Compound Action Potential Latency Research Articles

Development of the VIIIth nerve compound action potential evoked by low-intensity tone pips in the Mongolian gerbil

Maturation of the cochlea and afferent auditory units is reflected by changes in VIIIth nerve compound action potential (CAP) parameters. We studied auditory nerve CAPs evoked by low-intensity stimuli in Mongolian gerbils ( Meriones unguiculatus) ranging in age from 22 to 92 days after birth. The gerbil CAP development is characterized by marked changes in latency, threshold, and amplitude during the first few weeks of life. CAP latency and CAP threshold reach adult-like values at about 1 month of age. In contrast, the CAP amplitude continues to grow in size even after 2 months. This dichotomy suggests that the development of afferent auditory nerve function in the gerbil is preceded by maturation of the mechanical processes of the middle ear and cochlea.

Latency enhancement of the cochlear nerve compound action potential (CAP)

Forward maskers within two frequency-intensity domains are capable of decreasing (enhancing) CAP latency: one region flanks the low frequency tail, the other flanks the tip/high frequency slope regions of the latency tuning curve (TC). By contrast, amplitude enhancement typically does not flank the high frequency slope region.

Age-dependent extrasynaptic modulation of axonal conduction by exogenous and endogenous GABA in the rat optic nerve

To ascertain whether endogenous γ-aminobutyric acid (GABA) exists and exerts physiological effects in the optic nerve, we compared the effects of GABA and related drugs on the neonatal (1 to 22 days of age) and adult (>6 months) rat optic nerve in vitro. GABA (10 −4–10 −3 M) reversibly depressed the amplitude and increased the latency of compound action potentials in the neonatal optic nerve. In the adult optic nerve, GABA (10 −4–10 −3 M) had no significant effect on the compound action potential. The GABA-A receptor agonist, isoguvacine (10 −4–10 −3 M), mimicked these GABA effects on the neonate and adult optic nerve. Lower concentrations (10 −5 M) of GABA increased excitability of the neonatal optic nerve but produced no discernible effects on the adult optic nerve. The GABA-uptake inhibitor, nipecotic acid (10 −5 M), mimicked the effects of GABA (10 −5 M) on the neonatal optic nerve. The GABA-A receptor blockers, picrotoxin and bicuculline (10 −6–10 −3 M), decreased the latency of compound action potentials in the neonatal optic nerve. Membrane potential recordings indicate that while GABA (10 −5–10 −3 M) depolarized the neonatal optic nerve dose-dependently, pendently, picrotoxin hyperpolarized the axons. In the adult optic nerve, neither GABA-uptake inhibitors nor GABA-A receptor blockers had significant effects on the compound action potential. These results suggest that functional GABA-A receptors and GABA are present in the neonatal rat optic nerve and depolarize axons under physiological conditions. However, this does not appear to be the case in the adult optic nerve. While the biological role of GABA and GABA-A receptors in the neonatal optic nerve is not apparent, these results support our hypothesis that axonal conduction in white matter is subject to nonsynaptic modulation in an agedependent manner.

Auditory Brainstem Response (ABR) in Spontaneously Epileptic Rats (SER) and Their Parent Mutants.

Postnatal development of auditory brainstem response (ABR) in spontaneously epileptic rats (SER; zi/zi, tm/tm), a double mutant, their parent mutants, tremor rats (tm/tm) and zitter rats (zi/zi), and Kyo:Wistar rats (control), was studied by repeated ABR recordings from 2 to 13 weeks of age. In tremor rats and Kyo:Wistar rats at 2 weeks of age, ABR pattern was almost the same and 2 or 3 waves were identified. However, no further development in ABR was observed in tremor rats and prolongation of latency and lowering of amplitude were marked. Only wave I with prolonged latency and lowered amplitude was recognized in zitter rats, SER and SER-N (zitter phenotype without epilepsy; zi/zi, tm/+ or zi/zi, +/+). ABR pattern was almost the same from 2 to 13 weeks of age in them. Electrocochleography revealed delay of N1 latency of compound action potential in SER. Vacuolation was observed in the cochlear nuclei and the brainstem of tremor rats and SER from 3 weeks of age in histopathological examination. The organ of Corti and cochlear nerve of tremor rats and SER exhibited no remarkable histopathological findings. The deafness in SER and its parent mutants was considered to occur as a result of impairment of inner ear, cochlear nerve and brainstem as well.

