Central neural activity in rats with tinnitus evaluated with manganese-enhanced magnetic resonance imaging (MEMRI)

Brozoski, Thomas J.; Ciobanu, Luisa; Bauer, Carol A.

doi:10.1016/j.heares.2007.02.003

Cited by 125 publications

(121 citation statements)

References 35 publications

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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%

“…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: 99%

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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: 99%

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Mulders

Seluakumaran²,

Robertson³

2010

Journal of Neuroscience

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“…In addition, manganeseenhanced magnetic resonance imaging uses manganese as an activity-dependent, paramagnetic contrast agent to track structural and functional information on the central nervous system (Silva et al, 2004). Ex vivo scans of rats with behavioral evidence of tinnitus depict increased activity in the ipsilateral paraflocculus, the ipsilateral posteroventral cochlear nucleus, and the contralateral IC (Brozoski et al, 2007), while in vivo scans revealed increased activity in the dorsal cortex of the IC (Holt et al, 2010). Apparently, more work needs to be done to obtain detailed and consistent information using this new imaging tool.…”

Section: Introductionmentioning

confidence: 99%

Blast-Induced Tinnitus and Hearing Loss in Rats: Behavioral and Imaging Assays

Mao

Pace

Pierozynski

et al. 2012

Journal of Neurotrauma

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The current study used a rat model to investigate the underlying mechanisms of blast-induced tinnitus, hearing loss, and associated traumatic brain injury (TBI). Seven rats were used to evaluate behavioral evidence of tinnitus and hearing loss, and TBI using magnetic resonance imaging following a single 10-msec blast at 14 psi or 194 dB sound pressure level (SPL). The results demonstrated that the blast exposure induced early onset of tinnitus and central hearing impairment at a broad frequency range. The induced tinnitus and central hearing impairment tended to shift towards high frequencies over time. Hearing threshold measured with auditory brainstem responses also showed an immediate elevation followed by recovery on day 14, coinciding with behaviorally-measured results. Diffusion tensor magnetic resonance imaging results demonstrated significant damage and compensatory plastic changes to certain auditory brain regions, with the majority of changes occurring in the inferior colliculus and medial geniculate body. No significant microstructural changes found in the corpus callosum indicates that the currently adopted blast exposure mainly exerts effects through the auditory pathways rather than through direct impact onto the brain parenchyma. The results showed that this animal model is appropriate for investigation of the mechanisms underlying blast-induced tinnitus, hearing loss, and related TBI. Continued investigation along these lines will help identify pathology with injury/recovery patterns, aiding development of effective treatment strategies.

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“…We discussed the possibility that hyperactivity of the auditory nerve and brainstem nuclei up to the level of the inferior colliculus induces the decrease of thalamocortical input through enhanced subcortical GABA expression. Likewise, Brozoski et al (2007) observed elevated brainstem activity and decreased forebrain activity in rats with evidence of tinnitus using manganese-enhanced magnetic resonance imaging (Brozoski et al, 2007). Furthermore, high doses of salicylate have been shown to lead to a mean reduction in maximal field potential amplitudes in AC (Eggermont and Kenmochi, 1998), supporting the model of reduced thalamocortical input as a correlate of tinnitus.…”

Section: Discussionmentioning

confidence: 90%

Midazolam Reverses Salicylate-Induced Changes in Brain-Derived Neurotrophic Factor and Arg3.1 Expression: Implications for Tinnitus Perception and Auditory Plasticity

et al. 2008

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Tinnitus is a phantom auditory perception, which can be induced via application of concentrated sodium salicylate, and is known to be associated with hearing loss and altered neuronal excitability in peripheral and central auditory neurons. The molecular features of this excitability, however, has been poorly characterized to date. Brain-derived neurotrophic factor (BDNF), the activity-dependent cytoskeletal protein (Arg3.1, also known as Arc), and c-Fos are known to be affected by changes in excitability and plasticity. Using reverse transcription-polymerase chain reaction, in situ hybridization, and immunohistochemistry, the expression of these genes was monitored in the rat auditory system after local (cochlear) and systemic application of salicylate. Induction of tinnitus and hearing loss was verified in a behavioral model. Regardless of the mode of salicylate application, a common pattern became evident: 1) BDNF mRNA expression was increased in the spiral ganglion neurons of the cochlea; and 2) Arg3.1 expression was significantly reduced in the auditory cortex. Local application of the GABA A receptor modulator midazolam resulted in the reversal not only of salicylate-induced changes in cochlear BDNF expression, but also in cortical Arg3.1 expression, indicating that the tinnitus-associated changes in cochlear BDNF expression trigger the decline of cortical Arg3.1 expression. Furthermore, local midazolam application reduced tinnitus perception in the animal model. These findings support Arg3.1 and BDNF as markers for activity changes in the auditory system and suggest a role of GABAergic inhibition of cochlear neurons in the modulation of Arg3.1 plasticity changes in the auditory cortex and tinnitus perception.

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Central neural activity in rats with tinnitus evaluated with manganese-enhanced magnetic resonance imaging (MEMRI)

Cited by 125 publications

References 35 publications

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Blast-Induced Tinnitus and Hearing Loss in Rats: Behavioral and Imaging Assays

Midazolam Reverses Salicylate-Induced Changes in Brain-Derived Neurotrophic Factor and Arg3.1 Expression: Implications for Tinnitus Perception and Auditory Plasticity

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