Biomedical subjects

R B Patuzzi

Publications and source records attributed to R B Patuzzi.

At least 19 recordsLinked to original sources

PubMed2004

Transient focal cooling at the round window and cochlear nucleus shows round window CAP originates from cochlear neurones alone.

We have measured the compound action potential (CAP) evoked by very brief high-frequency tone-bursts (20 kHz, 1/4 ms) at the round window (RW) and at the surface of the cochlear nucleus (CN) in guinea pigs before, during and after a localised chilling of either the cochlea or CN, with a non-toxic 'freeze spray'. CN chilling almost abolished the negative-going component of the CAP measured in the CN (generated by the CN and here called the cochlear nucleus response or CNR), leaving a positive-going localised response from the cochlear neurones as they leave the internal auditory meatus. Within 3 min, the CNR recovered to control values. During that time, the N(1) component of the RW CAP was slightly increased and the P(1) was larger, even though the CNR was abolished, indicating that the P(1) was not due to electrotonic spread of current from the CN. The N(2) and successive peaks at the RW were also abolished, but returned after 30 s. When the cochlea was chilled, the RW CAP was initially reduced in amplitude, presumably due to a drop in the number of cochlear neurones spiking in response to sound, but recovered within 3 min to be larger than the control waveform, with a more prominent N(1) peak which was delayed slightly, making the CAP more monophasic. At the same time, the CNR was smaller, presumably due to fewer cochlear neurones responding, but overall the CN CAP was altered little in waveshape. These experiments indicate that that RW CAP is generated almost solely by cochlear neurones. We also suggest that some of the changes in the RW CAP during the chills were due to changes in the firing of the lateral olivo-cochlear system of efferent neurons.

Acoustic Stimulation↗

PubMed2004

K(+) currents produce P(1) in the RW CAP: evidence from DC current bias, K(+) channel blockade and recordings from cochlea and brainstem.

Tone-burst-evoked compound action potentials (CAP) from the guinea pig round window (RW) are altered by DC current injection through the RW. The CAP waveform consists of a series of interleaved negative and positive peaks (N(1), P(1), N(2), P(2) etc.) of decreasing amplitude. During positive DC current injection (around +50 microA) the positive peaks are depressed substantially and there is an overall negative baseline shift of the waveform following the N(1). Negative current injection (around -50 microA) increased the positive peaks, in particular P(1), and produced an overall positive baseline shift following the N(1) peak. Results support our hypothesis that the first and dominant N(1) peak in the RW CAP is due to depolarising Na(+) currents into the primary afferent dendrites and axons within the cochlea, and that the P(1) potential is largely due to the exit of the hyperpolarising K(+) currents in the same cells. We have reached this conclusion on the basis of the sign and latency of the N(1) and P(1) components at the RW, beneath the myelin layers around the spiral ganglion cells, at the internal auditory meatus (IAM) within the brain case, and on the basis of the differential susceptibility of the various peaks to perfusion of lidocaine in the cochlear nucleus, sectioning of the cochlear nerve at the IAM, application of the K(+) channel blockers 4-amino-pyridine and tetraethylammonium within the cochlea, and DC current biasing at the RW.

4-Aminopyridine↗

PubMed2004

Determinants of the spectrum of the neural electrical activity at the round window: transmitter release and neural depolarisation.

In this paper we summarise the changes we have observed in the electrical activity at the round window (RW) of guinea pigs during transient cooling of the RW or cochlear nucleus (CN), transient hypoxia, low frequency acoustic biasing, ablation of the CN, and DC current injection into the basal cochlear turn. We have measured the compound action potential (CAP), the spectrum of the average CAP waveform (SAW) evoked by brief tone-bursts, and the spectrum of the neural noise (SNN). We discuss how the changes we have observed can be understood in terms of changes in transmitter release from inner hair cells (that controls stochastic neural firing), or changes in the membrane potential of the primary afferent neurones (that controls the neural firing waveshape and the spectral content of the SAW and SNN). We note that changes in sound intensity produce a simple increase in the stochastic release of transmitter from inner hair cells, without much change in the waveform of the neural response, but manipulations of the auditory brainstem, cooling and current injection all appear to alter neural firing rate and the neural response waveform, producing a baseline shift in the CAP and changes in 1000 Hz peak and low frequency content of the SAW and SNN. We also discuss the use of the CAP, SAW and SNN as an indication of cochlear and auditory brainstem neural activity.

