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REPORT
1School of Psychological Science, La Trobe University, Bundoora, Victoria 3086; and 2Department of Otolaryngology, The University of Melbourne and 3The Bionic Ear Institute, East Melbourne, Victoria 3002, Australia
Submitted 31 March 2004; accepted in final form 10 May 2004
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ABSTRACT |
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INTRODUCTION |
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; Oertel et al. 1990), are narrowly tuned to tonal frequency, and their discharge rates are monotonically related to the spectral energy near their characteristic frequency (CF) (Blackburn and Sachs 1990; Yu and Young 2000). In response to CF tone bursts, these cells (termed choppers) exhibit an intrinsic and regular discharge pattern that is unrelated to stimulus frequency. Their discharge regularity is either maintained throughout a tone or decreases shortly after tone onset [sustained (CS) and transient (CT) chopper, respectively] (Blackburn and Sachs 1989; Smith and Rhode 1989; Young et al. 1988).
The VCN stellate population also includes D stellate cells (Oertel et al. 1990), which are inhibitory (glycinergic) neurons known to project on local as well as contralateral T stellate neurons (Cant and Gaston 1982; Doucet et al. 1999; Ferragamo et al. 1998; Needham and Paolini 2003; Schofield and Cant 1996; Wenthold 1987; Wu and Oertel 1986). D stellate cells are associated with onset chopper (OC) responses (Oertel et al. 1990; Paolini and Clark 1999), characterized by an initial, short series of regularly spaced action potentials (APs), followed by little or no activity for the remainder of a tone (Paolini and Clark 1999; Rhode and Smith 1986). These OC neurons are broadly tuned, reflecting the D stellate cell's diffuse dendritic arborization across isofrequency laminae (Doucet and Ryugo 1997; Smith and Rhode 1989), and have elevated thresholds to pure tones (Rhode and Smith 1986; Winter and Palmer 1995). D stellate cells are thought to provide wideband (lateral) inhibition to the narrowly tuned T stellate cells (Ferragamo et al. 1998). In turn, lateral inhibition is thought to fine tune the rate code by improving spectral contrast, particularly for signals in noise (Rhode and Greenberg 1994).
These wideband inhibitors are now known to provide fast (Joris and Smith 1998; Needham and Paolini 2003), short-duration (<10 ms) inhibition (Needham and Paolini 2003) to T stellate cells. Given their precisely timed and prominent onset responses, D stellate cells presumably have their greatest effect on the onset component of a T stellate cell's tonic response to a steady-state tonal stimulus. These experiments, using in vivo intracellular recording techniques, were designed to examine the effect of D stellate inhibition on the initial component of T stellate neurons' responses to pure tones. The results led us to reassess the traditional view of the role of wideband inhibition provided by D stellate cells and its contribution to frequency coding by T stellate cells.
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METHODS |
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). Briefly, animals were anesthetized with intraperitoneal urethane in water (20% wt/vol: total dose 2.6 g/kg; Sigma, Sydney, Australia), and supplemental doses were administered during the experiment if a corneal or paw reflex was observed. These procedures were in accordance with the Royal Victorian Eye and Ear Hospital Animal Research Ethics Committee guidelines (Project 95037). Following a craniotomy, the cerebellum was aspirated to expose a portion of the brain stem with the cochlear nucleus (CN) at the lateral extreme, enabling recording electrodes to be inserted into the VCN under visual control. Electrodes were oriented in a caudal-rostral direction away from the dorsal CN and octopus cell area of the posterior VCN. In some animals, a stimulating electrode was also inserted into the contralateral CN to activate commissural D stellate cell inhibition, as detailed by Needham and Paolini (2003). In this study, D stellate inhibition was induced by electrical stimuli consisting of 300-µA pulses.
Microelectrodes (quartz thin-walled; 1.0 mm OD; Sutter Instrument, Novato, CA) were filled with 1 M potassium acetate (70–80 M
) and advanced through the VCN in 2-µm steps by a motorized microdrive (Sutter Instrument), while presenting 70–80 dB white noise bursts (bandwidth, 0.45 Hz–50 kHz, 50-ms duration, 5-ms rise-fall time, repetition interval of 500 ms). Stable intracellular impalements were signaled by a prolonged (>3 min), stable drop (>30 mV) in the DC level and the presence of synaptic or large APs (>25 mV) with monophasic rise and fall times. Intracellular recordings typically lasted 20–40 min (maximum, 150 min).
