Investigates luminescence signatures in Ga2O3, suggesting links between defect disorder and emission.
Ion implantation in β-Ga 2 O 3 modifies the near-surface region, where disorder accumulation can drive local β↔γ polymorphic transformation, yet the mechanistic link between this structural transition and the resulting luminescence signatures remains unresolved. Here, Bi + implantation is employed as an isovalent, radiatively inactive disorder tracer to decouple lattice disorder from dopant-related recombination and isolate the role of Ga-sublattice disruption in luminescence evolution. High-fluence implantation generates a near-surface β/γ mixed layer, evidenced by channeling disorder and γ-related diffraction features, while Bi is incorporated predominantly as Bi 3+ , confirming negligible formation of Bi-related emission centers. Depth-resolved cathodoluminescence reveals a pronounced ∼2.0 eV orange luminescence (OL) band whose intensity tracks the implantation damage profile and coincides with suppression of the intrinsic self-trapped-hole (STH) UV emission. The OL band is attributed to recombination via implantation-induced deep acceptors, where migrating STHs are captured by Ga-vacancy complexes stabilized within γ-like environments. Annealing drives γ→β reordering, restores dominant STH emission and strongly suppresses the OL band, although residual intensity indicates persistent vacancy complexes. These results establish a strong correlation between β↔γ transition disorder and defect-mediated luminescence in β-Ga 2 O 3 .
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Matar et al. (2026) studied this question.
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