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

Chang, Henry; Chen, Kejian; Kaltenbach, James A.; Zhang, Jinsheng; Godfrey, Donald A.

doi:10.1016/s0378-5955(01)00410-5

Cited by 71 publications

(66 citation statements)

References 42 publications

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“…Our finding of increased expression of muscarinic acetylcholine receptors after unilateral cochlear ablation on the lesion side, relative to contralateral, may correlate with evidence for increased sensitivity of DCN neurons to the acetylcholine agonist carbachol after exposure to intense tones (Chang et al, 2002). Our results suggest that degeneration and removal of auditory nerve terminals may lead to increased cholinergic synaptic activity.…”

Section: Functional Implications Of Plasticity Of Muscarinic Acetylchsupporting

confidence: 65%

“…Studies have found that tinnitus may be related to increased spontaneous activity in the DCN in intense tone-exposed or cisplatin-treated animals (Zhang and Kaltenbach, 1998;Kaltenbach and Afman, 2000;Heffner and Harrington, 2002;Brozoski et al, 2002;Kaltenbach et al, 2002Kaltenbach et al, , 2004, particularly in fusiform cells (Brozoski et al, 2002). In a study of the DCN in brain slices from rats exposed to intense tones, the prevalence of bursting spontaneous activity increased as well as the sensitivity of bursting neurons to carbachol (Chang et al, 2002). These results suggest that changes in acetylcholine receptors may affect spontaneous activity and symptoms such as tinnitus.…”

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confidence: 95%

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Effects of cochlear ablation on muscarinic acetylcholine receptor binding in the rat cochlear nucleus

Jin

Godfrey

2006

J. Neurosci. Res.

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Cholinergic synapses in the cochlear nucleus (CN) have been reported to modulate spontaneous activity via muscarinic acetylcholine receptors. In this study, muscarinic receptor binding was measured as specific binding of 1-[N-methyl-(3)H]scopolamine in CN regions of control rats and 7 days, 1 month, and 2 months after unilateral cochlear ablation. In control rats, the strongest binding was found in granular regions, followed in order by fusiform soma, molecular, and deep layers of the dorsal cochlear nucleus (DCN), with much lower binding in the anteroventral CN (AVCN) and posteroventral CN (PVCN). After unilateral cochlear ablation, binding in the AVCN, PVCN, and their associated granular regions on the lesion side became progressively greater than on the control side through 2 months after lesion. A significant asymmetry, with binding higher on the lesion side, was also found in the DCN fusiform soma layer at 7 days, and there and in the DCN deep layer at 1 and 2 months after lesion. There was also evidence of increased binding on the control side in most CN regions. By contrast, binding in the ipsilateral facial nucleus decreased, compared with the control side, by 7 days after the lesion and showed some recovery toward symmetry by 2 months after lesion, and there was no evidence for contralateral changes. These muscarinic receptor binding changes reflect receptor plasticity after loss of auditory nerve innervation. Such plasticity may underlie some of the central auditory functional changes that occur following peripheral lesions, such as tinnitus and hyperacusis.

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Section: Functional Implications Of Plasticity Of Muscarinic Acetylchsupporting

confidence: 65%

mentioning

confidence: 95%

Effects of cochlear ablation on muscarinic acetylcholine receptor binding in the rat cochlear nucleus

Jin

Godfrey

2006

J. Neurosci. Res.

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“…Neurons with complex action potentials are, if anything, more prevalent in DCN slices cut from animals following acoustic trauma and they have non-zero spontaneous discharge rates (Chang et al, 2002). Thus, cartwheel cells should have been active in our preparations and should have presented recognizable spike patterns, even though we did not record from them.…”

Section: Source Of Tail Responsesmentioning

confidence: 98%

“…There are several reports of elevated spontaneous activity in the dorsal cochlear nucleus (DCN) after an acoustic trauma that is sufficient to produce behavioral signs of tinnitus in animals (Brozoski et al, 2002;Kaltenbach et al, 2004; but see Chang et al, 2002;Brozoski and Bauer, 2005), suggesting that DCN is the generator site for tinnitus. In addition, DCN principal cells receive excitatory and inhibitory inputs from a superficial granule-cell associated system (Mugnaini et al, 1980;Berrebi and Mugnaini, 1991) that carries non-auditory information from the somatosensory, vestibular, and other systems (Itoh et al, 1987;Burian and Gstoettner, 1988;Shore et al, 2000;Ohlrogge et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Dorsal cochlear nucleus response properties following acoustic trauma: Response maps and spontaneous activity

