THE EFFECT OF BUPIVACAINE ON COMPOUND ACTION POTENTIAL PARAMETERS OF SCIATIC NERVE FIBERS

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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Faculty Opinions recommendation of Contribution of auditory nerve fibers to compound action potential of the auditory nerve.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718409458.793532897 ◽

2017 ◽

Author(s):

M Charles Liberman

Keyword(s):

Action Potential ◽

Auditory Nerve ◽

Compound Action Potential ◽

Nerve Fibers ◽

Auditory Nerve Fibers ◽

Compound Action

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Bisphenol A depresses compound action potential of frog sciatic nerve in vitro involving Ca2+-dependent mechanisms

Neuroscience Letters ◽

10.1016/j.neulet.2012.04.044 ◽

2012 ◽

Vol 517 (2) ◽

pp. 128-132 ◽

Cited By ~ 15

Author(s):

Abhay K. Pandey ◽

Shripad B. Deshpande

Keyword(s):

Sciatic Nerve ◽

Bisphenol A ◽

Action Potential ◽

Compound Action Potential ◽

Frog Sciatic Nerve ◽

Compound Action

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

Journal of Neurophysiology ◽

10.1152/jn.00738.2013 ◽

2014 ◽

Vol 112 (5) ◽

pp. 1025-1039 ◽

Cited By ~ 109

Author(s):

Jérôme Bourien ◽

Yong Tang ◽

Charlène Batrel ◽

Antoine Huet ◽

Marc Lenoir ◽

...

Keyword(s):

Action Potential ◽

Auditory Nerve ◽

Computational Simulation ◽

Round Window ◽

Hearing Threshold ◽

Compound Action Potential ◽

Nerve Fibers ◽

Auditory Nerve Fibers ◽

Round Window Niche ◽

Compound Action

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.

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