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PubMed2006

The dorsal cochlear nucleus as a participant in the auditory, attentional and emotional components of tinnitus.

The dorsal cochlear nucleus (DCN) has been modeled in numerous studies as a possible source of tinnitus-generating signals. This hypothesis was originally developed on the basis of evidence that the DCN becomes hyperactive following exposure to intense noise. Since these early observations, evidence that the DCN is an important contributor to tinnitus has grown considerably. In this paper, the available evidence to date will be summarized. In addition, the DCN hypothesis of tinnitus can now be expanded to include possible involvement in other, non-auditory components of tinnitus. It will be shown by way of literature review that the DCN has direct connections with non-auditory brainstem structures, such as the locus coeruleus, reticular formation and raphe nuclei, that are implicated in the control of attention and emotional responses. The hypothesis will be presented that attentional and emotional disorders, such as anxiety and depression, which are commonly associated with tinnitus, may result from an interplay between these non-auditory brainstem structures and the DCN. Implicit in this hypothesis is that attempts to develop effective anti-tinnitus therapies are likely to benefit from a greater understanding of how the levels of activity in the DCN are influenced by different states of activation of these non-auditory brainstem structures and vice versa.

Anxiety↗
PubMed1994

Stimulus parameters affecting tissue injury during microstimulation in the cochlear nucleus of the cat.

We investigated the effects of continuous microstimulation in the cats' posteroventral cochlear nucleus, using chronically implanted activated iridium microelectrodes. We examined 51 electrode sites (39 pulsed sites, and 12 unpulsed sites). Seven hours of continuous stimulation at 500 Hz often produced tissue injury near the tips of the pulsed microelectrodes. The damage took the form of a region of vacuolated tissue extending 200 microns or more from the site of the electrode tip. Electron microscope studies showed the vacuoles to be severely edematous segments of myelinated axons. The statistical correlation between the amount of damaged tissue and the charge per phase was large and highly significant (P < 0.0001). When the electrodes were pulsed for 7 h at 500 Hz with charge-balanced biphasic pulse pairs, the threshold for the damage was approximately 3 nC/phase. The damage threshold was not appreciably lower than the stimulation protocol was extended to 35 h (7 h/day for 5 days). In contrast, the threshold for exciting neurons near the microelectrode is approximately 1 nC/phase, as determined by the evoked response recorded in the inferior colliculus. There was little correlation between the severity of the tissue damage and the geometric charge density at the surface of the electrodes, between the damage and amplitude of the cathodic phase of the voltage transient induced across the stimulating electrodes by the stimulus current pulses, or between the damage and the stimulus pulse duration.

Animals↗
PubMed1995

Glutamatergic inhibition of voltage-operated calcium channels in the avian cochlear nucleus.

The auditory nerve serves as the only excitatory input to neurons in the avian cochlear nucleus, nucleus magnocellularis (NM). NM neurons in immature animals are dependent upon auditory nerve signals; when deprived of them, many NM neurons die, and the rest atrophy. Auditory nerve terminals release glutamate, which can stimulate second messenger systems by activating a metabotropic glutamate receptor (mGluR). Therefore, it is possible that the effectors of mGluR-stimulated signal transduction systems are needed for NM neuronal survival. This study shows that mGluR activation in NM neurons attenuates voltage-dependent changes in [Ca2+]j. Voltage-dependent Ca2+ influx was also attenuated by increasing cAMP with forskolin, VIP, or 8-bromo-cAMP, indicating that mGluR activation may stimulate adenylate cyclase. The main results may be summarized as follows. NM neurons possess high voltage-activated Ca2+ channels that were modulated by quisqualate, glutamate, and (+/-)trans-ACPD, in that order of potency. Glutamatergic inhibition of Ca2+ influx was not blocked by L-AP3 or L-AP4, which antagonize the actions of mGluRs in other neural systems; it was blocked by serine-O-phosphate. Finally, the attenuation of voltage-dependent Ca2+ influx was duplicated by cAMP accumulators. Since NM neurons have high rates of spontaneous activity and higher rates of driven activity, the expression of this mGluR turns out to be very valuable: without it, [Ca2+]j could reach lethal concentrations. These results provide an important clue as to the identity of an intracellular signal that may play an important role in NM neuronal survival.

