The avian auditory brainstem displays parallel processing, a fundamental feature of vertebrate sensory systems. Nuclei specialized for temporal processing are largely separate from those processing other aspects of sound. One possible exception to this parallel organization is the inhibitory input provided by the superior olivary nucleus (SON) to nucleus angularis (NA), nucleus magnocellularis (NM), and nucleus laminaris (NL) and contralateral SON (SONc). We sought to determine whether single SON neurons project to multiple targets or separate neuronal populations project independently to individual target nuclei. We introduced two different fluorescent tracer molecules into pairs of target nuclei and quantified the extent to which retrogradely labeled SON neurons were double labeled. A large proportion of double-labeled SON somata were observed in all cases in which injections were made into any pair of ipsilateral targets (NA and NM, NA and NL, or NM and NL), suggesting that many individual SON neurons project to multiple targets. In contrast, when injections involved the SONc and any or all of the ipsilateral targets, double labeling was rare, suggesting that contralateral and ipsilateral targets are innervated by distinct populations of SON neurons arising largely from regionally segregated areas of SON. Therefore, at the earliest stages of auditory processing, there is interaction between pathways specialized to process temporal cues and those that process other acoustic features. We present a conceptual model that incorporates these results and suggest that SON circuitry, in part, functions to offset interaural intensity differences in interaural time difference processing.

Neurons in the inferior colliculus (IC) that are excited by one ear and inhibited by the other [excitatory-inhibitory (EI) neurons] can code interaural intensity disparities (IIDs), the cues animals use to localize high frequencies. Although EI properties are first formed in a lower nucleus and imposed on some IC cells via an excitatory projection, many other EI neurons are formed de novo in the IC. By reversibly inactivating the dorsal nucleus of the lateral lemniscus (DNLL) in Mexican free-tailed bats with kynurenic acid, we show that the EI properties of many IC cells are formed de novo via an inhibitory projection from the DNLL on the opposite side. We also show that signals excitatory to the IC evoke an inhibition in the opposite DNLL that persists for tens of milliseconds after the signal has ended. During that period, strongly suppressed EI cells in the IC are deprived of inhibition from the DNLL and respond to binaural signals as weakly inhibited or monaural cells. By relieving inhibition at the IC, we show that an initial binaural signal essentially reconfigures the circuit and thereby allows IC cells to respond to trailing binaural signals that were inhibitory when presented alone. Thus, DNLL innervation creates a property in the IC that is not possessed by lower neurons or by collicular EI neurons that are not innervated by the DNLL. That property is a change in responsiveness to binaural signals, a change dependent on the reception of an earlier sound. These features suggest that the circuitry linking the DNLL with the opposite central nucleus of the IC is important for the processing of IIDs that change over time, such as the IIDs generated by moving stimuli or by multiple sound sources that emanate from different regions of space. Key words: GABA; persistent inhibition; precedence effect; inferior colliculus; sound localization; dorsal nucleus of lateral lemniscusThe projections from the vast majority of lower auditory nuclei converge at a common destination in the central nucleus of the inferior colliculus (ICc) (for review, see Aitkin, 1986;Oliver and Huerta, 1992). This large convergence of inputs suggests that substantial transformations occur in the ICc; yet the response properties of ICc neurons appear to be similar to those of the lower nuclei from which they receive their innervation. An example is excitatory-inhibitory (EI) neurons in the ICc, neurons that are excited by one ear and inhibited by the other ear. These neurons are sensitive to interaural intensity disparities (IIDs), the cues animals use to localize high-frequency sounds (Erulkar, 1972;Mills, 1972). EI neurons are initially formed in the lateral superior olive (LSO) (Boudreau and Tsuchitani, 1968;Finlayson and Caspary, 1991). They are also the dominant type in the dorsal nucleus of the lateral lemniscus (DNLL), a nucleus the neurons of which are almost exclusively GABAergic (Brugge et al., 1970;Adams and Mugniani, 1984;Covey, 1993; Yang and Pollak, 1994a,b,c;Winer et al., 1995). The DNLL, like the ICc, is one of the principa...

