Contribution of auditory nerve fibers to compound action potential of the auditory nerve

2014 ◽  
Vol 112 (5) ◽  
pp. 1025-1039 ◽  
Author(s):  
Jérôme Bourien ◽  
Yong Tang ◽  
Charlène Batrel ◽  
Antoine Huet ◽  
Marc Lenoir ◽  
...  

Sound-evoked compound action potential (CAP), which captures the synchronous activation of the auditory nerve fibers (ANFs), is commonly used to probe deafness in experimental and clinical settings. All ANFs are believed to contribute to CAP threshold and amplitude: low sound pressure levels activate the high-spontaneous rate (SR) fibers, and increasing levels gradually recruit medium- and then low-SR fibers. In this study, we quantitatively analyze the contribution of the ANFs to CAP 6 days after 30-min infusion of ouabain into the round window niche. Anatomic examination showed a progressive ablation of ANFs following increasing concentration of ouabain. CAP amplitude and threshold plotted against loss of ANFs revealed three ANF pools: 1) a highly ouabain-sensitive pool, which does not participate in either CAP threshold or amplitude, 2) a less sensitive pool, which only encoded CAP amplitude, and 3) a ouabain-resistant pool, required for CAP threshold and amplitude. Remarkably, distribution of the three pools was similar to the SR-based ANF distribution (low-, medium-, and high-SR fibers), suggesting that the low-SR fiber loss leaves the CAP unaffected. Single-unit recordings from the auditory nerve confirmed this hypothesis and further showed that it is due to the delayed and broad first spike latency distribution of low-SR fibers. In addition to unraveling the neural mechanisms that encode CAP, our computational simulation of an assembly of guinea pig ANFs generalizes and extends our experimental findings to different species of mammals. Altogether, our data demonstrate that substantial ANF loss can coexist with normal hearing threshold and even unchanged CAP amplitude.

1994 ◽  
Vol 71 (5) ◽  
pp. 1826-1834 ◽  
Author(s):  
M. C. Brown

1. The antidromic compound action potential (ACAP) of the auditory nerve was evoked by shocks to the auditory nerve root and recorded at the round window of the cochlea in anesthetized guinea pigs. The goal of this study was to determine the characteristics of the ACAP and compare these characteristics with those of the orthodromic, sound-evoked compound action potential (CAP). 2. The ACAP consists of an initial complex of a positive peak (p1) followed by a negative peak (n1). In contrast, the CAP consists of a negative peak (N1) followed by a positive peak (P1). These differences in waveform are likely due to the differences in conduction direction, antidromic for the ACAP vs. orthodromic for the CAP. 3. After the initial complex, the ACAP has a second complex of peaks (p2, n2) at a latency of approximately 1 ms; this complex is much smaller in amplitude than the initial complex (p1, n1). It is likely that the initial ACAP complex reflects firing of auditory-nerve fibers whereas the second complex reflects firing of neurons further centrally, perhaps in the cochlear nucleus, that are activated by orthodromic firing of auditory-nerve fibers. 4. Experiments with shock pairs are consistent with the idea that for auditory nerve fibers, the absolute refractory period is < 0.5 ms, and the relative refractory period is between 0.5 and at least 5 ms. 5. Experiments with click-shock pairs indicate that a shock interferes with the response to a click when the click and shock are given at about the same time.(ABSTRACT TRUNCATED AT 250 WORDS)


2003 ◽  
Vol 112 (2) ◽  
pp. 163-168 ◽  
Author(s):  
Kentaro Ochi ◽  
Hirotsugu Kinoshita ◽  
Hirohito Nishino ◽  
Mutsumi Kenmochi ◽  
Toru Ohashi