Acoustic stimuli were synthesized digitally and generated by a Beyer DT48 transducer (Beyerdynamic, Farmingdale, NY) and controlled by a Tucker-Davis signal generator (Tucker-Davis Technologies, Gainesville, FL). The acoustic system was calibrated using a Bruel and Kjaer measuring amplifier (type 2606, Bruel and Kjaer, Naerum, Denmark) and a 0.5-in condenser microphone, coupled to a small probe tube positioned within the ear bar tube 
3 mm from the tympanic membrane. This enabled acoustic input to be measured in decibel sound pressure level (SPL).
Neurons were recorded intracellularly using an Axoclamp 2B amplifier (Axon Instruments, Union City, CA). The department's "Neurophysiology Laboratory System" (NLS software, by R. E. Millard), run on a PC, was used to control the Tucker-Davis unit and collate AP time information. A MacLab 4S data acquisition system (AD Instruments, Sydney, Australia) was used to store membrane potential records (traces) at a bandwidth of 20 or 40 kHz. Once impaled, the neuron's CF and input-output function at CF were determined (Liberman 1978). CF tone bursts (50-ms duration, 5-ms rise-fall time, repetition interval of 100 ms, usually 50 repetitions) were delivered in 5- or 10-dB steps in a sequential manner from subthreshold SPLs to SPLs that produced discharge rate saturation.
Classification of neurons was possible on the basis of their intracellular response profile. Averaging and superimposition of intracellular traces also aided in classification of neurons as did poststimulus time, interspike interval, and period histograms that were constructed on-line. The regularity of chopping behavior was determined, where possible, by calculating the CV (to suprathreshold CF tones) derived from the interspike interval histogram (Blackburn and Sachs 1989; Young et al. 1988). This measure differentiates between two chopper subtypes, both of which are recorded from T stellate cells. Neurons with low, consistent CV values (<0.2) were classified as CS, while CT neurons were those with an initial, low CV (<0.2) that increased during the tone (0.2 < CV < 0.5). Contour plots derived from the average intracellular traces over 25 stimulus repetitions were used to examine the relationship between stimulus SPL and membrane potential during CF tone presentation. The intracellular response profile of all chopper neurons recorded in this study were distinct from that of bushy cells (Paolini and Clark 1999; Paolini et al. 1997).
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RESULTS |
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Figure 1, A1–C1, depicts membrane potential changes in response to CF tones at different SPLs in neurons representative of each response type. The chopping behavior and time course of initial depolarization is clearly evident. Examples of single intracellular traces to CF tones, as well as peristimulus time histograms (PSTHs) with CV measures (Fig. 1, A2–C2), show that these cells' response characteristics are consistent with previous intracellular descriptions and PSTH-based classification of VCN stellate cells (Blackburn and Sachs 1989; Palmer et al. 2003; Paolini and Clark 1999; Rhode and Smith 1986; Rhode et al. 1983; Smith and Rhode 1989; Young et al. 1988). As expected, the latency of depolarization and the first AP decreased with increasing tone SPL in individual cells. The dynamic range of the latency of depolarization was lowest for OC neurons and was associated with a narrow depolarization band for the first evoked AP (Fig. 1C). Although OC neurons had higher thresholds, both neuron types (CS/T and OC) had similar latencies for depolarization across a range of SPLs when tones were presented at CF (Fig. 1, D, F, and H). This was also reflected in AP generation (Fig. 1, E, G, and I). However, when referenced to CF threshold, OC neurons showed significantly faster average depolarization latencies than CS/T neurons at 0 and 10 dB above threshold (respectively, t24 = 3.2 and t25 = 2.17, P < 0.05; Fig. 1J). There was also a tendency for OC neurons to have faster initial AP latencies than CS/T neurons at all SPLs; however, a significant difference was only observed at 30 dB above threshold (t18 = 2.1, P < 0.05).
