The ability of neurons to regulate their activity (homeostatic plasticity) is thought to be responsible for changes in neural responsiveness/gain induced by sensory deprivation, or augmented stimulation. For example, following auditory deprivation, excitatory and inhibitory synaptic transmission is strengthened and weakened, respectively. Abnormally high neural gain results in an 'over amplification' of spontaneous and stimulus-evoked firing rates, and may result in aberrant auditory perceptions including tinnitus and/or hyperacusis, respectively. The first manuscript in the thesis 'Pump up the Volume' (Chapter Three) provides a summary of the neural gain mechanism in the adult auditory system. Aspects of neural gain, including temporal characteristics and frequency specificity, had not been systematically investigated. Therefore, the aim of this thesis was to investigate characteristics of the neural gain mechanism. The thesis comprises three related studies involving normal hearing adult listeners: two studies involved short term sensory deprivation and one study involved short term augmented stimulation. The main outcome measures were the acoustic reflex threshold (ART), auditory brainstem response (ABR) and loudness. In Study One, the time course, frequency specificity and anatomical location of changes in the ART, following 6 days of unilateral earplug use (ca 30 dB attenuation at 2-4 kHz), were investigated. The reduction in ART in the treatment ear was greatest at day 4 and at frequencies most attenuated by the earplug. Ipsilateral and contralateral ARTs were similar when stimuli were presented to the treatment ear. ARTs were not statistically significant from baseline when measured 4 and 24 hours after earplug removal. In Study Two, the ART and ABR were measured at baseline and after 7 days of unilateral and bilateral hearing aid use (13-17 dB real ear insertion gain), to compare the effect of symmetrical and asymmetrical inputs. There was no change in ART and ABR after treatment, suggesting that the augmented stimulation was insufficient to modify neural gain. In Study Three, ARTs, ABRs and loudness were investigated after 4 days of unilateral earplug use (30 dB attenuation at 2-4 kHz). There was a significant reduction in ART (ca 6 dB) in the treatment ear, which returned to baseline within 1-2 hours of earplug removal. There was an unexpected but significant 35 nV decrease in the ABR wave V peak-to-trough amplitude in the treatment ear, and a 12 nV increase in the control ear. The change in ABR was opposite in direction to the change in ART. There was no change in loudness. The thesis has provided information on the threshold of deprivation/stimulation required to elicit a change in neural gain, along with the frequency specificity and temporal characteristics of the gain control mechanism. The anatomical location for changes in neural gain is around the level of the cochlear nucleus. The change in ABR was in the opposite direction to those predicted, but could be due a difference in the compensatory changes of contralateral and ipsilateral inputs at the level of the inferior colliculus.