Monte Carlo simulation of ultrafast processes in photoexcited semiconductors: Coherent and incoherent dynamics

The ultrafast dynamics of photoexcited carriers in a semiconductor is investigated by using a Monte Carlo simulation. In addition to a ‘‘conventional’’ Monte Carlo simulation, the coherence of the external light field and the resulting coherence in the carrier system are fully taken into account. This allows us to treat the correct time dependence of the generation process showing a time-dependent linewidth associated with a recombination from states off resonance due to stimulated emission. The subsequent dephasing of the carriers due to scattering processes is analyzed. In addition, the simulation contains the carrier-carrier interaction in Hartree-Fock approximation giving rise to a band-gap renormalization and excitonic effects which cannot be treated in a conventional Monte Carlo simulation where polarization effects are neglected. Thus the approach presents a unified numerical method for the investigation of phenomena occurring close to the band gap and those typical for the energy relaxation of hot carriers

Coupled free-carrier and exciton relaxation in optically excited semiconductors

The energy relaxation of coupled free-carrier and exciton populations in semiconductors after low-density ultrafast optical excitation is studied through a kinetic approach. The set of semiclassical Boltzmann equations, usually written for electron and hole populations only, is complemented by an additional equation for the exciton distribution. The equations are coupled by reaction terms describing phonon-mediated exciton binding and dissociation. All the other relevant scattering mechanisms, such as carrier-carrier, carrier-phonon, and exciton-phonon interactions, are also included. The resulting system of rate equations in reciprocal space is solved by an extended ensemble Monte Carlo method. As a first application, we show results for the dynamics of bulk GaAs in the range from 1 to ∼200 ps after photoexcitation. The build-up of an exciton population and its sensitivity to the excitation conditions are discussed in detail. As a consequence of the pronounced energy dependence of the LO-phonon-assisted transition probabilities between free-pair states and excitons, it is found that the efficiency of the exciton-formation process and the temporal evolution of the resulting population are sensitive to the excitation energy. We discuss the effects on luminescence experiments

ULTRAFAST WAVE PACKET DYNAMICS IN JAHN-TELLER SURFACES; Ag ATOMS TN Xe CRYSTALS

Author Institution: Fachbereich physik, FU BerlinThe dynamics on Jahn-Teller surfaces involving pseudorotation, radial oscillations and the symmetric breathing mode has been already explored in isolated triatomics like $Na_{3}$. This contribution deals with the additional effects occuring in the condensed phase and originating from the energy dissipation to the lattice by phonon emission. A study with femtosecond pump-probe spectroscopy is carried out for substitutional Ag atoms in a rare gas lattice (Xe) of cubic (fcc) symmetry. Excitation from the electronic ground state with s-symmetry to the p-orbitals of the Ag atom leads to a dynamic Jahn-Teller splitting which removes the degeneracy of the p-orbitals by a coupling to nontotally symmetric phonon modes. Energy dissipation of the initially pseudorotating wave packets leads to structural relaxation and to a thermalized population in a strongly statically deformed geometry according to the large Stokes shift of about 2 eV. The initial population in the Jahn-Teller state is probed by a transient bleaching of the ground state resulting in a life time of several ps. The observed subpicosecond dynamics is related to the cubic and noncubic modes derived from MCD experiments. The subsequent energy dissipation of about 0.4 eV corresponding to 80 phonons is detected by fluorescence dip spectroscopy. The static deformation and the thermalization in it is completed in 5-7 ps. This very fast energy relaxation cannot be attributed to single phonon emission events for a phonon period of about 1 ps and is discussed with respect to higher order terms in Jahn-Teller surfaces

Ketamine affects prediction errors about statistical regularities: A computational single-trial analysis of the mismatch negativity

The auditory mismatch negativity (MMN) is significantly reduced in schizophrenia. Notably, a similar MMN reduction can be achieved with NMDA receptor (NMDAR) antagonists. Both phenomena have been interpreted as reflecting an impairment of predictive coding or, more generally, the "Bayesian brain"notion that the brain continuously updates a hierarchical model to infer the causes of its sensory inputs. Specifically, neurobiological interpretations of predictive coding view perceptual inference as an NMDAR-dependent process of minimizing hierarchical precision-weighted prediction errors (PEs), and disturbances of this putative process play a key role in hierarchical Bayesian theories of schizophrenia. Here, we provide empirical evidence for this theory, demonstrating the existence of multiple, hierarchically related PEs in a "roving MMN"paradigm. We applied a hierarchical Bayesian model to single-trial EEG data from healthy human volunteers of either sex who received the NMDAR antagonist S-ketamine in a placebo-controlled, double-blind, within-subject fashion. Using an unrestricted analysis of the entire time-sensor space, our trial-by-trial analysis indicated that low-level PEs (about stimulus transitions) are expressed early (102-207 ms poststimulus), while high-level PEs (about transition probability) are reflected by later components (152-199 and 215-277 ms) of single-trial responses. Furthermore, we find that ketamine significantly diminished the expression of high-level PE responses, implying that NMDAR antagonism disrupts the inference on abstract statistical regularities. Our findings suggest that NMDAR dysfunction impairs hierarchical Bayesian inference about the world's statistical structure. Beyond the relevance of this finding for schizophrenia, our results illustrate the potential of computational singletrial analyses for assessing potential pathophysiological mechanisms

Mismatch negativity encoding of prediction errors predicts S-ketamine-induced cognitive impairments

Psychotomimetics like the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine and the 5-hydroxytryptamine2A receptor (5-HT(2A)R) agonist psilocybin induce psychotic symptoms in healthy volunteers that resemble those of schizophrenia. Recent theories of psychosis posit that aberrant encoding of prediction errors (PE) may underlie the expression of psychotic symptoms. This study used a roving mismatch negativity (MMN) paradigm to investigate whether the encoding of PE is affected by pharmacological manipulation of NMDAR or 5-HT(2A)R, and whether the encoding of PE under placebo can be used to predict drug-induced symptoms. Using a double-blind within-subject placebo-controlled design, S-ketamine and psilocybin, respectively, were administrated to two groups of healthy subjects. Psychological alterations were assessed using a revised version of the Altered States of Consciousness (ASC-R) questionnaire. As an index of PE, we computed changes in MMN amplitudes as a function of the number of preceding standards (MMN memory trace effect) during a roving paradigm. S-ketamine, but not psilocybin, disrupted PE processing as expressed by a frontally disrupted MMN memory trace effect. Although both drugs produced positive-like symptoms, the extent of PE processing under placebo only correlated significantly with the severity of cognitive impairments induced by S-ketamine. Our results suggest that the NMDAR, but not the 5-HT(2A)R system, is implicated in PE processing during the MMN paradigm, and that aberrant PE signaling may contribute to the formation of cognitive impairments. The assessment of the MMN memory trace in schizophrenia may allow detecting early phases of the illness and might also serve to assess the efficacy of novel pharmacological treatments, in particular of cognitive impairments.Neuropsychopharmacology advance online publication, 26 October 2011; doi:10.1038/npp.2011.261