Spontaneous activity in the inferior colliculus of CBA/J mice after manipulations that induce tinnitus

Ma, Wei Li Diana; Hidaka, Hiroshi; May, Bradford J.

doi:10.1016/j.heares.2005.10.003

Cited by 133 publications

(122 citation statements)

References 50 publications

(71 reference statements)

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“…These data are compared with the average spontaneous rates in the same CF regions seen 2 weeks after acoustic trauma (data from ). The increased incidence of neurons with a high spontaneous firing rate after acoustic trauma encountered in our experiments is in agreement with other studies (Wang et al, 1996(Wang et al, , 2002Imig and Durham, 2005;Ma et al, 2006;Brozoski et al, 2007;Bauer et al, 2008;Dong et al, 2009;). In the present study, only neurons with a spontaneous firing rate Ͼ8 spikes/s were selected for testing the effect of efferent stimulation.…”

Section: Cnic Neuronssupporting

confidence: 93%

“…Hyperactivity has been suggested to be involved in the generation of tinnitus, an auditory phantom perception (Brozoski et al, 2002;Kaltenbach et al, 2004;Bauer et al, 2008). This hypothesis is supported by the fact that the hyperactivity seems restricted to tonotopic regions broadly corresponding to the area of hearing loss as shown in cochlear nucleus (CN), the central nucleus of the inferior colliculus (CNIC), and the auditory cortex (Kaltenbach et al, 2000;Komiya and Eggermont, 2000;Seki and Eggermont, 2003;Ma et al, 2006;Dong et al, 2009;) and the observation in human studies that there is a strong correlation between the tinnitus pitch and the hearing loss frequencies (Mühlnickel et al, 1998;Norena et al, 2002;Eggermont and Roberts, 2004).…”

Section: Introductionmentioning

confidence: 98%

“…This plasticity has been demonstrated in a wide range of animal models, using either mechanically, acoustically, or drug-induced cochlear lesions (Kaltenbach et al, 2000;Seki and Eggermont, 2003;Kaltenbach et al, 2004;Ma et al, 2006;Brozoski et al, 2007;Bauer et al, 2008;Dong et al, 2009Dong et al, , 2010). Hyperactivity has been suggested to be involved in the generation of tinnitus, an auditory phantom perception (Brozoski et al, 2002;Kaltenbach et al, 2004;Bauer et al, 2008).…”

Section: Introductionmentioning

confidence: 98%

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Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Mulders

Seluakumaran²,

Robertson³

2010

Journal of Neuroscience

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Animal models have demonstrated that mild hearing loss caused by acoustic trauma results in spontaneous hyperactivity in the central auditory pathways. This hyperactivity has been hypothesized to be involved in the generation of tinnitus, a phantom auditory sensation. We have recently shown that such hyperactivity, recorded in the inferior colliculus, is still dependent on cochlear neural output for some time after recovery (up to 6 weeks). We have now studied the capacity of an intrinsic efferent system, i.e., the olivocochlear system, to alter hyperactivity. This system is known to modulate cochlear neural output. Anesthetized guinea pigs were exposed to a loud sound and after 2 or 3 weeks of recovery, single-neuron recordings in inferior colliculus were made to confirm hyperactivity. Olivocochlear axons were electrically stimulated and effects on cochlear neural output and on highly spontaneous neurons in inferior colliculus were assessed. Olivocochlear stimulation suppressed spontaneous hyperactivity in the inferior colliculus. This result is in agreement with our earlier finding that hyperactivity can be modulated by altering cochlear neural output. Interestingly, the central suppression was generally much larger and longer lasting than reported previously for primary afferents. Blockade of the intracochlear effects of olivocochlear system activation eliminated some but not all of the effects observed on spontaneous activity, suggesting also a central component to the effects of stimulation. More research is needed to investigate whether these central effects of olivocochlear efferent stimulation are due to central intrinsic circuitry or to coactivation of central efferent collaterals to the cochlear nucleus.

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Section: Cnic Neuronssupporting

confidence: 93%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 98%

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Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Mulders

Seluakumaran²,

Robertson³

2010

Journal of Neuroscience

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“…For the inferior colliculus, reported results are inconsistent. While Chen and Jastreboff (1995) find increases in firing rate following administration of salicylate to induce tinnitus, significant decreases relative to baseline were reported by Ma et al (2006) using doses of salicylate proven to be sufficient to induce tinnitus. Yet spontaneous firing rates increased after exposure to noise that was assumed to have induced tinnitus as reported by Ma et al Since both exposure to noise and the administration of salicylate were expected to have caused tinnitus enhanced firing of neurons in the inferior colliculus does not appear to be a consistent neuronal correlate of phantom sound perception.…”

Section: Insights From Animal Studiesmentioning

confidence: 94%

The relevance of spontaneous activity for the coding of the tinnitus sensation

Weisz

Dohrmann

Elbert

2007

Progress in Brain Research

149

133

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In this chapter we will present support for the hypothesis that synchronous neuronal activity of cell assemblies within the auditory cortex could be the underlying neural code of tinnitus. Such synchronous activity is reflected in the ongoing oscillatory activation pattern that can be recorded non-invasively using MEG and EEG techniques. We conclude that such an oscillatory model of tinnitus can explain many different observations regarding tinnitus.

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“…The presence of elevated levels of spontaneous neural firing (hyperactivity) after treatments that are associated with the development of tinnitus has been well documented in several stages of the central auditory pathways, including the auditory cortex, inferior colliculus, and cochlear nucleus Komiya and Eggermont, 2000;Brozoski et al, 2002;Seki and Eggermont, 2003;Kaltenbach et al, 2004;Ma et al, 2006;Bauer et al, 2008;Mulders and Robertson, 2009;Dong et al, 2010). The cochlear nucleus (CN) is the first brainstem auditory nucleus, and elevated activity at this level is of interest because it could either directly drive the hyperactivity seen in higher centers or, alternatively, it could trigger mechanisms that eventually lead to the de novo generation of hyperactivity in the higher parts of the pathway.…”

Section: Introductionmentioning

confidence: 99%

Hyperactivity in the Ventral Cochlear Nucleus after Cochlear Trauma

Vogler¹,

Robertson²,

Mulders³

2011

J. Neurosci.

121

100

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The emergence of hyperactivity in the form of elevated spontaneous firing rates after cochlear trauma has been well documented in a number of central auditory structures, including the auditory cortex, inferior colliculus, and dorsal subdivision of the cochlear nucleus. This hyperactivity is of interest as a possible neural substrate of tinnitus. Whether the ventral subdivision of the cochlear nucleus shows hyperactivity has never been investigated despite the fact that, like the dorsal division, it also receives direct input from the damaged cochlea and supplies major ascending inputs to brainstem and midbrain auditory centers. We investigated spontaneous neuronal firing rates in the ventral cochlear nucleus in a guinea pig model of cochlear trauma in which we have shown that hyperactivity consistently develops in the inferior colliculus (Mulders and Robertson, 2009). The mean spontaneous firing rates of ventral cochlear nucleus neurons was significantly elevated compared to sham controls. This hyperactivity was more evident in primary-like and onset categories of neurons. Hyperactivity in the ventral subdivision of cochlear nucleus therefore needs to be considered in relation to neural models of the genesis of tinnitus.

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Spontaneous activity in the inferior colliculus of CBA/J mice after manipulations that induce tinnitus

Cited by 133 publications

References 50 publications

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

The relevance of spontaneous activity for the coding of the tinnitus sensation

Hyperactivity in the Ventral Cochlear Nucleus after Cochlear Trauma

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