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This expectation was confirmed by examination of the intracellular traces and contour plots depicting regions of hyperpolarization and depolarization in CS/T neurons to off-CF tones. In the two neurons shown in Fig. 2, A–H, fast, short-duration inhibition is apparent at frequencies removed from CF and occurs before generation of the first spike. Inhibition of this type at frequencies removed from CF was observed in 60% (12/20) of T stellate cells tested at 80 dB SPL. Figure 2E shows that, if inhibition arrives during depolarization in response to an off-CF tone, the course of depolarization is altered (asterisk) and it takes longer for the cell to reach AP firing threshold (arrow); that is, the first AP is delayed. The time course of this inhibition precisely matched that previously described for D stellate inhibition produced by contralateral click stimulation (Fig. 2D, top, red trace) (Needham and Paolini 2003). In these same two cells, a long time base reveals an additional long latency, slow and sustained hyperpolarization to off-CF tones (Fig. 2, I and J, top and middle). Sustained hyperpolarization of this type was observed in all T stellate cells in which fast inhibition was also observed. In addition, it was sometimes observed in the absence of fast, short-duration inhibition (Fig. 2, I and J, bottom). These two hyperpolarization events have different latencies and time courses, and this is particularly evident when the short-duration inhibition at tone onset is compared with the slow time course of the return to RMP following tone cessation (Fig. 2J).
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). This paradigm evokes an inhibitory postsynaptic potential (IPSP) in ipsilaterally recorded CS/T neurons (Fig. 3A, top, *). By manipulating the interval between click and electrical stimulation, an IPSP can occur prior to AP generation in T stellate cells and significantly delay it (Fig. 3, A and B).
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). The timing of inputs from the auditory nerve does not appear to be altered in this two-tone paradigm because there are similar depolarization latencies observed under all conditions (Fig. 4, A–C). This indicates that AP delay is not simply a reflection of two-tone suppression effects that occur within the cochlea (Ruggero et al. 1992). A decrease in spike regularity associated with two-tone stimulation also suggest that inhibition mediates this delay in AP activation rather than it being a property of peripheral suppression (Blackburn and Sachs 1992).
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DISCUSSION |
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; Fujino and Oertel 2001; Rhode and Greenberg 1994). These regions of hyperpolarization were short-lived and followed the known time course of D stellate inhibition (Needham and Paolini 2003). At the edge of a T stellate cell's frequency response area, fast inhibition occurred during initial depolarization and was associated with longer AP latencies to off-CF tones. When a CF tone was presented in conjunction with a tone that fell outside a cell's response area, a delay in the T stellate cell's first AP was produced. This delay was not a result of a shift in threshold because the intracellular traces indicated that the threshold of depolarization was very similar in the two-tone and CF tone alone conditions. Therefore activation of a lateral inhibitory domain can delay a T stellate cell's response to an optimal (CF) tone.
In addition to the fast, short-duration inhibition, we showed that a longer latency, sustained hyperpolarization was evoked by off-CF tones in the same cells. The latter type of hyperpolarization would explain the sustained suppression of spontaneous activity (or activity evoked by continuous background noise) by off-CF tone bursts in chopper cells (Blackburn and Sachs 1992; Rhode and Greenberg 1994; Smith and Rhode 1989). This sustained component may reflect input from the subset of D stellate cells that show low level sustained activity throughout a tone burst (Paolini and Clark 1999; Rhode and Smith 1986; Winter and Palmer 1995). Alternatively, the different latencies and time courses of these two inhibitory events might reflect different sources. This conclusion is supported by the fact that sustained inhibition was sometimes observed in isolation and that T stellate cells receive inhibitory inputs from the DCN and other brain stem regions (Benson and Potashner 1990; Ostapoff et al. 1997; Wickesberg and Oertel 1990; Wickesberg et al. 1991). Regardless of the source of this slower inhibitory component, the presence and effects of fast, short-duration inhibition described here indicate that the classic view of lateral inhibition in VCN T stellate cells should include first spike delay as one of its outcomes.