Animals↗
PubMed1996

Response properties of units in the dorsal cochlear nucleus of unanesthetized decerebrate gerbil.

1. The electrophysiological responses of single units in the dorsal cochlear nucleus of unanesthetized decerebrate Mongolian gerbil (Meriones unguiculatus) were recorded. Units were classified according to the response map scheme of Evans and Nelson as modified by Young and Brownell, Young and Voigt, and Shofner and Young. Type II units have a V-shaped excitatory response map similar to typical auditory nerve tuning curves but little or no spontaneous activity (SpAc < 2.5 spikes/s) and little or no response to noise. Type I/III units also have a V-shaped excitatory map and SpAc < 2.5 spikes/s, but have an excitatory response to noise. Type III units have a V-shaped excitatory map with inhibitory sidebands, SpAc > 2.5 spikes/s, and an excitatory response to noise. Type IV-T units typically also have a V-shaped excitatory map with inhibitory sidebands, but have a highly nonmonotonic rate versus level response to best frequency (BF) tones like type IV units, SpAc > 2.5 spikes/s, and an excitatory response to noise. Type IV units have a predominantly inhibitory response map above an island of excitation of BF, SpAc > 2.5 spikes/s, and an excitatory response to noise. We present results for 133 units recorded with glass micropipette electrodes. The purpose of this study was to establish a normative response map data base in this species for ongoing structure/function and correlation studies. 2. The major types of units (type II, type I/III, type III, type IV-T, and type IV) found in decerebrate cat are found in decerebrate gerbil. However, the percentage of type II (7.5%) and type IV (11.3%) units encountered are smaller and the percentage of type III (62.4%) units is larger in decerebrate gerbil than in decerebrate cat. In comparison, Shofner and Young found 18.5% type II units, 30.6% type IV units, and 23.1% type III units using metal electrodes. 3. Two new unit subtypes are described in gerbil: type III-i and type IV-i units. Type III-i units are similar to type III units except that type III-i units are inhibited by low levels of noise and excited by high levels of noise whereas type III units have strictly excitatory responses to noise. Type IV-i units are similar to type IV units except that type IV-i units are excited by low levels of noise and become inhibited by high levels of noise whereas type IV units have strictly excitatory responses to noise. Type III-i units are approximately 30% of the type III population and type IV-i units are approximately 50% of the type IV population. 4. On the basis of the paucity of classic type II units and the reciprocal responses to broadband noise of type III-i and type IV-i units, we postulate that some gerbil type III-i units are the same cell type and have similar synaptic connections as cat type II units. 5. Type II and type I/III units are distinguished from one another on the basis of both their relative noise response, rho, and the normalized slope of the BF tone rate versus level functions beyond the first maximum. Previously, type II units were defined to be those nonspontaneously active units with rho values < 0.3 where rho is defined as the ratio of the maximum noise response minus spontaneous rate to the maximum BF tone response minus spontaneous rate. In the gerbil, the average rho value for type II units is 0.25, although a few values are > 0.3, and the rate-level curves are consistently nonmonotonic with normalized slopes steeper than than -0.007/dB. The average rho value for type I/III units is 0.54, although a few values are < 0.3, and the rate-level curves tend to saturate with slopes shallower than -0.006/dB. In general, the response properties of type II units recorded in gerbil are similar to those recorded in decerebrate cat. 6. In comparison to decerebrate cat, the lower percentage of type IV units recorded in decerebrate gerbil may be due to a species difference (a reduced number of type II units in gerbil) or an electrode bias.

Animals↗
PubMed1993

Maintenance of pharmacologically-immature glutamate receptors by aberrant synapses in the chick cochlear nucleus.

