Electrically driven compact hybrid lithium niobate microring laser

We demonstrate an electrically driven compact hybrid lithium niobate microring laser by butt coupling a commercial 980-nm pump laser diode chip with a high quality Er3+-doped lithium niobate microring chip. Single mode lasing emission at 1531 nm wavelength from the Er3+-doped lithium niobate microring can be observed with the integrated 980-nm laser pumping. The compact hybrid lithium niobate microring laser occupies the chip size of 3 mmx4mmx0.5 mm. The threshold pumping laser power is 6 mW and the threshold current is 0.5 A (operating voltage 1.64 V) in the atmospheric temperature. The spectrum featuring single mode lasing with small linewidth of 0.05 nm is observed. This work explores a robust hybrid lithium niobate microring laser source which has potential applications in coherent optical communication and precision metrology.Comment: 4 pages, 4 figure

OsbZIP18, a Positive Regulator of Serotonin Biosynthesis, Negatively Controls the UV-B Tolerance in Rice

Serotonin (5-hydroxytryptamine) plays an important role in many developmental processes and biotic/abiotic stress responses in plants. Although serotonin biosynthetic pathways in plants have been uncovered, knowledge of the mechanisms of serotonin accumulation is still limited, and no regulators have been identified to date. Here, we identified the basic leucine zipper transcription factor OsbZIP18 as a positive regulator of serotonin biosynthesis in rice. Overexpression of OsbZIP18 strongly induced the levels of serotonin and its early precursors (tryptophan and tryptamine), resulting in stunted growth and dark-brown phenotypes. A function analysis showed that OsbZIP18 activated serotonin biosynthesis genes (including tryptophan decarboxylase 1 (OsTDC1), tryptophan decarboxylase 3 (OsTDC3), and tryptamine 5-hydroxylase (OsT5H)) by directly binding to the ACE-containing or G-box cis-elements in their promoters. Furthermore, we demonstrated that OsbZIP18 is induced by UV-B stress, and experiments using UV-B radiation showed that transgenic plants overexpressing OsbZIP18 exhibited UV-B stress-sensitive phenotypes. Besides, exogenous serotonin significantly exacerbates UV-B stress of OsbZIP18_OE plants, suggesting that the excessive accumulation of serotonin may be responsible for the sensitivity of OsbZIP18_OE plants to UV-B stress. Overall, we identified a positive regulator of serotonin biosynthesis and demonstrated that UV-B-stress induced serotonin accumulation, partly in an OsbZIP18-dependent manner

Mechanisms Of Cannabinoid Cb 2 Receptor-Mediated Reduction Of Dopamine Neuronal Excitability In Mouse Ventral Tegmental Area

Background: We have recently reported that activation of cannabinoid type 2 receptors (CB 2 Rs)reduces dopamine (DA)neuron excitability in mouse ventral tegmental area (VTA). Here, we elucidate the underlying mechanisms. Methods: Patch-clamp recordings were performed in mouse VTA slices and dissociated single VTA DA neurons. Findings: Using cell-attached recording in VTA slices, bath-application of CB 2 R agonists (JWH133 or five other CB 2 R agonists)significantly reduced VTA DA neuron action potential (AP)firing rate. Under the patch-clamp whole-cell recording model, JWH133 (10 μM)mildly reduced the frequency of miniature excitatory postsynaptic currents (mEPSCs)but not miniature inhibitory postsynaptic currents (mIPSCs). JWH133 also did not alter evoked EPSCs or IPSCs. In freshly dissociated VTA DA neurons, JWH133 reduced AP firing rate, delayed AP initiation and enhanced AP after-hyperpolarization. In voltage-clamp recordings, JWH133 (1 μM)enhanced M-type K + currents and this effect was absent in CB 2−/− mice and abolished by co-administration of a selective CB 2 R antagonist (10 μM, AM630). CB 2 R-mediated inhibition in VTA DA neuron firing can be mimicked by M-current opener (10 μM retigabine)and blocked by M-current blocker (30 μM XE991). In addition, enhancement of neuronal cAMP by forskolin (10 μM)reduced M-current and increased DA neuron firing rate. Finally, pharmacological block of synaptic transmission by NBQX (10 μM), D-APV (50 μM)and picrotoxin (100 μM)in VTA slices failed to prevent CB 2 R-mediated inhibition, while intracellular infusion of guanosine 5\u27-O-2-thiodiphosphate (600 μM, GDP-β-S)through recording electrode to block postsynaptic G-protein function prevented JWH133-induced reduction in AP firing. Interpretation: Our results suggest that CB 2 Rs modulate VTA DA neuron excitability mainly through an intrinsic mechanism, including a CB 2 R-mediated reduction of intracellular cAMP, and in turn enhancement of M-type K + currents. Fund: This research was supported by the Barrow Neuroscience Foundation, the BNI-BMS Seed Fund, and CNSF (81771437)