Conductive Hearing Loss Disrupts Synaptic and Spike Adaptation in Developing Auditory Cortex

Abstract

Although sensorineural hearing loss (SNHL) is known to compromise central auditory structure and function, the impact of milder forms of hearing loss on cellular neurophysiology remains mostly undefined. We induced conductive hearing loss (CHL) in developing gerbils, reared the animals for 8 -13 d, and subsequently assessed the temporal features of auditory cortex layer 2/3 pyramidal neurons in a thalamocortical brain slice preparation with whole-cell recordings. Repetitive stimulation of the ventral medial geniculate nucleus (MGv) evoked robust short-term depression of the postsynaptic potentials in control neurons, and this depression increased monotonically at higher stimulation frequencies. In contrast, CHL neurons displayed a faster rate of synaptic depression and a smaller asymptotic amplitude. Moreover, the latency of MGv evoked potentials was consistently longer in CHL neurons for all stimulus rates. A separate assessment of spike frequency adaptation in response to trains of injected current pulses revealed that CHL neurons displayed less adaptation compared with controls, although there was an increase in temporal jitter. For each of these properties, nearly identical findings were observed for SNHL neurons. Together, these data show that CHL significantly alters the temporal properties of auditory cortex synapses and spikes, and this may contribute to processing deficits that attend mild to moderate hearing loss.

Experience-Dependent Intrinsic Plasticity in Interneurons of Barrel Cortex Layer IV

“…are determined by the sensory deprivation paradigm as well as cortical layers. Similar homeostatic intrinsic plasticity results have been reported in the auditory system, where hearing loss raised intrinsic biophysical excitabilities (Kotak et al 2005;Xu et al 2007). …”

“…To date, intrinsic plasticities have been described primarily in principal neurons in the visual (Cudmore and Turrigiano 2004;Maffei and Turrigiano 2008;Maffei et al 2004), auditory (Xu et al 2007), and somatosensory cortices (Barth et al 2004). In these studies, the intrinsic plasticities exhibited either enhanced or reduced excitabilities and are induced via different physiological mechanisms (e.g., sensory deprivation or acute long-term pairing), respectively.…”

“…How specific interneurons respond to sensory experiences is unclear. In principal neurons, both the strength of inhibitory synapses (Jiao et al 2006;Maffei and Turrigiano 2004;Maffei et al 2006) and the firing properties of principal neurons (Maffei and Turrigiano 2008;Maffei et al 2004Maffei et al , 2006Xu et al 2007) are regulated by sensoryinduced activities. So far, there is no evidence regarding sensory-dependent intrinsic plasticity in interneurons.…”

“…Although the idea of regulation of intrinsic plasticity has been described in sensory neural circuits (Maffei and Turrigiano 2008;Maffei et al 2004;Xu et al 2007), little is known about the underlying induction and expression mechanisms (Nelson and Turrigiano 2008). Here, I focused on answering the following two questions.…”

Consequences of unilateral hearing loss: Cortical adjustment to unilateral deprivation

“…Electrophysiological investigations of conductive hearing loss (CHL) in animals have shown that CHL changes the way sound is processed in the peripheral and central auditory system (e.g., Clopton and Silverman, 1978;Webster and Bobbin, 1986;Sumner et al, 2005;Xu and Jen, 2001;Jen and Xu, 2002;Xu et al, 2007). Centrally, unilateral CHL results in a decrease in glucose uptake as measured by the 2-deoxyglucose (2-DG) method, affecting cellular activity and metabolism in the major afferent projection from the manipulated ear (e.g., Tucci et al, 1999Tucci et al, , 2001.…”