Action Potentials↗

PubMed1999

Boltzmann analysis of CM waveforms using virtual instrument software.

We describe a modification to our technique for the rapid analysis of low-frequency cochlear microphonic (CM) waveforms in the basal turn of the guinea pig cochlea (Patuzzi and Moleirinho, 1998). The transfer curve relating instantaneous sound pressure in the ear canal to instantaneous receptor current through the outer hair cells (OHCs) is determined from the distorted microphonic waveform generated in the extracellular fluid near the hair cells, assuming a first-order Boltzmann activation curve. Previously, the analysis was done in real time using custom-built electronic circuitry. Here, the same task is performed numerically using virtual instrument software (National Instruments LabVIEW 4.1) running on a personal computer. The assumed theoretical function describing the CM waveform is Vcm = Voff + Vsat/[1 + exp[(Eo+Z.Po.sin(2pi f + phi(tot)))/kT]], where the six parameters are (i) a DC offset voltage (Voff); (ii) the frequency of the sinusoidal stimulus (f); (iii) the phase of the sinusoidal stimulus (phi(tot)); (iv) the maximal amplitude of the distorted microphonic signal (Vsat); (v) the sensitivity of the transduction process (Z); and (vi) the operating point on the sigmoidal transfer curve (Eo). The software obtains the least-squares fit to the CM waveforms by continuously deriving the six parameters at a speed of about one determination per second. The independent fitting of the frequency and phase allows the data to be analysed off-line from data previously recorded to tape (i.e. the frequency and phase of the microphonic response need not be known accurately beforehand). We present here an outline of the software we have used, and give an example of the changes which can be monitored using the technique (transient asphyxia). The method's advantages and limitations have been discussed in our previous paper. The virtual instrument described here is available from the authors on request.

Animals↗

PubMed1999

Basic properties of the sound-evoked post-auricular muscle response (PAMR).

One objective electrophysiological test for deafness involves presenting a brief acoustic stimulus to a subject and measuring the electrical activity evoked in the muscle located just behind the ear (the post-auricular muscle or PAM). Although this electrical response has been known for many years, it has been ignored by most clinicians and frequently misreported in the literature. This paper presents the fundamental properties of the PAM electrical response (the PAMR) and examines ways in which its measurement can be improved by altering the standard electrode position and filtering. The response consists of a simple bipolar compound action potential with a first peak latency of between 12.5 and 15 ms, depending on the stimulus intensity and PAM muscle tone. The largest recordings can be made with an active electrode over the PAM and with the reference electrode on the dorsal surface of the pinna. It can be obtained with click and tone-burst stimuli within 20 dB of the subjective detection threshold, can be evoked with tone-bursts between 500 Hz and 16 kHz and grows either linearly with the click level or approximately exponentially with the tone-burst level, reaching a maximum of as large as 250 microV pp in some subjects. It has a frequency spectrum mostly between 25 and 200 Hz. The response is often visible in raw recordings, with as few as 20 averages required for obtaining a stable waveform. There is very little amplitude and latency difference in stimulating the ear on the same side or opposite side to the recording electrodes and the binaurally evoked response is similar to the simple arithmetic sum of the waveforms obtained with monaural stimulation. The response latency and duration are longer in very young infants, but reach adult values by 12 months of age. In a companion paper, we describe a method of enhancing the PAMR using lateral eye movement (Patuzzi and O'Beirne, 1999a).

Acoustic Stimulation↗

PubMed1999

Effects of eye rotation on the sound-evoked post-auricular muscle response (PAMR).

One objective electrophysiological test for deafness involves presenting a brief acoustic stimulus to a subject and measuring the electrical activity evoked in the muscle located just behind the ear (the post-auricular muscle or PAM). We describe a method for enhancing this post-auricular muscle response (PAMR) using lateral eye movement, which increases both the tonic EMG activity in the PAM and the magnitude of the PAMR, and decreases response latency. EMG activity in most subjects tested (more than 30) increased almost instantly on rotation of the eyes, and thereafter grew more slowly with maintained lateral gaze, with the largest increase occurring with eye rotation towards rather than away from the measurement electrodes over the PAM. The EMG activity returned rapidly to near pre-rotation levels when the eyes were returned to the forwards position, with full recovery taking some minutes. While there was a similar increase and return of the PAMR amplitude with eye rotation, the time-course of these changes was somewhat different, largely because the EMG activity and the PAMR amplitude were not proportional. Rather the PAMR amplitude was a saturating function of EMG level, so that the PAMR response did not fall as markedly as the EMG when the eyes were returned to a forwards gaze, and the recovery of the PAMR amplitude to pre-rotation levels appeared to take longer. We discuss the neural mechanisms that may be responsible for this PAMR potentiation with eye movement and discuss its probable role in increasing variability in early studies which did not control for eye movement. We also discuss the utility of eye rotation in potentiating and stabilising the PAMR to allow its use in screening for deafness.

