scholarly journals Ventral Cochlear Nucleus Responses to Contralateral Sound Are Mediated by Commissural and Olivocochlear Pathways

2009 ◽  
Vol 102 (2) ◽  
pp. 886-900 ◽  
Author(s):  
Sanford C. Bledsoe ◽  
Seth Koehler ◽  
Debara L. Tucci ◽  
Jianxun Zhou ◽  
Colleen Le Prell ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Slow Component ◽  
Cholinergic Neurons ◽  
Tone Burst ◽  
Mechanical Destruction ◽  
Commissural Axons ◽  
Commissural Neurons ◽  
Glutamatergic Neurons ◽  
Ventral Cochlear Nucleus

In the normal guinea pig, contralateral sound inhibits more than a third of ventral cochlear nucleus (VCN) neurons but excites <4% of these neurons. However, unilateral conductive hearing loss (CHL) and cochlear ablation (CA) result in a major enhancement of contralateral excitation. The response properties of the contralateral excitation produced by CHL and CA are similar, suggesting similar pathways are involved for both types of hearing loss. Here we used the neurotoxin melittin to test the hypothesis that this “compensatory” contralateral excitation is mediated either by direct glutamatergic CN-commissural projections or by cholinergic neurons of the olivocochlear bundle (OCB) that send collaterals to the VCN. Unit responses were recorded from the left VCN of anesthetized, unilaterally deafened guinea pigs (CHL via ossicular disruption, or CA via mechanical destruction). Neural responses were obtained with 16-channel electrodes to enable simultaneous data collection from a large number of single- and multiunits in response to ipsi- and contralateral tone burst and noise stimuli. Lesions of each pathway had differential effects on the contralateral excitation. We conclude that contralateral excitation has a fast and a slow component. The fast excitation is likely mediated by glutamatergic neurons located in medial regions of VCN that send their commissural axons to the other CN via the dorsal/intermediate acoustic striae. The slow component is likely mediated by the OCB collateral projections to the CN. Commissural neurons that leave the CN via the trapezoid body are an additional source of fast, contralateral excitation.

scholarly journals Commissural Neurons in the Rat Ventral Cochlear Nucleus

2009 ◽  
Vol 10 (2) ◽  
pp. 269-280 ◽  
Author(s):  
John R. Doucet ◽  
Nicole M. Lenihan ◽  
Bradford J. May
Keyword(s):  
Cochlear Nucleus ◽  
Commissural Neurons ◽  
Ventral Cochlear Nucleus

scholarly journals Responses of Ventral Cochlear Nucleus Neurons to Contralateral Sound After Conductive Hearing Loss

2005 ◽  
Vol 94 (6) ◽  
pp. 4234-4243 ◽  
Author(s):  
Christian J. Sumner ◽  
Debara L. Tucci ◽  
Susan E. Shore
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Conductive Hearing Loss ◽  
Normal Hearing ◽  
Inhibitory Response ◽  
Broadband Noise ◽  
Central Auditory Processing ◽  
Ventral Cochlear Nucleus ◽  
Excitatory Responses ◽  
Conductive Hearing

Conductive hearing loss (CHL) is an attenuation of signals stimulating the cochlea, without damage to the auditory end organ. It can cause central auditory processing deficits that outlast the CHL itself. Measures of oxidative metabolism show a decrease in activity of nuclei receiving input originating at the affected ear but, surprisingly, an increase in the activity of second-order neurons of the opposite ear. In normal hearing animals, contralateral sound produces an inhibitory response to broadband noise in approximately one third of ventral cochlear nucleus (VCN) neurons. Excitatory responses also occur but are very rare. We looked for changes in the binaural properties of neurons in the VCN of guinea pigs at intervals immediately, 1 day, 1 wk, and 2 wk after the induction of a unilateral CHL by ossicular disruption. CHL was always induced in the ear ipsilateral to the VCN from which recordings were made. The main observations were as follows: 1) ipsilateral excitatory thresholds were raised by at least 40 dB; 2) contralateral inhibitory responses showed a small but statistically significant immediate decrease followed by an increase, returning to normal by 14 days; and 3) there was a large increase in the proportion of units with excitatory responses to contralateral BBN. The increase was immediate and lasting. The latencies of the excitatory responses were at least 6 ms, consistent with activation by a path involving several synapses and inconsistent with cross talk. The latencies and rate-level functions of contralateral excitation were similar to those seen occasionally in normal hearing animals, suggesting an upregulation of an existing pathway. In conclusion, contralateral excitatory inputs to the VCN exist, which are not normally effective, and can compensate rapidly for large changes in afferent input.

scholarly journals Ventral cochlear nucleus bushy cells encode hyperacusis in guinea pigs

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
David T. Martel ◽  
Susan E. Shore
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Wide Frequency Range ◽  
Neural Firing ◽  
Frequency Range ◽  
Neural Basis ◽  
Firing Rates ◽  
Ventral Cochlear Nucleus ◽  
Psychophysical Studies ◽  
Bushy Cells

AbstractPsychophysical studies characterize hyperacusis as increased loudness growth over a wide-frequency range, decreased tolerance to loud sounds and reduced behavioral reaction time latencies to high-intensity sounds. While commonly associated with hearing loss, hyperacusis can also occur without hearing loss, implicating the central nervous system in the generation of hyperacusis. Previous studies suggest that ventral cochlear nucleus bushy cells may be putative neural contributors to hyperacusis. Compared to other ventral cochlear nucleus output neurons, bushy cells show high firing rates as well as lower and less variable first-spike latencies at suprathreshold intensities. Following cochlear damage, bushy cells show increased spontaneous firing rates across a wide-frequency range, suggesting that they might also show increased sound-evoked responses and reduced latencies to higher-intensity sounds. However, no studies have examined bushy cells in relationship to hyperacusis. Herein, we test the hypothesis that bushy cells may contribute to the neural basis of hyperacusis by employing noise-overexposure and single-unit electrophysiology. We find that bushy cells exhibit hyperacusis-like neural firing patterns, which are comprised of enhanced sound-driven firing rates, reduced first-spike latencies and wideband increases in excitability.

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