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Antisite defects in plastically-deformed GaAs: An alternative analysis
Solid State Communications, Vol. 60, No. 11, pp. 867-870, 1986. Printed in Great Britain.
0038-1098/86 $3.00 + .00 Pergamon Journals Ltd.
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs: AN ALTERNATIVE ANALYSIS R. Bray* Max-Planck-Institut for Festk6rperforschung, 7000 Stuttgart 80, and Fakult/it fiir Physik, Universit/it Konstanz, 7750 Konstantz 1, FRG
(Received 15 June 1986 by M. Cardona) A revision is presented of the accepted view that the observed increase in electron paramagnetic resonance (EPR) with plastic deformation in GaAs is due to the generation of As antisite defects. It is proposed instead that only compensating deep acceptor defects are generated. The increase of the EPR signal from As antisites can then be attributed to the compensation of the neutral As antisites that were already present in the as-grown GaAs. The nonquenching extrinsic absorption can be attributed to the acceptors. The same analysis suggests that in the case of electron and neutron irradiation, both acceptors and As antisites are generated. These proposals succeed in eliminating some recently imposed complexities in the relationship between As antisites and EL2. INTRODUCTION THIS COMMUNICATION DEALS primarily with the nature of the defects generated in plastically deformed GaAs, and their relevance to the relation between the As antisites and EL2 centers. Our analysis was stimulated by the recent optical absorption and electron paramagnetic resonance (EPR) studies of plastically deformed GaAs by Omling et al. [ 1]. After reviewing their results and conclusions, we present a series of questions which lead to the formulation of an alternative analysis and a very different set of conclusions. The basic contention in [1], is that the defects generated by plastic deformation (PD) are "ASGa-related defects", and that the major portion of these defects is not EL2 related. We agree with the last part of this contention, that most of the defects generated are not EL2 related. But we believe that this is because the defects generated are, in fact, not AsGa-related, but rather, deep acceptors. In our model, these are held directly responsible for the nonquenching optical absorption induced by PD, and indirectly responsible for the observed increase in the EPR signal. Our analysis has important consequences not only for the nature of the defects generated by PD, but also for those generated by fast neutron [2] and electron [3] irradiation. Of particular interest is the application of our proposal to the question of the multiplicity of As6a-related defects, and the continuing controversial relationship between these defects and EL2 centers. * Permanent address: Department of Physics, Purdue University, West Lafayette, IN. 47907, USA.
It is necessary to first review and comment on the nature and identification of EL2. The mid-gap EL2 defects may be identified operationally by their role in various optical quenching or persistence phenomena. From these, it has been deduced that EL2 undergoes an optically-induced metastable transition at low temperature, and a thermal recovery near 130 K, which takes it back to its normal state [4]. It was originally suggested [5] that the EL2 concentration could be measured by the optical absorption (at certain photon energies). The work of [1 ] demonstrates conclusively that EL2 cannot always be measured straightforwardly from the extrinsic absorption. Nor can it be measured simply by the EPR signal, since only compensated EL2 centers which have lost an electron have the appropriate charge and spin state to give the EPR signal [ 6 - 8 ] . The quenchable part of the extrinsic absorption provides perhaps the best measure of the concentration of EL2 defects [1, 9]. Although there has been a long history of controversy over the identity of the EL2 defect, it is generally thought now to be some form of the As antisite AsGa. It is still controversial whether the latter is a point defect or part of one or more complexes, referred to in [1] as "As6a-related defects". In this paper, we shall use the designation "As6a" without regard to the precise form in which it exists. BACKGROUND REVIEW AND A CRITICAL COMMENTARY The study in [1 ] deals with the effects of PD of "undoped" semi-insulating GaAs on the optical absorption and on EPR. It is well-known that PD causes an
867
868
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs
