Role of acoustic striae in hearing: discrimination of sound-source elevation

After years of systematic experimentation, we finally uncovered one thing the dorsal system contributes to hearing which the ventral system may not – the mechanism for orienting to an elevated sound source [Sutherland, D.P., Masterton, R.B., Glendenning, K.K. (1998) Behav. Brain Res. in press]. This paper follows up this one positive result on a historical background of uniformly negative results. The focus of this report is on the fusiform cells of the dorsal cochlear nucleus whose axons course through the dorsal acoustic stria (DAS). Because electrophysiological studies have shown that the cues for sensing the elevation of a sound source would seem to be best analyzed by the dorsal cochlear nucleus, we tested, behaviorally, normal cats and cats deprived of their DAS or intermediate acoustic stria, bilaterally or ipsilaterally (with or without their contralateral ear deafened), for their ability to orient to elevated sources of broad-band noise. For behavioral testing, we made use of a conventional shock-avoidance procedure. The results lead to the conclusion that DCN and DAS may play no role in learned elevation discriminations. This result builds on that of another of our papers which suggests that a deficit in reflexive discrimination of elevation is strictly auditory in nature [Sutherland, D.P., Masterton, R.B., Glendenning, K.K. (1998) Behav. Brain Res. in press].     

Auditory Processing of Spectral Cues for Sound Localization in the Inferior Colliculus

The head-related transfer function (HRTF) of the cat adds directionally dependent energy minima to the amplitude spectrum of complex sounds. These spectral notches are a principal cue for the localization of sound source elevation. Physiological evidence suggests that the dorsal cochlear nucleus (DCN) plays a critical role in the brainstem processing of this directional feature. Type O units in the central nucleus of the inferior colliculus (ICC) are a primary target of ascending DCN projections and, therefore, may represent midbrain specializations for the auditory processing of spectral cues for sound localization. Behavioral studies confirm a loss of sound orientation accuracy when DCN projections to the inferior colliculus are surgically lesioned. This study used simple analogs of HRTF notches to characterize single-unit response patterns in the ICC of decerebrate cats that may contribute to the directional sensitivity of the brain's spectral processing pathways. Manipulations of notch frequency and bandwidth demonstrated frequency-specific excitatory responses that have the capacity to encode HRTF-based cues for sound source location. These response patterns were limited to type O units in the ICC and have not been observed for the projection neurons of the DCN. The unique spectral integration properties of type O units suggest that DCN influences are transformed into a more selective representation of sound source location by a local convergence of wideband excitatory and frequency-tuned inhibitory inputs.     

Development of hyperactivity after hearing loss in a computational model of the dorsal cochlear nucleus depends on neuron response type

Cochlear damage can change the spontaneous firing rates of neurons in the dorsal cochlear nucleus (DCN). Increased spontaneous firing rates (hyperactivity) after acoustic trauma have been observed in the DCN of rodents such as hamsters, chinchillas and rats. This hyperactivity has been interpreted as a neural correlate of tinnitus. In cats, however, the spontaneous firing rates of DCN neurons were not significantly elevated after acoustic trauma. Species-specific spontaneous firing rates after cochlear damage might be attributable to differences in the response types of DCN neurons: In gerbils, type III response characteristics are predominant, whereas in cats type IV responses are more frequent. To address the question of how the development of hyperactivity after cochlear damage depends on the response type of DCN neurons, we use a computational model of the basic circuit of the DCN. By changing the strength of two types of inhibition, we can reproduce salient features of the responses of DCN neurons. Simulated cochlear damage, which decreases the activity of auditory nerve fibers, is assumed to activate homeostatic plasticity in projection neurons (PNs) of the DCN. We find that the resulting spontaneous firing rates depend on the response type of DCN PNs: PNs with type III and type IV-T response characteristics may become hyperactive, whereas type IV PNs do not develop increased spontaneous firing rates after acoustic trauma. This theoretical framework for the mechanisms and circumstances of the development of hyperactivity in central auditory neurons might also provide new insights into the development of tinnitus.     