Young

2006

Hearing Research

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Recordings from single neurons in the dorsal cochlear nucleus (DCN) of unanesthetized (decerebrate) cats were done to characterize the effects of acoustic trauma. Trauma was produced by a 250 Hz band of noise centered at 10 kHz, presented at 105-120 dB SPL for 4 h. After a one-month recovery period, neurons were recorded in the DCN. The threshold shift, determined from compound actionpotential audiograms, showed a sharp threshold elevation of about 60 dB at BFs above an edge frequency of 5-10 kHz. The response maps of neurons with best frequencies (BFs) above the edge did not show the typical organization of excitatory and inhibitory areas seen in the DCN of unexposed animals. Instead, neurons showed no response to sound, weak responses that were hard to tune and characterize, or "tail" responses, consisting of broadly-tuned, predominantly excitatory responses, with a roughly low-pass shape similar to the tuning curves of auditory nerve fibers with similar threshold shifts. In some tail responses whose BFs were near the edge of the threshold elevation, a second weak high-frequency response was seen that suggests convergence of auditory nerve inputs with widely separated BFs on these cells. Spontaneous rates among neurons with elevated thresholds were not increased over those in populations of principal neurons in unexposed animals.

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“…The dorsal cochlear nucleus (DCN) is one of the first relays within the central auditory pathway (12). Hyperactivity in the DCN has been reported weeks after AOE in vivo and in brain slices and has been correlated with tinnitus (13)(14)(15). Our recent study showed the presence of bursts in DCN fusiform cells (FCs) just a few days after AOE (16).…”

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confidence: 92%

Mechanisms contributing to central excitability changes during hearing loss

Pilati¹,

Ison

Barker³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Exposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of hyperactivity, remain poorly explored. Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal cells that is overcome when additional multisensory fibers are recruited. Furthermore, gain modulation by inhibitory synaptic transmission is disabled in both auditory and multisensory pathways. These cellular mechanisms that contribute to decreased cellular excitability in the central auditory pathway are likely to represent early neurobiological markers of hearing loss and may suggest interventions to delay or stop the development of hyperactivity that has been associated with tinnitus.auditory brainstem | fusiform cell | parallel fiber | deafness | whole-cell patch I t is well established that exposure to loud sound causes damage to the cochlea and results in an elevation of hearing thresholds (1) often accompanied by a reduction of auditory nerve (AN) firing rate (2-4). Although peripheral cellular mechanisms contributing to hearing loss have been thoroughly described (5-11), mechanisms in the central auditory system involved in the early stages of hearing loss following acoustic overexposure (AOE) are poorly understood. The dorsal cochlear nucleus (DCN) is one of the first relays within the central auditory pathway (12). Hyperactivity in the DCN has been reported weeks after AOE in vivo and in brain slices and has been correlated with tinnitus (13-15). Our recent study showed the presence of bursts in DCN fusiform cells (FCs) just a few days after AOE (16). Therefore, the aim of the current study was to investigate synaptic transmission at this early time point after AOE and determine whether changes in auditory or multisensory (MS) inputs to FCs might contribute to the altered excitability in the DCN. We postulate that changes following AOE could represent the earliest modifications of the central auditory pathway preceding the later development of DCN hyperactivity and tinnitus. DCN FCs integrate the acoustic information from AN fibers with MS signals transmitted via granule cell axons (parallel fibers) (17-19). DCN granule cells and their parallel fiber axons represent a site of integration of multimodal sensory in...

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

Cited by 71 publications

References 42 publications

Effects of cochlear ablation on muscarinic acetylcholine receptor binding in the rat cochlear nucleus

Effects of cochlear ablation on muscarinic acetylcholine receptor binding in the rat cochlear nucleus

Dorsal cochlear nucleus response properties following acoustic trauma: Response maps and spontaneous activity

Mechanisms contributing to central excitability changes during hearing loss

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