Abstract
Tinnitus is often identified in animal models by using the gap prepulse inhibition of acoustic startle. Impaired gap detection following acoustic over-exposure (AOE) is thought to be caused by tinnitus “filling in” the gap, thus, reducing its salience. This presumably involves altered perception, and could conceivably be caused by changes at the level of the neocortex, i.e., cortical reorganization. Alternatively, reduced gap detection ability might reflect poorer temporal processing in the brainstem, caused by AOE; in which case, impaired gap detection would not be a reliable indicator of tinnitus. We tested the latter hypothesis by examining gap detection in inferior colliculus (IC) neurons following AOE. Seven of nine unilaterally noise-exposed guinea pigs exhibited behavioral evidence of tinnitus. In these tinnitus animals, neural gap detection thresholds (GDTs) in the IC significantly increased in response to broadband noise stimuli, but not to pure tones or narrow-band noise. In addition, when IC neurons were sub-divided according to temporal response profile (onset vs. sustained firing patterns), we found a significant increase in the proportion of onset-type responses after AOE. Importantly, however, GDTs were still considerably shorter than gap durations commonly used in objective behavioral tests for tinnitus. These data indicate that the neural changes observed in the IC are insufficient to explain deficits in behavioral gap detection that are commonly attributed to tinnitus. The subtle changes in IC neuron response profiles following AOE warrant further investigation.
Highlights
Tinnitus is a phantom sound percept that affects 10–15% of the populations of industrialized countries [1]
4–6 kHz was the most common background sound frequency at which significant gap detection deficits were found, some guinea pigs (GPs) showed a significant decrease in behavioral gap detection at multiple frequencies following acoustic over-exposure (AOE) (Figure 1)
The present study examined the effects of AOE, and the subsequent development of tinnitus, on neural gap detection in the inferior colliculus (IC)
Summary
Tinnitus is a phantom sound percept that affects 10–15% of the populations of industrialized countries [1]. The most commonly used behavioral model – gap prepulse inhibition of acoustic startle (GPIAS) – relies on measuring an innate reflex response to a startling stimulus. A loud sound evokes an acoustic startle reflex. When the startling sound is preceded by a gap in and otherwise continuous background noise, the magnitude of the startle response is reduced in size, a phenomenon known as prepulse inhibition [PPI; [6, 7]]. The impairment of gap detection (and subsequent PPI deficits) observed following acoustic over-exposure (AOE) or salicylate administration is thought to be caused by tinnitus “filling in” the gap, reducing its salience [7,8,9,10,11,12,13]. Others have suggested that behavioral deficits may reflect a deficit in temporal processing associated with the AOE, rather than tinnitus per se [9, 14]
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