Acoustic Stimulation↗

PubMed1999

A correlation method for detecting the sound-evoked post-auricular muscle response (PAMR).

We have made detailed measurements of the sound-evoked post-auricular muscle response (PAMR) in four adults and two infants, in an attempt to understand the inter-relationships between sound level, potentiation of the PAMR with voluntary PAM contraction or eye rotation, electromyographic (EMG) noise, amplitude of the PAMR, and a correlation measure of the presence of the PAMR. We have found that the amplitude of the PAMR is a simple linear function of the decibel level of a monophasic click (0.1 ms duration), and that the PAMR amplitude is also a saturating power function of the level of tonic EMG. As a result, PAMR=PAM(o).SL. (EMG-EMG(noise))(2)/[(EMG-EMG(noise))(2)+beta(2)], where SL is the decibel level of a click above subjective threshold, PAM(o) is a parameter accounting for the differing PAMR amplitude across individuals or with altered electrode placement, EMG(noise) is the component of EMG not associated with PAMR potentiation, and beta determines the initial rate of growth of PAMR at low levels of PAM activation. We have also found that the correlation measure (C) of the PAMR follows a saturating power function of the signal-to-noise ratio (SNR=PAMR/EMG), with C=SNR(2)/(SNR(2)+delta(2)), where delta determines the onset of saturation in the correlation as a function of SNR. The combination of these two relationships means that correlation is a non-monotonic function of the EMG (PAM activation): it can be large for moderate levels of EMG, but small for high levels of EMG, because the PAMR amplitude saturates but the EMG does not. The correlation is a fast, convenient means of detecting the PAMR, whether using clicks or tone-bursts, and can be used effectively in adults or infants, as long as the reflex is moderately activated. This moderate activation is most effectively produced by eye rotation towards the recording electrodes.

Acoustic Stimulation↗

PubMed1997

Microphonic and DPOAE measurements suggest a micromechanical mechanism for the 'bounce' phenomenon following low-frequency tones.

Neural auditory thresholds in the guinea pig can be temporarily improved by up to 6 dB about 2 min after the cessation of an moderately intense low-frequency tone (Kirk and Patuzzi, 1997). We have measured changes in the f2-f1 distortion product otoacoustic emission (DPOAE) and low-frequency microphonic potential in scala tympani before, during and after a low-frequency tone (200 Hz) to determine the cause of this so-called bounce phenomenon. In particular we have analysed the low-frequency microphonic waveform in detail to estimate changes in the maximal receptor current through the outer hair cells (OHCs), the sensitivity of the OHC forward transduction process and the change in OHC operating point on the mechano-electrical transduction transfer curve. Our results indicate that a 200 Hz tone changes the maximal current and sensitivity of the OHCs minimally, but more importantly, it transiently changes the operating point on the OHC transfer curve. In particular, the operating point changes are consistent with a movement of the OHC stereocilia away from the OHC basal body at the peak of the bounce. These changes detected using the microphonic potential are associated with changes in the level of the f2-f1 DPOAE that correlate well with the electrical measurements. We suggest that the shift in operating point is largely responsible for the increase in cochlear sensitivity, and is due to a disruption of the salt balance within the cochlea during the intense low-frequency tone.

Acoustic Stimulation↗

PubMed1997

Transient changes in cochlear potentials and DPOAEs after low-frequency tones: the 'two-minute bounce' revisited.

