Modeling adaptation in the auditory cortex to causally link neural synchrony to tinnitus
Tinnitus, the phantom perception of sound in the absence of an external stimulus, is widely thought to persist because of lasting changes in neural activity arising in the auditory cortex after hearing loss. Masking sounds presented for a set duration and then turned off, can reduce the severity of the tinnitus percept temporarily, a phenomenon known as residual inhibition (RI) [1]. The underlying mechanism for RI is not known; understanding it could provide insight into how changes in neural activity in the auditory cortex lead to persistent tinnitus. We propose that RI may be caused by long-term adaptation in the primary auditory cortex.
We have developed a network-level spiking model of the primary auditory cortex that includes tonotopically arranged excitatory and inhibitory neural units. The hearing loss region is represented as one where input firing rates are decreased. Our model includes a homeostatic plasticity mechanism that strengthens the weights on excitatory connections to the deafferented neurons. The novel contribution here is the addition of an adaptation mechanism to account for RI. The transient decrease in tinnitus perception that occurs after masker stimulus presentation is accounted for by adaptation that works on timescales as long as tens of seconds and has a similar effect on firing rates as has been found experimentally [2]. We simulate experimental findings regarding appropriate stimulus bandwidth and duration for RI in order to validate our model. Additionally, spontaneous firing rates and synchrony in neural firing before and after stimulus presentation are analyzed to shed light on their potential causal link to tinnitus.
Our simulations indicate that long-term adaptation in excitatory neurons of the primary auditory cortex can lead to a suppression in spontaneous firing rates that has a similar recovery timescale (15-45 seconds) as that of masker-induced tinnitus suppression. Furthermore, cross-correlation values between neural units in the hearing loss region are noticeably lower (average of 26.2%) 10 seconds after a 30-second masker stimulus is simulated. Before the stimulus, our model shows enhanced neural synchrony in the hearing loss region, which has been found empirically [3]. Thus, the masker presentation reduces firing synchrony to levels that are seen in the normal hearing regions of our model.
Studies where an auditory masker was shown to temporarily suppress the perception of tinnitus indicate that neural activity underlying the tinnitus percept is being transiently affected by the masker stimulus. We show that long-term adaptation is a plausible candidate mechanism underlying this temporary suppression. Furthermore, our simulations show that, with the presence of adaptation, the enhanced neural synchrony seen with induced hearing loss is temporarily reduced by an appropriate auditory masker. This supports the argument that there is a causal link between enhanced neural synchrony and the perception of tinnitus.
References
1. Roberts, L.E., Moffat, G., Bosnyak, D.J. (2007). Acta Oto-Laryngologica, 126:27-33.
2. Gourevitch, B. & Eggermont, J.J. (2008). European Journal of Neuroscience, 27:3310-3321.
3. Seki, S. & Eggermont, J.J. (2003). Hearing Research, 180:28-38.
Conference:
Computational and systems
neuroscience 2009, Salt Lake City, UT, United States, 26 Feb - 3 Mar, 2009.
Presentation Type:
Poster Presentation
Topic:
Poster Presentations
Citation:
(2009). Modeling adaptation in the auditory cortex to causally link neural synchrony to tinnitus.
Front. Syst. Neurosci.
Conference Abstract:
Computational and systems
neuroscience 2009.
doi: 10.3389/conf.neuro.06.2009.03.241
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Received:
03 Feb 2009;
Published Online:
03 Feb 2009.