Neurons in the central nucleus of the inferior colliculus (ICc) typically respond with phase-locked discharges to low rates of sinusoidal amplitude-modulated (SAM) signals and fail to phase-lock to higher SAM rates. Previous studies have shown that comparable phase-locking to SAM occurs in the dorsal nucleus of the lateral lemniscus (DNLL) and medial superior olive (MSO) of the mustache bat. The studies of MSO and DNLL also showed that the restricted phase-locking to low SAM rates is created by the coincidence of phase-locked excitatory and inhibitory inputs that have slightly different latencies. Here we tested the hypothesis that responses to SAM in the mustache bat IC are shaped by the same mechanism that shapes responses to SAM in the two lower nuclei. We recorded responses from ICc neurons evoked by SAM signals before and during the iontophoretic application of several pharmacological agents: bicuculline, a competitive antagonist for gamma-aminobutyric acid-A (GABAA) receptors; strychnine, a competitive antagonist for glycine receptors; the GABAB receptor blocker, phaclofen, and the N-methyl-D-aspartate (NMDA) receptor blocker, (-)-2-amino-5-phosphonopentanoic acid (AP5). The hypothesis that inhibition shapes responses to SAM signals in the ICc was not confirmed. In >90% of the ICc neurons tested, the range of SAM rates to which they phase-locked was unchanged after blocking inhibition with bicuculline, strychnine or phaclofen, applied either individually or in combination. We also considered the possibility that faster alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors follow high temporal rates of incoming excitation but that the slower NMDA receptors could follow only lower rates. Thus at higher SAM rates, NMDA receptors might generate a sustained excitation that "smears" the phase-locked excitation generated by the AMPA receptors. The NMDA hypothesis, like the inhibition hypothesis, was also not confirmed. In none of the cells that we tested did the application of AP5 by itself, or in combination with bicuculline, cause an increase in the range of SAM rates that evoked phase-locking. These results illustrate that the same response property, phase-locking restricted to low SAM rates, is formed in more than one way in the auditory brain stem. In the MSO and DNLL, the mechanism is coincidence of phase-locked excitation and inhibition, whereas in ICc the same response feature is formed by a different but unknown mechanism.

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Mature nucleus magnocellularis (NM) neurons, the avian homolog of bushy cells of the mammalian anteroventral cochlear nucleus, maintain high [ClϪ ] i and depolarize in response to GABA. Depolarizing GABAergic postsynaptic potentials (GPSPs) activate both the synaptic conductance and large outward currents, which, when coupled together, inhibit spikes via shunting and spike threshold accommodation. We studied the maturation of the synaptic and voltage-dependent components of inhibition in embryonic NM neurons using whole-cell and gramicidin-perforated patch-clamp techniques to measure Cl Ϫ reversal potential, GABAergic synaptic responses, and voltage-dependent outward currents. We found that GABA enhanced excitability in immature NM neurons, undergoing a switch to inhibitory between embryonic day 14 (E14) and E18. Low-voltage-activated Kv1-type (dendrotoxin-I sensitive) K ϩ currents increased in amplitude between E14 and E18, whereas Cl Ϫ reversal potential and synaptic conductances remained relatively stable during this period. GABA was rendered inhibitory because of this increase in low-voltage activated outward currents. GPSPs summed with other inputs to increase spike probability at E14. GPSPs shunted spikes at E18, but blocking Kv1 channels transformed this inhibition to excitation, similar to E14 neurons. Subthreshold depolarizing current steps, designed to activate outward currents similar to depolarizing GPSPs, enhanced excitability at E14 but inhibited spiking in E18 neurons. Blocking Kv1 channels reversed this effect, rendering current steps excitatory. We present the novel finding that the developmental transition of GABAergic processing from increasing neuronal excitability to inhibiting spiking can depend on changes in the expression of voltage-gated channels rather than on a change in Cl Ϫ reversal potential.

The morphology of clastic continental margins directly reflects their formative processes. These include interactions between plate movements and isostasy, which establish the characteristic stairstep shape of margins. Other factors are thermal and loading-induced subsidence, compaction and faulting/folding, which create and/or destroy accommodation space for sediment supplied by rivers and glaciers. These processes are primary controls on margin size and shape. Rivers and glaciers can also directly sculpt the margin surface when it is subaerially exposed by sea-level lowstands. Otherwise, they deposit their sediment load at or near the shoreline. Whether this deposition builds a delta depends on sea level and the energy of the ocean waves and currents. Delta formation will be prevented when sea level is rising faster than sediment supply can build the shoreline. Vigorous wave and current activity can slow or even arrest subaerial delta development by moving sediments seaward to form a subaqueous delta. This sediment movement is accomplished in part by wave-supported sediment gravity flows. Over the continental slope, turbidity currents are driven by gravity and, in combination with slides, cut submarine canyons and gullies. However, turbidity currents also deposit sediment across the continental slope. The average angle of continental slopes (~4°) lies near the threshold angle above which turbidity currents will erode the seafloor and below which they will deposit their sediment load. Therefore, turbidity currents may help regulate the dip of the continental slope. Internal waves exert a maximum shear on the continental-slope surface at about the same angle, and may be another controlling factor.

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