Acute changes in frequency responses of inferior colliculus central nucleus (ICC) neurons following progressively enlarged restricted spiral ganglion lesions

Abstract

Immediate effects of sequential and progressively enlarged spiral ganglion (SG) lesions were recorded from cochleas and inferior colliculi. Small SG-lesions produced modest elevations in cochlear tone-evoked compound action potential (CAP) thresholds across narrow frequency ranges; progressively enlarged lesions produced progressively higher CAP-threshold elevations across progressively wider frequency ranges. No comparable changes in distortion product otoacoustic emissions (DPOAEs) amplitudes were observed consistent with silencing of auditory nerve sectors without affecting organ of Corti function.Frequency response areas (FRAs) of inferior colliculus (IC) neurons were recorded before and immediately after SG-lesions using multi-site silicon arrays fixed in place with recording sites arrayed along IC frequency gradient. Individual post-lesion FRAs exhibited progressively elevated response thresholds and diminished response amplitudes at lesion frequencies, whereas responses at non-lesion frequencies were either unchanged or enhanced. Characteristic frequencies were shifted and silent areas were introduced within these FRAs. Sequentially larger lesions produced sequentially larger shifts in CF and/or enlarged silent areas within affected FRAs, producing immediate changes in IC frequency organization.These results contrast with those from the auditory nerve, extend previous reports of experienceinduced plasticity in the auditory CNS, and support results indicating afferent convergence onto ICC neurons across broad frequency bands.

Effects of Brain-Derived Neurotrophic Factor (BDNF) and Electrical Stimulation on Survival and Function of Cochlear Spiral Ganglion Neurons in Deafened, Developing Cats

“…These recording methods have been described in detail in previous publications Snyder et al 2008). Briefly, under sodium pentobarbital anesthesia, the right IC was exposed, and a 32-channel silicon probe (32 sites, 100-μm spacing on a single shank; NeuroNexus Technologies, Ann Arbor, MI) was inserted along a standardized trajectory parallel to the tonotopic axis of the IC.…”

“…Two to four probe penetrations were made in each subject, recording responses to charge-balanced biphasic current pulses (200 μs/phase), delivered by each of the six individual intracochlear CI electrodes in monopolar mode, and also for all five contiguous bipolar electrode combinations (1-2, 2-3, 3-4, 4-5, 5-6). Minimum response thresholds and response widths were determined by evaluating spatial tuning curves (STCs;Snyder et al 2008) for each recording probe penetration within the ICC and each CI channel. For a given stimulating channel, the STC describes the strength of response on each recording site (abscissa) for different stimulus levels (ordinate).…”

Temporary off-frequency listening after noise trauma

“…Any decrease of this spontaneous and stimulusinduced peripheral activity, due to a lesioned sensory epithelium (Liberman and Dodds, 1984;Heinz and Young, 2004), could induce a decrease in central inhibition (Garraghty and Muja, 1996;Garraghty et al, 2006). Ultimately, the release from inhibition, if sufficient, could result in neural hyperactivity and tonotopic map reorganization (Snyder et al, 2000;Snyder and Sinex, 2002;Snyder et al, 2008;Noreña, 2011 for a review). Importantly, the release from inhibition could be proportional to the extent of sensory deprivation, suggesting that the extent of central changes (including those involved in tinnitus generation) may be proportional to the severity of hearing loss.…”

“…The extent of central changes may depend on the severity of hearing loss. Extensive sensory deprivation has been shown to induce a systematic shift of the tuning curve of neurons corresponding to the projection area of the peripheral lesion toward the edge frequency of the hearing loss (Robertson and Irvine, 1989;Rajan et al, 1993;Snyder et al, 2000;Snyder and Sinex, 2002;Snyder et al, 2008). As a consequence, the tonotopic map is altered, such that high frequencies are no longer represented (in terms of characteristic frequencies of central neurons) and the edge frequency of the hearing loss is over-represented.…”

Tonotopic reorganization and spontaneous firing in inferior colliculus during both short and long recovery periods after noise overexposure

“…The reorganization of the frequency topographic map (FTM) has shown to be a direct outcome from hearing loss [4-7]. This could be associated with an increase of spontaneous firing in the brain auditory center [8,9].…”