Response of the cochlear nucleus neurons of the cat to tone-burst-trains

Although both posteroventral cochlear nucleus (PVCN) and dorsal cochlear nucleus (DCN) are innervated by the descending branch of auditory nerve fibers, their intrinsic morphological organizations are so different that their physiological roles are expected to be different in signal processing. Temporal information coding of acoustic signals in the cochlear nucleus was examined by using stimuli of "tone-burst-trains (TBT)". Responses of cochlear nucleus neurons of anesthetized cats were recorded either intracellularly or extracellularly. Responses of the neurons to TBT stimuli were classified into "adaptive type" and "non-adaptive type". The "adaptive type" neurons were mainly recorded from PVCN. Responses of these neurons to TBT stimuli decayed exponentially, because of short-term adaptation, in the subsequent tone-bursts. These neurons faithfully preserve the adaptative behavior of auditory nerve fibers. On the contrary, the "non-adaptive type" neurons were mainly found in DCN. They showed variety of responses to TBT stimuli including facilitation, disinhibition and inhibition depending on duration and/or interval of tone-bursts. Our results suggest that some "non-adaptive type" neurons, showing facilitative and/or inhibitory responses to TBT stimuli, act as temporal filters that extract temporal information from acoustic signals.     

The Structural Development of the Mouse Dorsal Cochlear Nucleus

The dorsal cochlear nucleus (DCN) is a major subdivision of the mammalian cochlear nucleus (CN) that is thought to be involved in sound localization in the vertical plane and in feature extraction of sound stimuli. The main principal cell type (pyramidal cells) integrates auditory and non-auditory inputs, which are considered to be important in performing sound localization tasks. This study aimed to investigate the histological development of the CD-1 mouse DCN, focussing on the postnatal period spanning the onset of hearing (P12). Fluorescent Nissl staining revealed that the three layers of the DCN were identifiable as early as P6 with subsequent expansion of all layers with age. Significant increases in the size of pyramidal and cartwheel cells were observed between birth and P12. Immunohistochemistry showed substantial changes in synaptic distribution during the first two postnatal weeks with subsequent maturation of the presumed mossy fibre terminals. In addition, GFAP immunolabelling identified several glial cell types in the DCN including the observation of putative tanycytes for the first time. Each glial cell type had specific spatial and temporal patterns of maturation with apparent rapid development during the first two postnatal weeks but little change thereafter. The rapid maturation of the structural organization and DCN components prior to the onset of hearing possibly reflects an influence from spontaneous activity originating in the cochlea/auditory nerve. Further refinement of these connections and development of the non-auditory connections may result from the arrival of acoustic input and experience dependent mechanisms.     

Changes in the tonotopic map of the dorsal cochlear nucleus following induction of cochlear lesions by exposure to intense sound.

Hamsters were exposed to intense tones (10 kHz) at levels and durations sufficient to cause stereocilia lesions. The purpose was to determine how the tonotopic map of the dorsal cochlear nucleus (DCN) readjusts to loss of receptor sensitivity. Neural population thresholds and tonotopic organization was mapped over the surface of the DCN in normal unexposed animals and those showing tone-induced lesions. The results indicate that cochlear lesions characterized mainly by loss of stereocilia in a restricted portion of the organ of Corti cause changes in a corresponding region of the tonotopic map which reflect primarily changes in the shape and thresholds of neural tuning curves. In many cases the center of the lesion was represented in the DCN as a distinct characteristic frequency (CF) gap in the tonotopic map in which responses were either extremely weak or absent. In almost all cases the map area representing the center of the lesion was bordered by an expanded region of near-constant CF, a feature superficially suggestive of map reorganization. These expanded map areas had abnormal tip thresholds and showed other features suggesting that their CFs had been shifted downward by distortion and deterioration of their original tips. Such changes in neural tuning are similar to those observed by others in the auditory nerve following acoustic trauma, and thus would seem to have a peripheral origin. Thus, it is not necessary to invoke plastic changes in the cochlear nucleus to explain the changes observed in the tonotopic map.     