Surgical destruction of the otocyst in chick embryos prevents formation of the *** ear, abolishes normal cochlear input to the cochlear nucleus (nucleus magnocellularis, NM) and results in axons from the contralateral NM forming (in addition to their normal bilateral endings in nucleus laminaris, NL) a novel and functional aberrant projection to the deafferented NM. We studied the pharmacology of synaptic transmission at aberrant synapses in an in vitro preparation of the brainstem in chick embryos and hatchlings. Transmission at the aberrant synapses (as with cochlear nerve synapses in NM and NM synapses in NL) is blocked by the quinoxalinedione antagonists CNQX and NBQX, confirming the presence of excitatory amino acid receptors of the non-NMDA subtype. At cochlear nerve synapses in NM, the antagonist potency of NBQX normally decreases rapidly after embryonic day (E)18 (IC50 = 0.69 +/- 0.06 microM, mean +/- S.E.M.), reaching an asymptotic value by E21 (IC50 = 2.7 +/- 0.4 microM) that is maintained at least through posthatching day (P)14 (IC50 = 3.6 +/- 0.3 microM). In the case of the aberrant endings, the potency of NBQX remained (from E21 [IC50 = 0.6 +/- 0.1 microM] through at least P14[IC50 = 0.5 +/- 0.1 microM]) at levels that are statistically indistinguishable from the E18 value for normal cochlear nerve synapses.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1983

Pharmacologic evidence for synaptic transmission mediated by non-N-methyl-D-aspartate receptors in the avian cochlear nucleus.

The hypothesis that synaptic transmission between the auditory nerve and the cochlear nucleus is mediated by an excitatory amino acid acting through N-methyl-D-aspartate (NMDA) receptors was examined in an in vitro preparation of the chicken brainstem. The ability of various bath-applied excitatory amino acid receptor antagonists to inhibit synaptically-evoked responses was assessed by recording field potentials from nucleus magnocellularis (NM) following electrical stimulation of the cochlear nerve. Antagonists that selectively block responses mediated by NMDA receptors, such as D-alpha-aminoadipate and 2-amino-5-phosphonovalerate, were without effect on evoked transmission in NM. In contrast, antagonists that additionally act on non-NMDA receptors, such as cis-2,3-piperidine dicarboxylate and gamma-D-glutamylglycine, reversibly suppressed transmission. The results indicate that (1) transmission in the chicken auditory system is mediated by non-NMDA receptors, and (2) a substance(s) chemically akin to aspartate and glutamate may be the transmitter used by the auditory nerve in NM.

Animals↗
PubMed1983

Differential uptake of H3-amino acids in the cat cochlear nucleus.

A fresh brain-slice preparation that allows simultaneous characterization of the anatomic localization of radioactively labeled substances in a variety of different auditory brain stem areas has been used to examine localization patterns for a number of putative neurotransmitter amino acids in the anteroventral and dorsal cochlear nuclei of the cat. Following incubation of fresh brain sections in oxygenated salt solutions containing micromolar amounts of the tritiated amino acids, differences in the pattern of label localization are revealed by light microscopic autoradiography. Electron microscopic autoradiography of the same material demonstrates that the label is restricted to different synaptic terminal populations. In the dorsal cochlear nucleus, gamma aminobutyric acid (GABA) and glutamic acid incubations label two different terminal populations in the molecular layer. Glycine incubation labels a population more uniformly distributed among the molecular, fusiform cell, and deep layers. In the anteroventral cochlear nucleus the pattern after GABA and glycine incubations is similar, with multiple endings on all spherical cells labeled. Studies are underway to characterize fully the different labeling patterns and the conditions under which they occur.

Amino Acids↗
PubMed2000

An immunogold investigation of the relationship between the amino acids GABA and glycine and their transporters in terminals in the guinea-pig anteroventral cochlear nucleus.

The majority of terminals contacting spherical bushy cell bodies in the guinea-pig anteroventral cochlear nucleus contain GABA, glycine or both (colocalizing). Double labeling with antibodies to each amino acid and the plasma membrane transporter for the other was performed using different sizes of gold particles. The transporter for GABA occurs in the plasma membranes of some terminals containing glycine and vice versa suggesting that colocalizing terminals can retrieve both amino acids.