increase in the dislocation density, and also in the point defects and point defect clusters. The basic experimental findings and the related inferences and conclusions of [1] can be summarized as follows: (1) The extrinsic absorption (in the range 0 . 8 1.4eV) is shown to consist of two components, a nonquenchable part which increases strongly with deformation, and a quenchable part which remains constant, and hence is unaffected by PD. The inference is made that the increase in nonquenchable absorption is not related to quenchable EL2, and that the quenchable EL2 concentration is unaffected by PD. (2) The nonquenchable part of the extrinsic absorption is observed to be proportional to the increase in the EPR signal. Since the latter is generally taken as a signature of AsGa-containing defects, it is therefore inferred that the increase of the EPR signal reflects an increase in ASGa-containing defects produced during PD, and that these defects are responsible for the increase in the nonquenchable absorption. (3) The PD-induced defects, presumed to be ASGarelated, are found to anneal at T ~ 650°C; this is in contrast with the ASGa-related defects in as-grown "undoped" GaAs, which are stable at least up to 950°C. From the existence of these different annealing temperatures it is inferred that there is a family of AsGacontaining defects. It is suggested that perhaps only a select portion of them (perhaps only the ones that are stable to very high temperatures, >950°C) are responsible for the EL2 level. We agree with the inferences in (1) above, but take issue with those in (2) and (3), where several aspects of the analysis are disturbing: (I) We question how the generation of ASGa defects by PD can increase the EPR signal. If only ASGa defects are being generated, one would expect them to be neutral. How can they acquire the appropriate charge state and spin to give EPR signals? In as-grown "undoped" GaAs, the EPR signal is obtained only for the ASGa defects which have become positively-charged through compensation by the residual shallow acceptors [6, 7]. Since the latter are already fully compensated before PD of the as-grown semi-insulating material, they are not available to provide a similar service for the additional PD-generated ASGa defects. This argument implies that any generation of AsGa-containing defects which show up in the EPR measurements must be accompanied by the generation of corresponding, compensating acceptor defects (which may have their own signature !). (2) No account is taken in [1] of the fact that the PD-induced EPR signal undergoes substantial opticallyinduced quenching. That this indeed happens is a central
V~. 60, No. 11
point in earlier EPR studies of plastically deformed GaAs [10]. We question how nonquenchable absorption can be associated, and be compatible, with quenchable EPR for the same ASGa defect, as is implicit in [ 1]. (3) It was inferred that in a family of different As6a-Containing defects (identified by the same EPR signature) some members are capable of undergoing absorption quenching and others not. We question why only the quenchable members appear in as-grown material, and only nonquenchable ones are generated by PD? One might have expected that both types would show up in either means of defect-formation. Some of the assumptions and inferences made for PD also show up in the analysis of neutron [1, 2] and electron [3] irradiated GaAs. The scope of the alternative analysis presented below covers all three types of deformation. The analysis leads to a significant difference between the defects generated by PD and particle irradiation. AN ALTERNATIVE PROPOSAL The questions raised above led to our attempt to provide an alternative analysis of the experimental findings of [1]. The central point of our proposal is to change the type of defect assumed to be generated by PD. Instead of assuming that (predominantly) ASGa defects are introduced, we propose that deep acceptors are generated. These acceptors serve the function of compensating the residual neutral ASGa deIects that were originally present in the as-grown material, prior to PD. The effect of this compensation is to increase the EPR signal by increasing the necessary Asia concentration. The precedent for this assumption is the important role of compensation demonstrated in as-grown "undoped" GaAs [ 6 - 8 ] . The concentration of deep donor defects ASGa in such material can be substantially higher than the residual compensating shallow acceptors [6]. Suppose e.g., that we consider an "undoped" semi-insulating sample with 4 x 1016 cm -3 antisites. If there are ~< 1016 cm -3 shallow acceptors, then most of the antisites will be neutral and not contribute to the EPR signal. Only the singly positively-charged compensated antisites A s ~ , which are equal in concentration to the compensating, residual shallow acceptors, will have the appropriate spin to contribute to the EPR signal. If more compensating acceptors are generated by plastic deformation, this provides the means for converting the residual neutral ASGa to Asia, and thus increasing the EPR signal strength. We then attribute the corresponding increase in nonquenching absorption directly to the deep acceptors; this consists of optically-induced transitions of carriers from the acceptors to the conduction and valence bands.
