We report the demonstration of CW lasing at room temperature in a GaN-based vertical-cavity surface-emitting laser (VCSEL) by current injection. The active region of the VCSEL consisted of a two-pair InGaN/GaN quantum well active layer. The optical cavity consisted of a 7-λ-thick GaN semiconductor layer and an indium tin oxide layer for p-contact embedded between two SiO2/Nb2O5 dielectric distributed Bragg reflectors. The VCSEL was mounted on a Si substrate by wafer bonding and the sapphire substrate was removed by laser lift-off. Under CW operation for an 8-µm aperture device, the threshold current was 7.0 mA and the emission wavelength was approximately 414 nm.

We realized room-temperature lasing of blue and green GaN-based vertical-cavity surface-emitting lasers (VCSELs), for the first time, by current injection. The blue GaN-based VCSEL had a threshold current of 1.5 mA and a threshold voltage of 3.3 V under continuous-wave operation. Its maximum output power was 0.70 mW and its laser emission wavelength was 451 nm. The green GaN-based VCSEL had a threshold current of 22 mA and a threshold voltage of 6.3 V under pulsed current operation. Its maximum output power was estimated to be over 0.80 mW and the laser emission wavelength was 503 nm.

We compared the lasing characteristics of GaN-based vertical-cavity surface-emitting lasers (VCSELs) fabricated using a GaN substrate with those fabricated using a sapphire substrate. The original substrates are removed from the devices after the devices have been bonded to Si substrates. Consequently, with the exception of the cavity length, the two kinds of fabricated VCSELs have almost the same structures. The VCSELs fabricated using a GaN substrate have a higher maximum output power (0.62 mW) and longer lifetimes than those fabricated using a sapphire substrate. Even for the VCSELs fabricated with a GaN substrate, 10-min operation causes their threshold current to increase.

GD3 is an intracellular mediator of apoptotic signaling. Although GD3 is known to directly act on mitochondria, the dynamic responses of individual mitochondria to GD3 remain to be elucidated. In the current study, the membrane potential of single mitochondria is observed in the presence of GD3 or its analogues. Here, we report that (1) GD3 specifically induces gradual depolarizations of the inner membrane by a mechanism that differs from the permeability transition, and (2) the GD3-induced depolarizations are suppressed by cyclosporin A. These results suggest that GD3 depolarizes mitochondria by a mechanism distinct from but relevant to the permeability transition.