Amino Acid Transport Systems, Neutral↗
PubMed2000

Calretinin expression in the chick cochlear nucleus after deafferentation.

The expression of the calcium-binding protein calretinin (CR) in the chick cochlear nucleus, nucleus magnocellularis (NM), was examined after unilateral cochlea removal in hatchlings and 3-week-old birds. Following survival times of 3, 6 or 12 h or 1, 3 or 7 days, CR mRNA was localized by in situ hybridization using a radiolabeled chick CR probe. Levels of CR protein were assessed by CR-immunoreactivity (CR-I) using a calcium-independent CR antiserum and immunohistochemistry. At survival times of 1 day or less, cochlea removal did not change relative levels of CR mRNA or CR-I in NM between the deafferented and the unoperated sides of the brain. Decreases in CR expression on the cochlea removal side were observed, however, at times that coincide with deafferentation-induced cell loss (3 and 7 days). Additionally, bilateral cochlea removal had no apparent effect on CR-I in NM neurons when compared to those in normal animals. Thus, CR mRNA and protein appear to be constitutively expressed in NM neurons and are not affected by sensory deprivation.

Afferent Pathways↗
PubMed2001

Representation of harmonic complex stimuli in the ventral cochlear nucleus of the chinchilla.

The representation of Schroeder-phase harmonic complex sounds in the ventral cochlear nucleus (VCN) of the anesthetized chinchilla was studied. Stimuli consisted of a series of harmonically related sinusoids, multiples of a fundamental frequency (f0), summed in either negative (-SCHR) or positive (+SCHR) Schroeder phase. Psychoacoustic experiments performed in humans by other investigators have revealed that masking effects of -SCHR stimuli are larger than those found using +SCHR stimuli as maskers. In our laboratory, basilar membrane measurements at the base of the chinchilla cochlea show that responses to -SCHR stimuli are less "peaked," or modulated, than responses to +SCHR stimuli. We also found that suppression of a characteristic-frequency (CF) tone by -SCHR stimuli is larger than that evoked by +SCHR stimuli. Rate-intensity functions display higher firing rates in responses to -SCHR stimuli than in those produced by +SCHR stimuli. Firing rates evoked by either -SCHR or +SCHR stimuli saturate at lower values than those obtained in responses to CF tones. Rate and synchrony suppressions by -SCHR stimuli were larger than those evoked by +SCHR stimuli. Auditory nerve fiber responses to Schroeder complex stimuli share most of the properties of VCN responses, indicating little additional processing by the VCN.

Animals↗
PubMed2003

[Risk functions and expected spike density functions for neurons in the cat cochlear nucleus].

The temporal properties of spontaneous and (or) evoked discharges of 157 neurons localized in dorsal cochlear nucleus of anaesthetized cats have been studied. Tone bursts were presented at stimulus best frequency in a free field from the side of ipsilateral ear. About half of cells were characterized by paused or build-up types of the discharge. For all such units a long lasting post-spike decrease in excitability could be seen from the analysis of hazard functions of spontaneous and evoked activity. As a result, the time dependence of conditional probability of the first crossing of the threshold (under condition of an absence of previous response spikes) or expecting probability function (EPF) were over the usual peristimulus histograms. Units with chopper discharges usually did not demonstrate alternative peaks in EPF. We interpreted this fact as evidence that chopper discharge pattern is a result of strong post spike decrease in excitability. Such pattern doesn't demonstrate an existence of real periodicity of the unit. In primary-like units the hazard functions demonstrated only minor after-spike decrease of excitability, and the EPFs were similar to the initial part of peristimulus histograms. Type II units (presumably inhibitory cells) were characterized by non-monotonous hazard functions and by a tendency to burst response patterns. In some cells, we observed a tendency to existence of real intrinsic oscillations both in the EPFs and hazard functions.