Vol. 60, No. 11
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs
If the increased absorption is to lie in the same photon energy range as that of the ASGa defects, as is apparently observed in Fig. 1 of [ I ] , the PD-generated acceptors must lie fairly close to, but below them, near the middle of the gap. We also note from that figure that the increased absorption clearly does not have the same shape as that of the ASGa in the undeformed case. This supports our conclusion that the defects generated by PD differ from ASGa. The fact that the absorption is nonquenchable, tells us that the acceptor defects do not undergo a metastable transition. We next apply this model to the observed quenching phenomena. Since the concentration of the original ASGa defects is not affected by PD in our model, their quenchable contribution to the absorption should remain constant, as is indeed observed. Their quenchability has been attributed to their ability to undergo an optically-induced metastable transition. The transition to a metastable state has been shown to occur only from the neutral state of the antisites [8, 11]. This ability is not affected by the compensation-induced change in their charge state. During their normal, prequench state all the antisites are, at some time, in the neutral state as a result of the dynamic processes during optical excitation. Finally, when the absorption of the antisites is quenched, they are all frozen in their neutral state by the metastable transition and their EPR signal must also be quenched. In the meantime, the acceptors must be restored to their neutral state, in which they can continue to contribute to the absorption. Thus, there is no conflict in this picture between the observation of "unquenchable absorption" and "quenchable EPR". They refer here to phenomena occurring on different defects! This model predicts a natural, sample-dependent limit to the increase in the EPR signal. The limit is determined by the concentration of neutral ASGa that is present in the particular as-grown GaAs sample. In the case of plastically deformed material, the highest EPR signal reported in [1] is less than 5 × 10 ~6 cm -3. This poses no problem since it is within the range quoted for as-grown material. On the other hand, we run into a difficulty with the high increase in EPR signal for neutron [1, 2] and electron [3] irradiated material, where defect concentrations as high as I0 TM cm -3 are measured. This is far beyond the limit of ASGa that is present naturally in the as-grown material. This result requires that the defect generation mechanism proposed for PD is not applicable for particle irradiation. The implication is that the irradiation (or, for that matter, even the plastic deformation to a much smaller extent) can form high concentrations of ASGaantitsites. But this has to occur in conjunction with the formation of compensating acceptor defects if the increase in EPR signal strength to very high levels is to be manifested.
869
With regard to this extension to irradiated material, there are two interesting pieces of substantiating evidence. (i) An EPR study [3] of electron-irradiated n-type GaAs demonstrates that the original free electron population is completely compensated before the EPR signal from As antisites can show up. This demonstrates that only after all the free electrons are trapped, necessarily on newly-generated acceptor defects, can the mechanism of compensation of the donor As antisites by acceptor defects produce Asia and permit the observation of their EPR signal. The necessity of the generation of compensating acceptor defects in conjunction with As antisites is clearcut. (ii) The confirming evidence in neutron irradiated material [2] is more indirect. A new EPR signal is reported, a singlet from an unidentified "S" center that is induced simultaneously and with matching concentration to the quadruplet from Asia. It is very tempting to suggest that the S center is the acceptor that provides the compensation for the newly generated ASGa antisites. It may even be the same center we postulate in plastically deformed material, but at concentrations 10-100 times smaller, and not yet detected or recognized because it lies under the antistite spectrum [2]. One of the problems in [1] was the different EPR thermal anneal temperatures for the ASGa antisites in as-grown material (>950°C), and for the PD-induced defects (650°C). In fact, the reports of different anneal temperatures in as-grown, PD, and neutron-irradiated GaAs, has led to the suggestion that more than one ASGa-containing defect can give the same EPR signal [1]. In our model, the resolution of the problem is very much simpler. We can attribute the lower anneal temperature(s) to compensating acceptor defects. When they are annealed, the EPR signal is also necessarily lost because the Asia antisites are restored to their neutral charge status. This permits some or all of the variability in anneal temperatures to be transferred to the acceptor defects. Our model thus demonstrates the lack of validity of attributing everything that happens to the EPR signal, to the variability of the ASGa-containing defects. In [1], it was concluded that since the defects generated by PD are ASGa, then the increased absorption due to PD must come from defects and cannot be due to dislocations. In contrast, in our model, PD induces acceptors. These may be present as defects, but they may also be associated with dislocations. Therefore, the dislocations can no longer be excluded as a possible contributor to the PD-induced absorption. In summary, we have drastically altered a basic assumption of previous analyses of PD and electron-and neutron-irradiated GaAs, namely that the generally observed increase in EPR signal represents an increase in donor ASGa defects alone. In the case of PD, we
870
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs
conclude that compensating deep acceptors are the dominant defects generated, as opposed to the electronand neutron-irradiated materials where very high populations of both types of defects appear to be generated. By introducing the important role of compensating acceptor defects, we not only explain the increase in the As6a-related EPR signal, but greatly simplify the analysis of various other aspects of the experimental results. The assumption of the generation of acceptor defects supplies a mechanism for explaining such features as nonquenchable absorption but quenchable EPR. The anomalous EPR annealing temperatures, previously attributed to peculiar members of the ASGadefect family, can now be attributed to the acceptor defects. Thus the "family" of AsGa defects may not be as large or as varied as was supposed. In particular, there remains no evidence for a class of As6a-defects with characteristics that deviate from those of EL2.
