A novel concept for dynamic adjustment of auditory space.

Traditionally, the auditory system is thought to serve reliable sound localization. Stimulus-history driven feedback circuits in the early binaural pathway, however, contradict this canonical concept and raise questions about their functional significance. Here we show that stimulus-history dependent changes in absolute space perception are poorly captured by the traditional labeled-line and hemispheric-difference models of auditory space coding. We therefore developed a new decoding model incorporating recent electrophysiological findings in which sound location is initially computed in both brain hemispheres independently and combined to yield a hemispherically balanced code. This model closely captures the observed absolute localization errors caused by stimulus history, and furthermore predicts a selective dilation and compression of perceptional space. These model predictions are confirmed by improvement and degradation of spatial resolution in human listeners. Thus, dynamic perception of auditory space facilitates focal sound source segregation at the expense of absolute sound localization, questioning existing concepts of spatial hearing.

Mapping time.

Neuronal coding of temporal stimulus features can occur by means of delay lines. Given that neuronal activity is conducted through many parallel axons, there has to be a mechanism guaranteeing minimal temporal dispersion. We argue that plastic changes in synaptic transmission that are unspecifically propagated along presynaptic axons are a basis for the development of delay-line topologies. Furthermore, we show how two populations of afferents form a map of interaural time differences as found, for instance, in the laminar nucleus of the barn owl.

Temporal map formation in the barn owl's brain.

Barn owls provide an experimentally well-specified example of a temporal map, a neuronal representation of the outside world in the brain by means of time. Their laminar nucleus exhibits a place code of interaural time differences, a cue which is used to determine the azimuthal location of a sound stimulus, e.g., prey. We analyze a model of synaptic plasticity that explains the formation of such a representation in the young bird and show how in a large parameter regime a combination of local and nonlocal synaptic plasticity yields the temporal map as found experimentally. Our analysis includes the effect of nonlinearities as well as the influence of neuronal noise.

Temporal receptive fields, spikes, and Hebbian delay selection.

The intriguing concept of a receptive field evolving through Hebbian learning, mostly during ontogeny, has been discussed extensively in the context of the visual cortex receiving spatial input from the retina. Here, we analyze an extension of this idea to the temporal domain. In doing so, we indicate how a particular spike-based learning rule can be described by means of a mean-field learning equation and present a solution for a couple of illustrative examples. We argue that the success of the learning procedure strongly depends on an interplay of, in particular, the temporal parameters of neuron (model) and learning window, and show under what conditions the noisy synaptic dynamics can be regarded as a diffusion process.

Formation of temporal-feature maps by axonal propagation of synaptic learning.

Computational maps are of central importance to a neuronal representation of the outside world. In a map, neighboring neurons respond to similar sensory features. A well studied example is the computational map of interaural time differences (ITDs), which is essential to sound localization in a variety of species and allows resolution of ITDs of the order of 10 micros. Nevertheless, it is unclear how such an orderly representation of temporal features arises. We address this problem by modeling the ontogenetic development of an ITD map in the laminar nucleus of the barn owl. We show how the owl's ITD map can emerge from a combined action of homosynaptic spike-based Hebbian learning and its propagation along the presynaptic axon. In spike-based Hebbian learning, synaptic strengths are modified according to the timing of pre- and postsynaptic action potentials. In unspecific axonal learning, a synapse's modification gives rise to a factor that propagates along the presynaptic axon and affects the properties of synapses at neighboring neurons. Our results indicate that both Hebbian learning and its presynaptic propagation are necessary for map formation in the laminar nucleus, but the latter can be orders of magnitude weaker than the former. We argue that the algorithm is important for the formation of computational maps, when, in particular, time plays a key role.

Wide distribution of the cysteine string proteins in Drosophila tissues revealed by targeted mutagenesis.

The "cysteine string protein" (CSP) genes of higher eukaryotes code for a novel family of proteins characterized by a "J" domain and an unusual cysteine-rich region. Previous studies had localized the proteins in neuropil and synaptic terminals of larval and adult Drosophila and linked the temperature-sensitive paralysis of the mutants described here to conditional failure of synaptic transmission. We now use the null mutants as negative controls in order to reliably detect even low concentrations of CSPs by immunohistochemistry, employing three monoclonal antibodies. In wild-type flies high levels of cysteine string proteins are found not only in apparently all synaptic terminals of the embryonic, larval, and adult nervous systems, but also in the "tall cells" of the cardia, in the follicle cells of the ovary, in specific structures of the female spermatheca, and in the male testis and ejaculatory bulb. In addition, low levels of CSPs appear to be present in all tissues examined, including neuronal perikarya, axons, muscles, Malpighian tubules, and salivary glands. Western blots of isolated tissues demonstrate that of the four isoforms expressed in heads only the largest is found in non-neural organs. The wide expression of CSPs suggests that at least some of the various phenotypes of the null mutants observed at permissive temperatures, such as delayed development, short adult lifespan, modified electroretinogram, and optomotor behavior, may be caused by the lack of CSPs outside synaptic terminals.