Effects of acoustic trauma on dorsal cochlear nucleus neuron activity in slices

Previous studies found increased multi-unit spontaneous activity in the dorsal cochlear nucleus (DCN) of animals that had been exposed to intense sound. Such activity may be related to tinnitus. Our study examined effects of previous exposure to intense sound on single neurons in the DCN, by measuring spontaneous activities and sensitivities to acetylcholine, an important neurotransmitter of centrifugal pathways to the cochlear nucleus, in brain slices. Spontaneous discharges were recorded extracellularly in the DCN portion of brain slices from control and intense-tone-exposed rats. Slices from exposed rats showed increased prevalence of bursting and decreased regular spontaneous activity. Since regular neurons include fusiform cells, and bursting neurons include cartwheel cells, intense tone exposure may lead to increased activity of DCN cartwheel cells and decreased activity of fusiform cells. Alternatively, the activity of some fusiform cells might change to bursting. Intense tone exposure also appeared to increase bursting neuron sensitivity to carbachol. This suggests that changes in DCN cartwheel cell spontaneous activity may reflect changes in effects of cholinergic centrifugal pathways following intense tone exposure. We conclude that acoustic trauma may lead to changes in the physiology and pharmacology of DCN neurons. These changes may be related to underlying mechanisms of central tinnitus.     

Electrophysiological and HRP studies of the direct afferent inputs from the cochlear nuclei to the tensor tympani muscle motoneurons in the cat

The direct fiber connections from the cochlear nuclei to the tensor tympani muscle (TTM) motoneurons were investigated by means of electrophysiological and horseradish peroxidase (HRP) methods, using cats. When HRP was injected into motoneuron region of the TTM, HRP-labelled cells were found bilaterally in the dorsal cochlear nucleus (DCN) and ventral cochlear nucleus (VCN). When the electrical stimulus was applied to the cochlear nucleus, the TTM motoneurons fired spikes monosynaptically with s short latency. These histological and electrophysiological results indicate the existence of direct fiber connections from the bilateral cochlear nuclei to the TTM motoneurons.     

The effect of brainstem lesions on brainstem auditory evoked potentials in the cat

Brainstem auditory evoked potentials (BAEPs) were recorded before and after cuts were made in either the midline trapezoid body (TB), the lateral lemniscus (LL), or the combined dorsal and intermediate acoustic striae (DAS/IAS) in 23 anesthetized cats. Monaural and binaural rarefaction clicks were presented at a rate of 10 per s, and the potentials recorded from a vertex electrode referenced to either earbar or to the neck. The potentials were filtered so that fast and slow components could be examined separately and special efforts were exerted to obtain stable conditions so that small changes in waveforms could be significant. Lesions of the DAS/IAS produced negligible changes in either the fast or slow waves. Lesions of the midline TB reduced the amplitudes of peaks P3 through P5, while greatly reducing the amplitude of the slow wave. Complete lesions of the LL always reduced the amplitude of the slow wave. Lesions of the ventral part of the LL were more likely to reduce the amplitude of P4-P5. Our interpretations of these lesion experiments are based on the idea that individual fast peaks of the BAEP represent compound action potentials of fiber pathways. According to this view, only synchronized activity generated in populations of neurons that are both favorably oriented in space and significant in number, will contribute to the fast peak.     

The cochlear nuclei in two patients with Usher syndrome type I

Hypothesis: Does long-term sound deprivation lead to degeneration of the cochlear nuclei in two Usher type I patients? Methods: The cochlear nuclei of these patients were morphometrically analyzed and compared with two age-matched controls. Routine autopsy of the brainstems was performed before the design of this study was known. During this procedure, the ventral cochlear nucleus (VCN) can easily be damaged. Five partially damaged VCN could nevertheless be analyzed for this study, including the right VCN of Usher patient I and both VCN of Usher patient 2. Using 15 μm thick serial paraffine sections of the cochlear nuclei, estimates of volume, neuronal densities, number of cells and mean cell diameter of the dorsal cochlear nucleus (DCN) and VCN were obtained. Results: This study presents unique material of the cochlear nuclei in two patients with Usher syndrome type I. Data regarding volume and total cell number of the VCN are influenced by the absence of a part of the VCN. Results suggest a decrease in mean cell diameter of the VCN in Usher patients. Other parameters of the VCN and DCN, however, showed no major differences between Usher type I patients and controls. Conclusion: Only minor degenerative changes are apparent in the cochlear nuclei of two patients with Usher type I, who were deprived of acoustic stimuli since birth.     