Acknowledgements - This work was partially supported by the National Science Foundation through Grant No. DMR-82-17442. An Alexander von Humboldt Senior U.S. Scientist Award permitted me to enjoy the stimulating environment and hospitality provided by K. Dransfeld at the Universitiit Konstanz and by M. Cardona at the Max-Planck-lnstitut fiir Festkorperforschung in Stuttgart. I am grateful to M. Cardona for
Vol. 60, No. 11
calling my attention to the work on plastic deformation of GaAs. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.
10. 11.
P. Omling, E.R. Weber & L. Samuelson, Phys. Rev. B33, 5880 (1986). A. Goltzene, B. Meyer, C. Schwab, S.G. Greenbaum, R.J. Wagner & T.A. Kennedy, J. Appl. Phys. 56, 3394 (1984). N.K. Goswami, R.C. Newman & J.E. Whitehouse, Solid State Commun. 40, 473 (1981). G. Vincent & D. Bois, Solid State Commun. 27, 431 (1978); G. Vincent, D. Bois & A. Chantre, J. Appl. Phys. 53, 3643 (1982). G.M. Martin, Appl. Phys. Lett. 39,747 (1981). K. EUiott, R.T. Chen. S.G. Greenbaum & R.J. Wagner, AppL Phys. Lett. 44, 907 (1984). K. Wan & Ralph Bray, Phys. Rev. B32, 5265 (1985). R. Bray, K. Wan & J.C. Parker, to be published. L. Samuelson, P. Omling, E.R. Weber & H.G. Grimmeis, in Semi-insulating I I I - V Materials, p. 268, (Edited by D.C. Look and J.S. Blakemore) Shiva, Nantwich (1984). E.R. Weber, H. Ennen, U. Kaufman, J. Windsheif, J. Schnedier & T. Wosinski, J. AppL Phys. 53, 6140 (1982). M. Skowronski, J. Lagowski & H.C. Gatos, Phys. Rev. B32, 4264 (1985).
0038-1098/86 $3.00 + .00 Pergamon Journals Ltd.
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs: AN ALTERNATIVE ANALYSIS R. Bray* Max-Planck-Institut for Festk6rperforschung, 7000 Stuttgart 80, and Fakult/it fiir Physik, Universit/it Konstanz, 7750 Konstantz 1, FRG
(Received 15 June 1986 by M. Cardona) A revision is presented of the accepted view that the observed increase in electron paramagnetic resonance (EPR) with plastic deformation in GaAs is due to the generation of As antisite defects. It is proposed instead that only compensating deep acceptor defects are generated. The increase of the EPR signal from As antisites can then be attributed to the compensation of the neutral As antisites that were already present in the as-grown GaAs. The nonquenching extrinsic absorption can be attributed to the acceptors. The same analysis suggests that in the case of electron and neutron irradiation, both acceptors and As antisites are generated. These proposals succeed in eliminating some recently imposed complexities in the relationship between As antisites and EL2. INTRODUCTION THIS COMMUNICATION DEALS primarily with the nature of the defects generated in plastically deformed GaAs, and their relevance to the relation between the As antisites and EL2 centers. Our analysis was stimulated by the recent optical absorption and electron paramagnetic resonance (EPR) studies of plastically deformed GaAs by Omling et al. [ 1]. After reviewing their results and conclusions, we present a series of questions which lead to the formulation of an alternative analysis and a very different set of conclusions. The basic contention in [1], is that the defects generated by plastic deformation (PD) are "ASGa-related defects", and that the major portion of these defects is not EL2 related. We agree with the last part of this contention, that most of the defects generated are not EL2 related. But we believe that this is because the defects generated are, in fact, not AsGa-related, but rather, deep acceptors. In our model, these are held directly responsible for the nonquenching optical absorption induced by PD, and indirectly responsible for the observed increase in the EPR signal. Our analysis has important consequences not only for the nature of the defects generated by PD, but also for those generated by fast neutron [2] and electron [3] irradiation. Of particular interest is the application of our proposal to the question of the multiplicity of As6a-related defects, and the continuing controversial relationship between these defects and EL2 centers. * Permanent address: Department of Physics, Purdue University, West Lafayette, IN. 47907, USA.