Effect of Ligating Peripheral Branches on Facial Nerve Regeneration

Douglas Mattox, MD, of the Department of Otolaryngology–Head and Neck Surgery, Johns Hopkins Hospital, Baltimore, presented the results of his investigation into the effect of selectively ligating peripheral branches of the facial nerve in promoting regeneration of more important branches of the nerve at the American Neurotology Society Meeting, Denver, April 24 to 25, 1987. Based on clinical observations made by his coauthor, Dr Ugo Fisch, Zurich, that ligation of the central branches of the facial nerve after grafting or primary anastomosis will promote regeneration at the mouth and eye, Drs Mattox, Fisch, and Jacob Felix, Baltimore, designed an animal (rat) model for the study of this phenomenon. Bilateral common trunk facial nerve transections were performed. Following reanastomosis, all peripheral branches except the mandibular branch were ligated on one side. The contralateral side served as a nonligated control. Over a six-month period, selective electrophysiologic studies (compound action potential latencies) and

The influence of cochlear hearing loss and probe tone level on compound action potential tuning curves in humans

The effect of cochlear hearing loss and of probe tone level on slopes and sharpness of compound action potential tuning curves was investigated. Thirty-one simultaneously masked isoreduction (50%) tuning curves were determined in 26 adults with cochlear hearing losses up to 60 dB. Probe tone frequency was 2 or 3 kHz. Probe tone level was chosen as close as possible to the action potential threshold, usually within 30 dB. In 5 cases a second tuning curve was determined at a 20–30 dB higher probe tone level in order to differentiate between effects of hearing loss and of probe tone level itself on decrease of selectivity. Tuning was analysed in terms of high- and low-frequency slopes of the tuning curves, both in the steepest parts near the tip and overall, and in terms of Q10dB. Slopes and tuning quality diminished with increasing hearing loss up to 60 dB. Part of the decrease in Q10 could be attributed to increased probe tone level, implying that frequency selectivity is also a level-dependent property. In the same group of subjects so called ‘narrow-band’ (or ‘derived response’) compound action potential latencies were determined at 90 dB per SPL and a derived frequency similar to the probe tone in the tuning curve experiments. Narrow band latencies did not change significantly out of the normal range (2 periods) with increasing hearing loss. This implies that narow band latencies are not related to hearing loss, but reflect only the probe-level dependent impulse response delay. Analysis shows that it is possible to derived Q10dB from narrow band latencies with probe level as a parameter.

The temperature dependency of neural and hair cell responses evoked by high frequencies.

A fine thermocouple, placed on the round window of the guinea pig cochlea, was used to measure temperature and electrical potentials. In acute experiments, rectal temperature was held constant at 38 degrees C while cochlear temperature was varied between 38 degrees C and 31.5 degrees C. Cochlear cooling to 36 degrees C caused elevated thresholds for the compound action potential (CAP) in response to tone bursts with frequencies above 24 kHz. CAP latencies increased for all frequencies tested (2 to 40 kHz). Cooling to lower temperatures produced larger latency increases and greater threshold shifts which extended to CAPs evoked by frequencies as low as 16 kHz. These CAP changes were fully reversible after a cochlear temperature of 38 degrees C was restored. In an attempt to create more uniform cooling of the cochlea, experiments were also conducted with round window thermo-couples chronically implanted in guinea pigs. After cooling the entire anesthetized animal to 36 degrees C, CAP thresholds were again elevated only for frequencies above 24 kHz. In other acute experiments, extracellular dc receptor potentials were recorded from the organ of Corti with micropipettes. Cooling caused a decreased sensitivity to tones at the characteristic frequency of the recording location (20 kHz) and had less effect on responses to lower frequencies. The receptor potential usually recovered after rewarming the cochlea. These data emphasize that temperature is an important parameter when electrophysiological measurements are being made. They also suggest an explanation for the reported discrepancy between behavioral and electrophysiological thresholds at high frequencies.