The effect of dorsal cochlear nucleus ablation on tinnitus in rats

A growing body of evidence implies that the dorsal cochlear nucleus (DCN) plays an important role in tinnitus. To test the hypothesis that the rostral output of the DCN is necessary for the experience of chronic tinnitus, the dorsal DCN and the dorsal acoustic stria of rats with psychophysical evidence of tinnitus was ablated. If the DCN plays a necessary role in the generation of chronic tinnitus, ablating the DCN should decrease the evidence of tinnitus in subjects previously shown to have tinnitus. Contrary to prediction, bilateral dorsal DCN ablation did not significantly (n=11, p=0.707) affect the psychophysical evidence of tinnitus, and ipsilateral dorsal DCN ablation appeared to increase the evidence of tinnitus (n=9, p=0.018) compared to pre-ablation performance. It was concluded that the DCN does not act as a simple feed-forward source of chronic tinnitus. Alternative hypotheses were considered, among them that elevated DCN activity following acoustic trauma triggers persistent pathological changes distributed across more than one level of the auditory system. In addition to serving as a trigger, the DCN may also modify the experience of tinnitus, since the evidence of tinnitus was enhanced by ipsilateral DCN ablation.     

Inner ear lesion alters acoustically induced c-Fos expression in the rat auditory rhomboencephalic brainstem.

The pattern of c-Fos expression was mapped in the adult rat's brain following unilateral cochlear lesions. In normal and cochlear lesioned rats, c-Fos expression was induced with sound stimuli. Acoustic stimulation consisted of pulses of four tones. An additional control group consisted of non-stimulated rats. In the cochlear nuclei (CN), c-Fos activation was scarce in isolated rats and increased strongly following sound stimulation. Following unilateral cochlear lesion, acoustically driven expression was decreased in all CN in both the lesioned and the untreated sides. The ventromedial periolivary nucleus and the rostral periolivary nucleus showed c-Fos activation in isolated conditions and were strongly activated following sound stimulation. The rest of the superior olivary complex showed no c-Fos activation in isolated rats and a weak activation following sound stimulation. Following unilateral cochlear lesions, acoustically driven expression was decreased in some, but not all superior olivary nuclei in both the lesioned and the untreated sides. In the lateral lemniscus complex, c-Fos activation was scarce in isolated rats and increased strongly after stimulation. Following unilateral cochlear lesion, acoustically driven expression decreased bilaterally in all nuclei. We have found that unilateral inner ear lesions lead to bilateral impairment of the capability of acoustic pathway neurons, to being c-Fos-activated following sound stimulation.     

Development of mature microcystic lesions in the cochlear nuclei of the Mongolian gerbil, Meriones unguiculatus

Microcystic lesions are a persistent final stage in a neurodegenerative disorder characteristic of the cochlear nuclei of gerbils. When gerbils of various ages raised under known acoustic conditions were examined, the volume density and number of lesions increased with age, however, the affected region was restricted to the posteroventral cochlear nucleus and adjacent portions of the dorsal cochlear nucleus, interstitial nucleus and posterior anteroventral cochlear nucleus. Lesions were also noted in a separate locus in the auditory nerve trunk associated with the acoustic nerve nucleus. The fusiform and molecular layers of the dorsal cochlear nucleus were spared at all ages observed. The spherical cell region of the anteroventral cochlear nucleus was also largely spared. A good correlation was observed between the cumulative input from the auditory nerve fibers caused by the ambient acoustic environment acting over the life of the animal and the number of lesions in tonotopic subdivisions of the cochlear nuclei. The earliest microcysts formed in regions receiving auditory nerve fibers most strongly stimulated by the ambient noise. Thereafter, short exposures to higher levels of input or long exposures to lower levels of input were quantitatively equivalent in producing microcystic lesions.     