It is necessary to first review and comment on the nature and identification of EL2. The mid-gap EL2 defects may be identified operationally by their role in various optical quenching or persistence phenomena. From these, it has been deduced that EL2 undergoes an optically-induced metastable transition at low temperature, and a thermal recovery near 130 K, which takes it back to its normal state [4]. It was originally suggested [5] that the EL2 concentration could be measured by the optical absorption (at certain photon energies). The work of [1 ] demonstrates conclusively that EL2 cannot always be measured straightforwardly from the extrinsic absorption. Nor can it be measured simply by the EPR signal, since only compensated EL2 centers which have lost an electron have the appropriate charge and spin state to give the EPR signal [ 6 - 8 ] . The quenchable part of the extrinsic absorption provides perhaps the best measure of the concentration of EL2 defects [1, 9]. Although there has been a long history of controversy over the identity of the EL2 defect, it is generally thought now to be some form of the As antisite AsGa. It is still controversial whether the latter is a point defect or part of one or more complexes, referred to in [1] as "As6a-related defects". In this paper, we shall use the designation "As6a" without regard to the precise form in which it exists. BACKGROUND REVIEW AND A CRITICAL COMMENTARY The study in [1 ] deals with the effects of PD of "undoped" semi-insulating GaAs on the optical absorption and on EPR. It is well-known that PD causes an
867
868
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs
increase in the dislocation density, and also in the point defects and point defect clusters. The basic experimental findings and the related inferences and conclusions of [1] can be summarized as follows: (1) The extrinsic absorption (in the range 0 . 8 1.4eV) is shown to consist of two components, a nonquenchable part which increases strongly with deformation, and a quenchable part which remains constant, and hence is unaffected by PD. The inference is made that the increase in nonquenchable absorption is not related to quenchable EL2, and that the quenchable EL2 concentration is unaffected by PD. (2) The nonquenchable part of the extrinsic absorption is observed to be proportional to the increase in the EPR signal. Since the latter is generally taken as a signature of AsGa-containing defects, it is therefore inferred that the increase of the EPR signal reflects an increase in ASGa-containing defects produced during PD, and that these defects are responsible for the increase in the nonquenchable absorption. (3) The PD-induced defects, presumed to be ASGarelated, are found to anneal at T ~ 650°C; this is in contrast with the ASGa-related defects in as-grown "undoped" GaAs, which are stable at least up to 950°C. From the existence of these different annealing temperatures it is inferred that there is a family of AsGacontaining defects. It is suggested that perhaps only a select portion of them (perhaps only the ones that are stable to very high temperatures, >950°C) are responsible for the EL2 level. We agree with the inferences in (1) above, but take issue with those in (2) and (3), where several aspects of the analysis are disturbing: (I) We question how the generation of ASGa defects by PD can increase the EPR signal. If only ASGa defects are being generated, one would expect them to be neutral. How can they acquire the appropriate charge state and spin to give EPR signals? In as-grown "undoped" GaAs, the EPR signal is obtained only for the ASGa defects which have become positively-charged through compensation by the residual shallow acceptors [6, 7]. Since the latter are already fully compensated before PD of the as-grown semi-insulating material, they are not available to provide a similar service for the additional PD-generated ASGa defects. This argument implies that any generation of AsGa-containing defects which show up in the EPR measurements must be accompanied by the generation of corresponding, compensating acceptor defects (which may have their own signature !). (2) No account is taken in [1] of the fact that the PD-induced EPR signal undergoes substantial opticallyinduced quenching. That this indeed happens is a central
V~. 60, No. 11
