestered into synaptic vesicles and, hence, the kind of signal transmitted to postsynaptic neurons. Glutamate is the prominent excitatory neurotransmitter in retina; GABA and glycine are the main inhibitory neurotransmitters. Little is known about the ontogeny of vesicular neurotransmission in retina. We investigated expression of glutamatergic [vesicular glutamate transporter 1 (VGLUT1)] and GABA/glycinergic [vesicular GABA/glycine transporter (VGAT)] vesicular transporters in postnatal retina. VGLUT1 labels glutamatergic synapses. VGLUT1 and synaptic vesicle 2 colocalized to photoreceptor terminals. VGLUT1 colocalized with PKC to rod bipolar terminals and to ON bipolar terminals in metabotropic glutamate receptor 6+/- mice. Developmentally, VGAT expression precedes VGLUT1. In rat and mouse retina, VGAT occurred in the inner retina by postnatal day 1 (P1). In rat retina, VGLUT1 was in the outer retina by P5-P7 and the inner retina by P7. In the mouse retina, VGLUT1 expression was in the outer retina by P3 and the inner retina by P5. Both rat and mouse retina had an adult pattern of VGLUT1 expression by P14. VGLUT1 expression precedes ribbon synapses, which are first observed in the inner retina at P11 (Fisher, 1979) in mouse and P13 (Horsburgh and Sefton, 1987) in rat. The ribbon synapse marker RIBEYE was not detected in inner retina of P5 or P7 rat. Spontaneous EPSCs in mouse ganglion cells were recorded as early as P7. Together, these findings indicate that vesicular GABA and glycine transmission precedes vesicular glutamate transmission in developing rodent retina. Furthermore, vesicular glutamate transmission likely occurs before ribbon synapse formation in the inner retina.

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CeO2/g-C3N4 n–n type heterojunction was successfully constructed via a facile in situ co-pyrolysis route by employing Ce(IO3)3 and melamine as precursors. It exhibits high photo-induced oxidation and reduction properties for degradation of phenol, NO removal and hydrogen evolution.

Solar‐driven conversion of CO2 into high value‐added fuels is expected to be an environmental‐friendly and sustainable approach for relieving the greenhouse gas effect and countering energy crisis. Metal sulfide semiconductors with wide photoresponsive range and favorable band structures are suitable photocatalysts for CO2 photoreduction. This review summarizes the recent progress on metal sulfide semiconductors for photocatalytic CO2 reduction. First, the fundamentals, mechanisms and some principles, like product selectivity, of photocatalytic CO2 reduction are introduced. Then, according to the elemental composition, the metal sulfide photocatalysts applied for CO2 reduction are classified into binary (CdS, ZnS, MoS2, SnS2, Bi2S3, In2S3,Cu2S, NiS/NiS2, and CoS2), ternary (ZnIn2S4, CdIn2S4, CuInS2, Cu3SnS4, and CuGaS2), and quaternary (Cu2ZnSnS4) systems, in which their crystal structures, photochemical characteristics, and photocatalytic CO2 reduction applications are systematically demonstrated. Especially, the diverse modification strategies for improving the activity and product selectivity of photocatalytic CO2 reduction on these metal sulfides are summarized. Finally, the current challenges and future directions for the development of metal sulfide photocatalysts for CO2 reduction are proposed. This review is expected to serve as a powerful reference for exploiting high‐efficiency metal sulfide photocatalysts for CO2 conversion and furthering related mechanism understanding.

Utilizing mechanical energy to produce hydrogen is emerging as a promising way to generate renewable energy, but is challenged by low efficiency and scanty cognition. In this work, graphitic carbon nitride (g‐C3N4) with an atomically thin sheet‐like structure is applied for prominent piezocatalytic and photo‐enhanced piezocatalytic H2 production. It is revealed that the anomalous piezoelectricity in g‐C3N4 originates from the strong in‐plane polarization along the a‐axis, contributed by the superimposed polar tri‐s‐triazine units and flexoelectric effect derived from the structured triangular cavities, which provides powerful electrochemical driving force for the water reduction reaction. Furthermore, the photo‐enhanced charge transfer enables g‐C3N4 nanosheets to reserve more energized polarization charges to fully participate in the reaction at the surface reactive sites enriched by strain‐induced carbon vacancies. Without any cocatalysts, an exceptional photo‐piezocatalytic H2 evolution rate of 12.16 mmol g−1 h−1 is delivered by the g‐C3N4 nanosheets, far exceeding that of previously reported piezocatalysts and g‐C3N4 photocatalysts. Further, high pure‐water‐splitting performance with production of the value‐added oxidation product H2O2 via photo‐piezocatalysis is also disclosed. This work not only exposes the potential of g‐C3N4 as a piezo‐semiconductor for catalytic H2 evolution, but also breaks a new ground for the conversion of solar and mechanical energy by photomediated piezocatalytic reaction.