Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2014 May 23;8:110. doi: 10.3389/fnins.2014.00110

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2014 Gold and Bajo.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Gap-prepulse inhibition of the acoustic startle reflex (GPIAS) in rodents acts as a marker for underlying neurobiological changes following auditory insult. (A) In a cohort of adult guinea pigs, acoustic overexposure (1/4 octave band noise centered at 7 kHz, 93 dB SPL, 2 h; twice-exposed, separated by 6–8 weeks) yielded a subset of animals that displayed significantly decreased normalized startle response inhibition for background masking in the 4–16 kHz bandwidths. Sham controls = white bars; GPIAS-unimpaired animals = gray bars; GPIAS-impaired animals = pink bars. Star = significantly different (p < 0.05) from other bars in the same frequency band (B) On the basis of categorization according to the presence of GPIAS deficits, this subset of animals displayed significantly different stimulus-timing dependent plasticity functions for bimodal somatosensory-auditory stimulation compared with both sham controls, and exposed but unimpaired animals. Sham = gray; GPIAS-unimpaired = pink; GPIAS-impaired = red. Modified with permission from Koehler and Shore (2013a). (C–E) Following exposure to acoustic trauma (octave band noise centered at 16 kHz, 115 dB SPL, 1 h), adult rats underwent daily pairing of tonal stimuli outside the 8–10 kHz frequency bandwidth, either with vagal nerve stimulation (VNS) (C) or sham stimulation (D). VNS-tone pairing was found to produce rapid and long-lasting remediation of GPIAS impairments for 8–10 kHz background masking; sham-tone pairing produced no such improvement, with startle suppression ratios remaining depressed throughout the testing period following trauma. Time points: i, before trauma; ii, 4 weeks after exposure; iii, 10 days after initiation of VNS-tone or sham-tone pairing therapy; iv, 20 days after therapy initiation; v, 1 week after conclusion of therapy; vi, 3 weeks after conclusion of therapy. Broadband noise (thick line), non-tinnitus frequency (thin line), putative tinnitus frequency (dashed line). (E) In addition, VNS-tone pairing was found to remediate and normalize with respect to control measurements, aspects of primary auditory cortex neuronal operation which had been significantly enhanced following trauma, including tonotopic map distortion, frequency receptive field bandwidth, evoked spike response number, and neural spike-timing synchrony. For each bar plot, leftmost bar = naive; middle bar (gray) = sham-tone pairing therapy; rightmost bar = VNS-tone pairing therapy. Asterisk = significantly different (p < 0.05) compared with controls. Modified with permission from Engineer et al. (2011).