Acoustic Stimulation↗
PubMed2004

Noise trauma alters D-[3H]aspartate release and AMPA binding in chinchilla cochlear nucleus.

Exposure of adults to loud noise can overstimulate the auditory system, damage the cochlea, and destroy cochlear nerve axons and their synaptic endings in the brain. Cochlear nerve loss probably results from the death of cochlear inner hair cells (IHC). Additional degeneration in the cochlear nucleus (CN) is hypothesized to stem from overstimulation of the system, which may produce excitotoxicity. This study tested these predictions by exposing one ear of anesthetized adult chinchillas to a loud noise, which damaged the ipsilateral cochlea and induced degeneration in the glutamatergic cochlear nerve. During the first postexposure week, before cochlear nerve axons degenerated, glutamatergic synaptic release in the ipsilateral CN was elevated and uptake was depressed, consistent with hyperactivity of glutamatergic transmission and perhaps with the operation of an excitotoxic mechanism. By 14 days, when cochlear nerve fibers degenerated, glutamatergic synaptic release and uptake in the CN became deficient. By 90 days, a resurgence of transmitter release and an elevation of AMPA receptor binding suggested transmission upregulation through plasticity that resembled changes after mechanical cochlear damage. These changes may contribute to tinnitus and other pathologic symptoms that precede and accompany hearing loss. In contrast, the other ear, protected with a silicone plug during the noise exposure, exhibited virtually no damage in the cochlea or the cochlear nerve. Altered glutamatergic release and AMPA receptor binding activity in the CN suggested upregulatory plasticity driven by signals emanating from the CN on the noise-exposed side.

Animals↗
PubMed2006

Summary of evidence pointing to a role of the dorsal cochlear nucleus in the etiology of tinnitus.

Evidence has accumulated in the last decade that the dorsal cochlear nucleus (DCN) may be an important site in the etiology of tinnitus. This evidence comes from a combination of studies conducted in animals and humans. This paper will review the key findings, as follows. 1) Direct electrical stimulation of the DCN leads to changes in the loudness of tinnitus. This suggests that the loudness of tinnitus may be linked to changes in the level of neural activity in the DCN. 2) Exposure to tinnitus inducers, such as intense sound or cisplatin, causes neural activity in the DCN to become chronically elevated, a condition known as neuronal hyperactivity. 3) This hyperactivity is very similar to the activity that is evoked in the DCN by sound stimulation, suggesting that the hyperactivity represents a code that signals the presence of sound, even when there is no longer any sound stimulus. 4) Noise-induced hyperactivity in the DCN is correlated with tinnitus. Behavioral studies have demonstrated that animals exposed to the same intense sound that causes hyperactivity in the DCN develop tinnitus-like percepts. The correlation between the level of hyperactivity and the behavioral index of tinnitus was found to be statistically significant. 5) The DCN is a polysensory integration center, and electrophysiological studies have shown that both spontaneous activity and hyperactivity of neurons in the DCN can be modulated by stimulation of certain ipsilateral cranial nerves, such as the sensory branch of the trigeminal nerve. This ipsilateral modulation of DCN activity offers a plausible explanation of how tinnitus, when perceived on one side, can be modulated by certain manipulations of the head and neck on the side ipsilateral to the tinnitus, but rarely on the contralateral side. 6) The DCN exhibits various forms of neuronal plasticity that parallel the various forms of plasticity that characterize tinnitus. These findings collectively strengthen the view that the DCN may be a key structure that should be included as a target of anti-tinnitus treatment.

Acoustic Stimulation↗
PubMedDate not supplied

Mathematical models of cochlear nucleus onset neurons: II. model with dynamic spike-blocking state.

