A semiclassical theory relating the molecular resonance Rayleigh scattering intensity to the extinction coefficient of an electronic transition is presented. For isotropic molecules, the theory is shown to be equivalent to classical fluctuation theory. The semiclassical theory is then extended to include anisotropic polarizabilities. Depolarized scattering intensities and depolarization ratios are calculated for a model system, and the general features of previous experimental data are explained. Inclusion of inhomogeneous broadening in the theory predicts increased scattering intensities and decreased vibrational resolution of the scattering profile. Depolarized Rayleigh linewidths and intensity profiles are presented for a series of diphenylpolyenes, several coumarin laser dyes, and 3,4-dinitrophenol in its neutral and ionic forms. The ideal molecular properties and experimental conditions for the use of resonance enhanced dynamic Rayleigh scattering are deduced.

No abstract

We have used animal models of long term neonatal cochlear hearing loss to study developmental plasticity of the central auditory pathways. Newborn chinchilla pups and feline kittens were treated with the ototoxic drug amikacin, so as to induce basal lesions in the cochlea. At maturity these animals were used in single unit electrophysiological mapping studies, in which the cochleotopic organization of primary auditory cortex (of the cat) and the inferior colliculus of the midbrain (in the chinchilla) were mapped. We have observed, both in the midbrain and auditory cortex, massive reorganization of frequency representation. Most striking were the presence of large monotonic regions (i.e. large areas in which all neurons have similar tuning properties). Cochlear lesions which involve inner hair cells clearly modify the normal development of cochleotopic representation in the midbrain and cortical regions. We suggest that similar abnormal patterns of frequency representation will exist in human subjects with long term neonatal hearing loss.

In the present study, anatomical projections from the medial geniculate body (MGB) to primary auditory cortex (AI) were investigated in normal adult cats and in animals that were neonatally deafened with the ototoxic drug amikacin. Cochleotopic/tonotopic maps in AI (based on neural response characteristic frequency) were obtained with microelectrode recording techniques, and single or multiple injections of retrograde tracers (horseradish peroxidase and fluorescent dyes) were introduced into AI. The AI maps of the amikacin-treated cats had an abnormal cochleotopic organization, such that deprived cortical areas exhibited an expanded representation of intact regions of the damaged cochlea. However, retrograde tracer injections into different regions of AI produced a normal pattern of labeling in the ventral division of the medial geniculate body (MGBv). In both experimental and control animals, the main mass of labeled thalamic cells was found in the MGBv. Different isofrequency contours in AI receive input from different portions of the MGBv. Thus, cell arrays labeled by anterior AI injections were situated medially in MGBv, and injections into posterior AI labeled MGBv more laterally. Furthermore, the deafened cats did not develop a more divergent thalamocortical projection compared with normal control animals, indicating that an abnormal spread of the thalamocortical afferents across the frequency domain in AI (anterior-posterior axis) is not responsible for the altered cochleotopic map in these neonatally deafened animals. The relatively normal thalamocortical projection pattern suggests that, after neonatal cochlear lesions, the major reorganization of cochleotopic maps occurs at subthalamic levels.