The effects we observed are consistent with the broad frequency tuning of D stellate cells and the response latency data that indicated D stellate cells can be activated before T stellate cells to frequencies at the edge of a T stellate cell's response area. We used the fast, monosynaptic connection between D stellate and T stellate cells in the opposite cochlear nucleus (Needham and Paolini 2003) to confirm that, when inhibition occurred during depolarization in a T stellate cell, the course of this event was altered, and the initial AP was significantly delayed. Overall, these results indicate that inhibition can alter the timing of tone-evoked APs in neurons at the lowest level of the auditory brain stem. The importance of the interaction between inhibition and excitation in determining spike timing has been revealed in previous studies of the auditory brain stem, including the inferior colliculus (Casseday et al. 2000; Faure et al. 2003) and the medial superior olive (Brand et al. 2002; Grothe et al. 1992).
Our results (Fig. 1), and those of other groups (Rhode and Smith 1986; Winter and Palmer 1995), indicate that D stellate cells have higher CF tone thresholds than T stellate cells. Therefore in response to a CF tone, inhibition would arrive after the first AP produced by a T stellate cell. In auditory cortex, inhibition following initial excitation improves temporal precision by reducing the spike time variability associated with the initial "barrage" of excitatory inputs that impinge on cortical neurons (Wehr and Zador 2003). A similar effect may be occurring in T stellate cells and is consistent with the findings of Young et al. (1988) who found very low first spike variability in VCN chopper neurons.
The classic view of lateral inhibition in T stellate cells depicts a wideband inhibitor (D stellate cell input) superimposed on its narrow frequency tuning curve (Ferragamo et al. 1998; Fujino and Oertel 2001). In higher auditory centers, surround inhibition can improve spectral selectivity (Jen et al. 2002; Yang et al. 1992); however, in T stellate cells, this does not appear to be the case. When glycinergic transmission is blocked (by iontophoretic application of the antagonist strychnine), there is very little or no change in the width of frequency tuning of T stellate neurons (Caspary et al. 1994). T stellate neurons also have similar widths of frequency tuning to primary-like neurons, another of the major projection neurons that show less extensive and intensive lateral inhibition than T stellate cells (Rhode and Greenberg 1994; Rhode and Smith 1986). In response to pure tones, our data indicate that the main effect of D stellate inhibition is to delay the response to tones at the edge of a cell's frequency response area. This presumably results in a greater difference in the response latency to CF versus "edge" tones than would exist in the absence of inhibition. This outcome could form the basis of an improvement in spectral selectivity if neurons at the next level of the pathway were sensitive to the time of arrival of inputs. For example, a coincidence detector receiving tonotopically mapped inputs will be optimally activated by the subset of inputs that arrives during an initial, narrow time window. Empirically, and in principle, the relative timing of inputs can be just as crucial as response magnitude to feature extractors at various levels of the auditory pathway (Brand et al. 2002; Cariani 1994; Faure et al. 2003; Park and Pollak 1993; Wehr and Zador 2003).
Thus far, we have interpreted our results in terms of their pure tone responses, and these are not particularly relevant to the spectrally and temporally complex sounds that animals encounter in their environment. D stellate cells receive input from auditory nerve fibers across isofrequency lamina and are not optimally activated by pure tones. They can show more sustained responses and lower thresholds to broadband compared with narrowband sounds, although they do retain their prominent and precise onset response (Winter and Palmer 1995). D stellate cells also respond vigorously and precisely to amplitude modulated sounds, including synthetic vowels (Palmer and Winter 1993; Rhode 1994; Wang and Sachs 1994). Therefore the extent to which D stellate cells can alter the timing and/or discharge rate of T stellate neurons would depend on the complexity of the stimulus. Finally, the effect of D stellate cell activation would not be restricted to T stellate cells with matching CFs because these inhibitory neurons are known to project quite widely within the VCN (Palmer et al. 2003; Smith and Rhode 1989). Thus they have the potential to alter the timing of the first spike response of T stellate cells in other isofrequency lamina.
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GRANTS |
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Address for reprint requests and other correspondence: A. G. Paolini, School of Psychological Science, La Trobe Univ., Bundoora, Victoria 3086, Australia (E-mail: a.paolini{at}latrobe.edu.au).
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ABSTRACT
INTRODUCTION
0.05 < P < 0.1 (t-test).
20 repetitions of a given stimulus. Cal.D: max amp = 1.8, 3, 25 mV, respectively.