Onset (On) neurons in the cochlear nucleus (CN), characterized by their prominent response to the onset followed by little or no response to the steady-state of sustained stimuli, have a remarkable ability to entrain (firing 1 spike per cycle of a periodic stimulus) to low-frequency tones up to 1000 Hz. In this article, we present a point-neuron model with independent, excitatory auditory-nerve (AN) inputs that accounts for the ability of On neurons to both produce onset responses for high-frequency tone bursts and entrain to a wide range of low-frequency tones. With a fixed-duration spike-blocking state after a spike (an absolute refractory period), the model produces entrainment to a broad range of low-frequency tones and an On response with short interspike intervals (chopping) for high-frequency tone bursts. To produce On response patterns with no chopping, we introduce a novel, more complex, active membrane model in which the spike-blocking state is maintained until the instantaneous membrane voltage falls below a transition voltage. During the sustained depolarization for a high-frequency tone burst, the new model does not chop because it enters a spike-blocking state after the first spike and fails to leave this state until the membrane voltage returns toward rest at the end of the stimulus. The model entrains to low-frequency tones because the membrane voltage falls below the transition voltage on every cycle when the AN inputs are phase-locked. With the complex membrane model, On response patterns having moderate steady-state activity for high-frequency tone bursts (On-L) are distinguished from those having no steady-state activity (On-I) by requiring fewer AN inputs. Voltage-gated ion channels found in On-responding neurons of the CN may underlie the hypothesized dynamic spike-blocking state. These results provide a mechanistic rationale for distinguishing between the different physiological classes of CN On neurons.

Acoustic Stimulation↗
PubMed1997

Performance over time of adult patients using the Ineraid or nucleus cochlear implant.

This study examined the average and individual performance over time of 49 adult cochlear implant subjects. Subjects were randomly assigned to receive either the Ineraid cochlear implant, with analog processing, or the Nucleus cochlear implant, with feature-extraction processing. All subjects had postlingual profound bilateral sensorineural hearing loss and received no significant benefit from hearing aids before implantation. Group data were examined in two ways. First, only subjects who had complete data over the test period were examined. Second, an analysis of all available data was carried out by mixed linear-model analysis. In this analysis, to account for missed follow-ups at the planned intervals, data consisting of the observations closest in time to the planned test times were modeled by natural splines with knots at the planned follow-up times. Contrasts between all pairs of planned follow-up times for each device were tested, as were contrasts between devices at each planned follow-up time. Results indicated little difference between the performance of the Ineraid and Nucleus subjects in their level of performance or their rate of learning. Postimplantation performance was typically superior to preimplantation performance within 9 months, and continued to improve up to 18-30 months depending on the speech perception measure. In some subjects, improvements in speech perception measures were observed up to four or five years postimplantation. There was also evidence that three subjects had a decrement in overall speech perception performance, although their postimplantation scores were always higher than their preimplantation scores. In at least one subjects this was likely a result of age-related cognition decrements.

Adult↗
PubMed1994

Two separate inhibitory mechanisms shape the responses of dorsal cochlear nucleus type IV units to narrowband and wideband stimuli.

1. The principal cells of the dorsal cochlear nucleus (DCN) are mostly inhibited by best frequency (BF) tones but are mostly excited by broadband noise (BBN), producing the so-called type IV response characteristic. The narrowband inhibitory responses can be explained by the inhibitory influence of interneurons with type II response characteristics. However, it is not clear that all the details of the type IV responses can be accounted for by this neural circuit. In particular, many type IV units are inhibited by band-reject noise (notch noise); type II units tend to be only weakly excited by these stimuli, if at all. In this paper we study the relationships between the narrowband, inhibitory and the wideband, excitatory regimens of the type IV responses and present the case for the existence of a second inhibitory source in DCN, called the wideband inhibitor (WBI) below. 2. Type IV units were studied using pure tones, noise bands arithmetically centered on BF, notch noise centered on BF, and BBN. We measured the rate-level function (response rate as function of stimulus level) for each stimulus. This paper is based on the responses of 28 type IV units. 3. Evidence for low-threshold inhibitory input to type IV units is derived from analysis of rate-level functions at sound levels just above threshold. Notch noise stimuli of the appropriate notch width produce inhibition at threshold in this regime. When BBN is presented, this inhibition appears to summate with excitation produced by energy in the band of noise centered on BF, resulting in BBN rate-level functions with decreased slope and maximum firing rate. A range of slopes and maximal firing rates is observed, but these variables are strongly correlated and they are negatively correlated with the strength of the inhibition produced by notch noise; this result supports the conclusion that a single inhibitory source is responsible for these effects. 4. By contrast, there is a weak (nonsignificant) positive correlation between the strength of the inhibitory effect of notch noise and the slope/maximal firing rate in response to narrowband stimuli, including BF tones. The contrast between this positive nonsignificant correlation and the significant negative correlation mentioned above suggests that more than one inhibitory effect operates: specifically, the type II input is responsible for inhibition by narrowband stimuli and a different inhibitory source, the WBI, produces inhibition by notch stimuli. 5. Several lines of evidence are given to show that type II units cannot produce the inhibition seen with notch noise stimuli.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Dorsal cochlear nucleus single neurons can enhance temporal processing capabilities in background noise.