point in earlier EPR studies of plastically deformed GaAs [10]. We question how nonquenchable absorption can be associated, and be compatible, with quenchable EPR for the same ASGa defect, as is implicit in [ 1]. (3) It was inferred that in a family of different As6a-Containing defects (identified by the same EPR signature) some members are capable of undergoing absorption quenching and others not. We question why only the quenchable members appear in as-grown material, and only nonquenchable ones are generated by PD? One might have expected that both types would show up in either means of defect-formation. Some of the assumptions and inferences made for PD also show up in the analysis of neutron [1, 2] and electron [3] irradiated GaAs. The scope of the alternative analysis presented below covers all three types of deformation. The analysis leads to a significant difference between the defects generated by PD and particle irradiation. AN ALTERNATIVE PROPOSAL The questions raised above led to our attempt to provide an alternative analysis of the experimental findings of [1]. The central point of our proposal is to change the type of defect assumed to be generated by PD. Instead of assuming that (predominantly) ASGa defects are introduced, we propose that deep acceptors are generated. These acceptors serve the function of compensating the residual neutral ASGa deIects that were originally present in the as-grown material, prior to PD. The effect of this compensation is to increase the EPR signal by increasing the necessary Asia concentration. The precedent for this assumption is the important role of compensation demonstrated in as-grown "undoped" GaAs [ 6 - 8 ] . The concentration of deep donor defects ASGa in such material can be substantially higher than the residual compensating shallow acceptors [6]. Suppose e.g., that we consider an "undoped" semi-insulating sample with 4 x 1016 cm -3 antisites. If there are ~< 1016 cm -3 shallow acceptors, then most of the antisites will be neutral and not contribute to the EPR signal. Only the singly positively-charged compensated antisites A s ~ , which are equal in concentration to the compensating, residual shallow acceptors, will have the appropriate spin to contribute to the EPR signal. If more compensating acceptors are generated by plastic deformation, this provides the means for converting the residual neutral ASGa to Asia, and thus increasing the EPR signal strength. We then attribute the corresponding increase in nonquenching absorption directly to the deep acceptors; this consists of optically-induced transitions of carriers from the acceptors to the conduction and valence bands.
Vol. 60, No. 11
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs
If the increased absorption is to lie in the same photon energy range as that of the ASGa defects, as is apparently observed in Fig. 1 of [ I ] , the PD-generated acceptors must lie fairly close to, but below them, near the middle of the gap. We also note from that figure that the increased absorption clearly does not have the same shape as that of the ASGa in the undeformed case. This supports our conclusion that the defects generated by PD differ from ASGa. The fact that the absorption is nonquenchable, tells us that the acceptor defects do not undergo a metastable transition. We next apply this model to the observed quenching phenomena. Since the concentration of the original ASGa defects is not affected by PD in our model, their quenchable contribution to the absorption should remain constant, as is indeed observed. Their quenchability has been attributed to their ability to undergo an optically-induced metastable transition. The transition to a metastable state has been shown to occur only from the neutral state of the antisites [8, 11]. This ability is not affected by the compensation-induced change in their charge state. During their normal, prequench state all the antisites are, at some time, in the neutral state as a result of the dynamic processes during optical excitation. Finally, when the absorption of the antisites is quenched, they are all frozen in their neutral state by the metastable transition and their EPR signal must also be quenched. In the meantime, the acceptors must be restored to their neutral state, in which they can continue to contribute to the absorption. Thus, there is no conflict in this picture between the observation of "unquenchable absorption" and "quenchable EPR". They refer here to phenomena occurring on different defects! This model predicts a natural, sample-dependent limit to the increase in the EPR signal. The limit is determined by the concentration of neutral ASGa that is present in the particular as-grown GaAs sample. In the case of plastically deformed material, the highest EPR signal reported in [1] is less than 5 × 10 ~6 cm -3. This poses no problem since it is within the range quoted for as-grown material. On the other hand, we run into a difficulty with the high increase in EPR signal for neutron [1, 2] and electron [3] irradiated material, where defect concentrations as high as I0 TM cm -3 are measured. This is far beyond the limit of ASGa that is present naturally in the as-grown material. This result requires that the defect generation mechanism proposed for PD is not applicable for particle irradiation. The implication is that the irradiation (or, for that matter, even the plastic deformation to a much smaller extent) can form high concentrations of ASGaantitsites. But this has to occur in conjunction with the formation of compensating acceptor defects if the increase in EPR signal strength to very high levels is to be manifested.