Development of mature microcystic lesions in the cochlear nuclei of the mongolian gerbil, Meriones unguiculatus

Microcystic lesions are a persistent final stage in a neurodegenerative disorder characteristic of the cochlear nuclei of gerbils. When gerbils of various ages raised under known acoustic conditions were examined, the volume density and number of lesions increased with age, however, the affected region was restricted to the posteroventral cochlear nucleus and adjacent portions of the dorsal cochlear nucleus, interstitial nucleus and posterior anteroventral cochlear nucleus. Lesions were also noted in a separate locus in the auditory nerve trunk associated with the acoustic nerve nucleus. The fusiform and molecular layers of the dorsal cochlear nucleus were spared at all ages observed. The spherical cell region of the anteroventral cochlear nucleus was also largely spared. A good correlation was observed between the cumulative input from the auditory nerve fibers caused by the ambient acoustic environment acting over the life of the animal and the number of lesions in tonotopic subdivisions of the cochlear nuclei. The earliest microcysts formed in regions receiving auditory nerve fibers most strongly stimulated by the ambient noise. Thereafter, short exposures to higher levels of input or long exposures to lower levels of input were quantitatively equivalent in producing microcystic lesions.     

Mechanisms of synaptic plasticity in the dorsal cochlear nucleus: plasticity-induced changes that could underlie tinnitus

PURPOSE: Tinnitus is the persistent perception of a subjective sound. Tinnitus is almost universally experienced in some forms. In most cases, recovery may occur in seconds, hours, or days. How does tinnitus shift from a transient condition to a lifelong disorder? Several lines of evidence, including clinical studies and animal models, indicate that the brain, rather than the inner ear, may in some cases be the site of maintenance of tinnitus. One hypothesis is that normal electrical activity in the auditory system becomes pathologically persistent due to plasticity-like mechanisms that can lead to long-term changes in the communication between neurons. A candidate site for the expression of this so-called synaptic plasticity is a region of the brainstem called the dorsal cochlear nucleus (DCN), a site of integration of acoustic and multimodal, sensory inputs. CONCLUSIONS: Here we review recent findings on cellular mechanisms observed in the DCN that can lead to long-term changes in the synaptic strength between different neurons in the DCN. These cellular mechanisms could provide candidate signaling pathways underlying the induction (ignition) and/or the expression (maintenance) of tinnitus.     

Contralateral Effects and Binaural Interactions in Dorsal Cochlear Nucleus

The dorsal cochlear nucleus (DCN) receives afferent input from the auditory nerve and is thus usually thought of as a monaural nucleus, but it also receives inputs from the contralateral cochlear nucleus as well as descending projections from binaural nuclei. Evidence suggests that some of these commissural and efferent projections are excitatory, whereas others are inhibitory. The goals of this study were to investigate the nature and effects of these inputs in the DCN by measuring DCN principal cell (type IV unit) responses to a variety of contralateral monaural and binaural stimuli. As expected, the results of contralateral stimulation demonstrate a mixture of excitatory and inhibitory influences, although inhibitory effects predominate. Most type IV units are weakly, if at all, inhibited by tones but are strongly inhibited by broadband noise (BBN). The inhibition evoked by BBN is also low threshold and short latency. This inhibition is abolished and excitation is revealed when strychnine, a glycine-receptor antagonist, is applied to the DCN; application of bicuculline, a GABA_A-receptor antagonist, has similar effects but does not block the onset of inhibition. Manipulations of discrete fiber bundles suggest that the inhibitory, but not excitatory, inputs to DCN principal cells enter the DCN via its output pathway, and that the short latency inhibition is carried by commissural axons. Consistent with their respective monaural effects, responses to binaural tones as a function of interaural level difference are essentially the same as responses to ipsilateral tones, whereas binaural BBN responses decrease with increasing contralateral level. In comparison to monaural responses, binaural responses to virtual space stimuli show enhanced sensitivity to the elevation of a sound source in ipsilateral space but reduced sensitivity in contralateral space. These results show that the contralateral inputs to the DCN are functionally relevant in natural listening conditions, and that one role of these inputs is to enhance DCN processing of spectral sound localization cues produced by the pinna.     