Envelope temporal fluctuations are critical for effective processing of biologically relevant sounds including speech, animal vocalizations, sound-source location and pitch. Amplitude modulation (AM) of sound envelopes can be encoded in quiet with high fidelity by some auditory neurons, including those of the cochlear nucleus. From both neurophysiological and clinical perspectives, it is important to understand the effects of background noise on the processing of AM. To further this goal, single-unit recordings were made from dorsal cochlear nucleus (DCN) units in urethane-anesthetized chinchillas. All units of this study were classified as pauser/buildup or On-s units according to PSTH response patterns, first spike latencies, and shape of best-frequency (BF) rate-intensity functions. BF pure-tone and AM (10-500 Hz) tone bursts were presented at several sound levels, in quiet and in the presence of a continuous wideband masker. The following was found: (1) DCN units can enhance their AM coding relative to quiet in the presence of loud noise (+14 or +19 dB S/N) and at high signal levels (e.g. 75 dB SPL); (2) for the sample of units of the present study, this is usually achieved by lowering the average firing rate and increasing the synchronous (fundamental frequency) response; (3) for some units, the AM coding stays the same or declines in the background noise. The nature of these findings suggests that part of a DCN unit's abilities to preserve or enhance AM coding with masking noise results from peripheral operating range shifts, whereas part comes from intrinsic circuitry (inhibitory inputs) or cellular mechanisms (dendritic filtering of sound temporal features) within the DCN.

Acoustic Stimulation↗
PubMed1992

Rapid changes in protein synthesis and cell size in the cochlear nucleus following eighth nerve activity blockade or cochlea ablation.

Destruction of the cochlea causes secondary changes in the central auditory pathway through transynaptic regulation. These changes appear to be mediated by an activity-dependent process and can be detected in the avian auditory system as early as 30 minutes after deafferentation. We compared the early changes in cochlear nucleus neurons following deafferentation by cochlea ablation with those seen following activity deprivation by perilymphatic tetrodotoxin (TTX) exposure. Protein synthesis and size of large spherical cells in the anteroventral cochlear nucleus (AVCN) of 14-day-old gerbils were measured during the first 48 hours after the manipulations. Both cochlea ablation and TTX produced a reliable decrease in protein synthesis by AVCN neurons (30-40%) by 1 hour. The magnitude of change in tritiated leucine incorporation was similar at all survival times, in both experimental groups. In contrast to the rapid changes in protein synthesis, the decrease in cell size was first evident 18 hours after TTX exposure and 48 hours after cochlea ablation. There was no significant change in protein synthesis or cell size in control groups at any of the survival times. These findings are consistent with changes in the avian auditory system in response to deafferentation and TTX exposure. Cochlea ablation and TTX exposure induced similar transneuronal changes, supporting the hypotheses that activity of auditory afferents in young mammals plays a regulatory role in the metabolism and morphology of their target neurons in the central auditory pathway, and that early changes following destruction of the peripheral receptor are due to reduction of activity-dependent interactions of presynaptic and postsynaptic cells.

Analysis of Variance↗