869
With regard to this extension to irradiated material, there are two interesting pieces of substantiating evidence. (i) An EPR study [3] of electron-irradiated n-type GaAs demonstrates that the original free electron population is completely compensated before the EPR signal from As antisites can show up. This demonstrates that only after all the free electrons are trapped, necessarily on newly-generated acceptor defects, can the mechanism of compensation of the donor As antisites by acceptor defects produce Asia and permit the observation of their EPR signal. The necessity of the generation of compensating acceptor defects in conjunction with As antisites is clearcut. (ii) The confirming evidence in neutron irradiated material [2] is more indirect. A new EPR signal is reported, a singlet from an unidentified "S" center that is induced simultaneously and with matching concentration to the quadruplet from Asia. It is very tempting to suggest that the S center is the acceptor that provides the compensation for the newly generated ASGa antisites. It may even be the same center we postulate in plastically deformed material, but at concentrations 10-100 times smaller, and not yet detected or recognized because it lies under the antistite spectrum [2]. One of the problems in [1] was the different EPR thermal anneal temperatures for the ASGa antisites in as-grown material (>950°C), and for the PD-induced defects (650°C). In fact, the reports of different anneal temperatures in as-grown, PD, and neutron-irradiated GaAs, has led to the suggestion that more than one ASGa-containing defect can give the same EPR signal [1]. In our model, the resolution of the problem is very much simpler. We can attribute the lower anneal temperature(s) to compensating acceptor defects. When they are annealed, the EPR signal is also necessarily lost because the Asia antisites are restored to their neutral charge status. This permits some or all of the variability in anneal temperatures to be transferred to the acceptor defects. Our model thus demonstrates the lack of validity of attributing everything that happens to the EPR signal, to the variability of the ASGa-containing defects. In [1], it was concluded that since the defects generated by PD are ASGa, then the increased absorption due to PD must come from defects and cannot be due to dislocations. In contrast, in our model, PD induces acceptors. These may be present as defects, but they may also be associated with dislocations. Therefore, the dislocations can no longer be excluded as a possible contributor to the PD-induced absorption. In summary, we have drastically altered a basic assumption of previous analyses of PD and electron-and neutron-irradiated GaAs, namely that the generally observed increase in EPR signal represents an increase in donor ASGa defects alone. In the case of PD, we
870
ANTISITE DEFECTS IN PLASTICALLY-DEFORMED GaAs
conclude that compensating deep acceptors are the dominant defects generated, as opposed to the electronand neutron-irradiated materials where very high populations of both types of defects appear to be generated. By introducing the important role of compensating acceptor defects, we not only explain the increase in the As6a-related EPR signal, but greatly simplify the analysis of various other aspects of the experimental results. The assumption of the generation of acceptor defects supplies a mechanism for explaining such features as nonquenchable absorption but quenchable EPR. The anomalous EPR annealing temperatures, previously attributed to peculiar members of the ASGadefect family, can now be attributed to the acceptor defects. Thus the "family" of AsGa defects may not be as large or as varied as was supposed. In particular, there remains no evidence for a class of As6a-defects with characteristics that deviate from those of EL2.
Acknowledgements - This work was partially supported by the National Science Foundation through Grant No. DMR-82-17442. An Alexander von Humboldt Senior U.S. Scientist Award permitted me to enjoy the stimulating environment and hospitality provided by K. Dransfeld at the Universitiit Konstanz and by M. Cardona at the Max-Planck-lnstitut fiir Festkorperforschung in Stuttgart. I am grateful to M. Cardona for
Vol. 60, No. 11
calling my attention to the work on plastic deformation of GaAs. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.
10. 11.
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