Hyperactivity in the dorsal cochlear nucleus after intense sound exposure and its resemblance to tone-evoked activity: a physiological model for tinnitus

Intense tone exposure induces increased spontaneous activity (hyperactivity) in the dorsal cochlear nucleus (DCN) of hamsters. This increase may represent an important neural correlate of noise-induced tinnitus, a condition in which sound, typically of very high pitch, is perceived in the absence of a corresponding acoustic stimulus. Since high pitch sounds are thought to be represented in central auditory structures by the place of activation across the tonotopic array; it is therefore possible that the high pitch of noise-induced tinnitus occurs because intense sound exposure induces a tonotopic distribution of chronic hyperactivity in the DCN similar to that normally evoked only under conditions of high frequency stimulation. To investigate this possibility we compared this tone-induced hyperactivity with the activity evoked in normal animals by presentation of a tone. This comparison revealed that the activity in the DCN of animals which had been exposed to an intense 10 kHz tone 1 month previously showed a striking similarity to the activity in the DCN of normal animals during presentation of low to moderate level tonal stimuli of the same frequency. In both test conditions similar patterns were seen in the topographic distribution of the increased activity along the tonotopic axis. The magnitude of hyperactivity in exposed animals was similar to the evoked activity in the normal DCN responding to a stimulus at a level of 20 dB SL. These results suggest that the altered DCN following intense tone exposure behaves physiologically as though it is responding to a tone in the absence of a corresponding acoustic stimulus. The relevance of these findings to noise-induced tinnitus and their implications for understanding its underlying mechanisms are discussed.     

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.     

Effects of cochlear ablation on noise induced hyperactivity in the hamster dorsal cochlear nucleus: implications for the origin of noise induced tinnitus

Chronic increases in multiunit spontaneous activity are induced in the dorsal cochlear nucleus (DCN) following exposures to intense sound. This hyperactivity has been implicated as a neurophysiological correlate of noise induced tinnitus. However, it is not known whether this hyperactivity originates centrally, or instead, reflects an increase in the level of spontaneous input from the auditory nerve. In the present study we addressed this issue by testing whether hyperactivity, induced in the DCN by previous exposure to intense sound, persists after ipsilateral cochlear input to the DCN has been removed. To induce hyperactivity, Syrian golden hamsters were exposed under anesthesia to an intense pure tone (122-127 dB SPL at 10 kHz) for 4 h. Additional hamsters, which were anesthetized for 4 h, but not tone exposed, served as controls. Electrophysiological recordings of spontaneous activity were performed on the surface of the left DCN in animals in which the ipsilateral cochlea was either intact or ablated. The degree of cochlear removal was determined by microdissection and histologic evaluation of the cochlea after completion of each recording session. Comparisons between the levels of activity recorded in animals with and without intact cochleas revealed that the induced hyperactivity in the DCN persisted after both partial and complete cochlear ablations. These results indicate that the maintenance of hyperactivity is not dependent on input from the ipsilateral cochlea, implying that hyperactivity originates centrally.     

Bilateral Dorsal Cochlear Nucleus Lesions Prevent Acoustic-Trauma Induced Tinnitus in an Animal Model

Animal experiments suggest that chronic tinnitus (“ringing in the ears”) may result from processes that overcompensate for lost afferent input. Abnormally elevated spontaneous neural activity has been found in the dorsal cochlear nucleus (DCN) of animals with psychophysical evidence of tinnitus. However, it has also been reported that DCN ablation fails to reduce established tinnitus. Since other auditory areas have been implicated in tinnitus, the role of the DCN is unresolved. The apparently conflicting electrophysiological and lesion data can be reconciled if the DCN serves as a necessary trigger zone rather than a chronic generator of tinnitus. The present experiment used lesion procedures identical to those that failed to decrease pre-existing tinnitus. The exception was that lesions were done prior to tinnitus induction. Young adult rats were trained and tested using a psychophysical procedure shown to detect tinnitus. Tinnitus was induced by a single unilateral high-level noise exposure. Consistent with the trigger hypothesis, bilateral dorsal DCN lesions made before high-level noise exposure prevented the development of tinnitus. A protective effect stemming from disruption of the afferent pathway could not explain the outcome because unilateral lesions ipsilateral to the noise exposure did not prevent tinnitus and unilateral lesions contralateral to the noise exposure actually exacerbated the tinnitus. The DCN trigger mechanism may involve plastic circuits that, through loss of inhibition, or upregulation of excitation, increase spontaneous neural output to rostral areas such as the inferior colliculus. The increased drive could produce persistent pathological changes in the rostral areas, such as high-frequency bursting and decreased interspike variance, that comprise the chronic tinnitus signal.