Test of the thermal equilibration model for persistent photoconductivity in doping-modulated amorphous silicon.
The persistent photoconductivity effect in doping modulated amorphous silicon is compared to the light-induced conductivity changes in compensated amorphous silicon. The recent proposal that the defect structure of doped amorphous silicon is in metastable thermal equilibrium is able to account for the metastable excess conductivity in both systems, and for the several orders of magnitude difference in exposure times needed.
Power-law dependence of persistent photoconductivity on exposure time in compensated a-Si : H
Abstract The exposure time dependence of the persistent photoconductivity (PPC) in compensated films of hydrogenated amorphous silicon ( a -Si : H) has been investigated as a function of illumination temperature. It is found that the conductivity in the PPC state follows a power-law dependence on the exposure time when the Fermi level of the sample lies in the conduction band tails. The power-law exponent is inversely proportional to the illumination temperature, which is well predicted by a simple theory based on Staebler-Wronski defect creation. These results are compared with the predictions of the thermal-equilibration model.
Effects of dopants and defects on light-induced metastable states in a-Si:H.
Using photothermal deflection spectroscopy we measure the gap-state optical absorption of light-induced metastable defects in undoped, singly-doped, and compensated a-Si:H. We observe an enhancement in the gap-state absorption after illumination which is shown to be due to the creation of new silicon dangling-bond defects and not to a shift in the Fermi level. For singly-doped material, the number of light-induced defects scales with dopant concentration, while full compensation (counter doping) drastically minimizes the density of these defects. The results provide evidence that the doping level influences the light-induced defect formation mechanism, and imply that simply breaking Si--Si bonds may not be the primary mechanism.