The compound action potential (CAP) in response to a click train stimulus was recorded at the round window of guinea pigs. Administration of quinine hydrochloride (200 mg/kg) significantly elevated the CAP thresholds by 5 to 25 dB (p < .05), and the CAP waveform elicited by the click train stimulus was abnormal. The amplitude of the CAP elicited by the second click was bigger than that elicited by the first click. These changes may be caused by an abnormally broadened N1 response to the first click in the click train. In contrast, CAP waveforms elicited by the second and subsequent clicks appeared normal. After administration of nimodipine (2 mg/kg), the CAP thresholds and waveforms elicited by the click train stimulus were unchanged. Simultaneous administration of both quinine (200 mg/kg) and nimodipine (2 mg/kg) resulted in the same electrophysiological changes as those induced by quinine alone. These results suggest that nimodipine prevents neither the deterioration in the CAP nor the abnormal properties in the response to a click train stimulus.


2002 ◽  
Vol 23 (5) ◽  
pp. 784-788 ◽  
Author(s):  
René Chabert ◽  
Jacques Magnan ◽  
Jean–Gabriel Lallemant ◽  
Alain Uziel ◽  
Jean–Luc Puel

2004 ◽  
Vol 114 (1) ◽  
pp. 1-16 ◽  
Author(s):  
NIZAMETTIN DALKILIC ◽  
HULAGU BARISKANER ◽  
NECDET DOGAN ◽  
ILHAMI DEMIREL ◽  
BARKIN ILHAN

2018 ◽  
Vol 95 (4) ◽  
pp. 99-120
Author(s):  
D. S. Klyachko ◽  
◽  
A. V. Pashkov ◽  
S. V. Gadaleva ◽  
I. V. Naumova ◽  
...  

1988 ◽  
Vol 60 (6) ◽  
pp. 2168-2179 ◽  
Author(s):  
D. L. Eng ◽  
T. R. Gordon ◽  
J. D. Kocsis ◽  
S. G. Waxman

1. The sensitivities of mammalian myelinated axons to potassium channel blockers was studied over the course of development using in vitro sucrose gap and intra-axonal recording techniques. 2. Application of 4-aminopyridine (4-AP; 1.0 mM) to young nerves led to a delay in return to base line of the sciatic nerve compound action potential and to a postspike positivity (indicative of hyperpolarization) lasting for tens of milliseconds. These effects were very much attenuated during the course of maturation. 3. Tetraethylammonium chloride (TEA; 10 mM) application alone had little effect on the waveform of the compound action potential at any age. However, the 4-AP-induced postspike positivity was blocked by TEA, Ba/+, and Cs+. This block was observed in Ca2+-free electrolyte solutions containing EGTA (1.0 mM). 4. Immature sciatic nerves (approximately 3 wk postnatal) were incubated in a potassium-free electrolyte solution containing 120 mM CsCl for up to 1 h in an attempt to replace internal potassium with cesium. When the nerves were tested in the sucrose gap chamber using solutions containing 3.0 mM CsCl substituted for KCl, the compound action potential was broadened and a prolonged depolarization appeared, but there was no postspike positivity; the CsCl effect was similar to the combined effects of 4-AP and TEA. 5. Intra-axonal recordings were obtained to study the effects of 4-AP and TEA on individual axons. In the presence of 4-AP a single stimulus led to a burst of action potentials followed by a pronounced afterhyperpolarization (AHP) in sensory fibers. The AHP was blocked by TEA. In motor fibers 4-AP application resulted in action potential broadening with no AHP. 6. Repetitive stimulation (200-500 Hz; 100 ms) was followed by a pronounced AHP in both sensory and motor fibers at all ages studied. This activity-elicited AHP was sensitive to TEA at all ages. 7. The results indicate that 4-AP and TEA sensitivity change over the course of development in rat sciatic nerve. The effects of 4-AP are much more pronounced in immature nerves than in mature nerves, suggesting that 4-AP-sensitive channels become masked as they are covered by myelin during maturation. However, the TEA-sensitive channels, demonstrable after repetitive firing, remain accessible to TEA after myelination. These channels therefore may have a nodal representation.


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