After exposure to a loud, non-traumatic low-frequency tone, auditory thresholds are elevated. Thresholds recover to normal in a non-monotonic manner, decreasing rapidly at first before increasing again, until they finally decrease monotonically towards normal. Although the transient elevation of thresholds after the initial improvement was originally called a 'bounce' by Hirsh and Ward (1952), Kemp (1986) suggests that the initial rapid recovery is the oddity: under some conditions a low-frequency tone can produce hypersensitivity in otoacoustic emissions, psychophysical thresholds, and perceived loudness (Kemp's 'bounce') without a later elevation of threshold (Hirsh and Ward's 'bounce'). Kemp also suggested that the transient hypersensitivity was caused by changes in the sensitivity of the active process within the cochlea. We have investigated the origin of this transient hypersensitivity (Kemp's bounce) in guinea pigs, recording cochlear potentials (CM, CAP, SP and EP) and otoacoustic emissions (DPOAEs at f2-f1, 2f1-f2, 2f2-2f1 and 3f1-2f2). Our results indicate that the bounce does not require neural activity, but is probably produced by non-neural cochlear mechanisms, possibly a transient decrease in the permeability of the organ of Corti which produces a small but significant change in standing current through outer hair cells. At least part of these changes, which are reduced as the stimulation frequency increases, and absent above 2 kHz, seem due to a small and transient movement of the cochlear partition towards scala tympani, probably due to a transient osmotic imbalance.

Acoustic Stimulation↗

PubMed1992

Mechanical preprocessing in the mammalian cochlea.

The mammalian cochlea responds with exquisite sensitivity to the small fluctuations in air pressure that make up the stimulus of sound. Moreover, it responds to pressure fluctuations that occur extremely rapidly and that vary over a wide range of intensities--in both cases, to an extent outside the capabilities of unaided nerve fibres. Research performed during the past decade has shown that these properties are dependent on a physiological source of mechanical energy that operates probably within the outer hair cells of the organ of Corti. These cells, which are anatomically and functionally similar to the primary receptor cells, the inner hair cells, are believed to function as a source of mechanical power to assist the mechanical sensitivity of the cochlea, by mechanisms that currently are not understood. Several possible mechanisms have been proposed, but each has limitations that may make it an unsuitable candidate. Recent work has also demonstrated the likely role of mechanoelectrical transduction in outer hair cells in controlling the power source and thereby influencing the sensitivity and amplitude range of the cochlea.

Animals↗

PubMed1992

Additivity of threshold losses produced by acute acoustic trauma.

We have previously [Patuzzi and Rajan, Hear. Res. 60, 165-177, 1992] formulated a model to describe how the threshold elevations produced by a variety of independent, short-term cochlear manipulations add when the manipulations are combined. The manipulations were presumed to affect only the 'active process' in the cochlea. The present report applied this model to the effects observed after acute acoustic trauma in normal-hearing guinea pigs and in guinea pigs with idiopathic threshold losses. Successive loud pure-tone exposures were presented to the normal-hearing guinea pigs, while only a single exposure was presented to the guinea pigs with idiopathic hearing losses. Various parameters of exposure and inter-exposure delays were used to create a variety of threshold elevations, and the total hearing losses observed in the various groups were compared to the total hearing losses predicted by the model. In most cases a statistically-valid 1:1 relationship was obtained between the predicted values and the observed values. In cases where the model's predictions were found not to fit the data, this appeared to be due to inclusion of data previously defined to be outside the scope of the model. When such data were excluded, there was good agreement between the model's predictions and the observed data. The model was further tested by comparing its predictions with data obtained in studies of acute noise trauma in chinchillas and humans by other researchers. The model's predictions were found to agree with these data as well. Thus, across a number of different types and conditions of exposures, the model appears to provide a very good description of the additivity of threshold losses produced by acute acoustic trauma. The generality of and constraints on the model are discussed.

Acoustic Stimulation↗

PubMed1991

Cochlear efferent neurones and protection against acoustic trauma: protection of outer hair cell receptor current and interanimal variability.

We have measured the changes in neural and microphonic sensitivity in the basal turn of the guinea-pig cochlea produced by intense acoustic overstimulation (10 kHz, 115 dB SPL for 60 s and 150 s). As reported previously, the drop in neural and microphonic sensitivities observed after overstimulation were highly correlated [Patuzzi et al. (1989) Hear. Res. 39, 189-202]. Presentation of a non-traumatizing pure-tone to the contralateral ear (10 kHz, 80 dB SPL) during acoustic overstimulation reduced the amount of acoustic trauma measured using the neural response or the microphonic response. Transection of the medial olivo-cochlear system of efferent fibres at the floor of the fourth ventricle abolished this protective effect of contralateral sound and dramatically reduced the variability in the data. Since the low-frequency microphonic is a simple measure of the receptor current through the outer hair cells, and this current probably plays a part in enhancing the mechanical sensitivity of the cochlea, the protection of the microphonic we have observed suggests that the efferent system protects neural sensitivity by protecting the mechano-electrical transduction of outer hair cells. The drop in variability after sectioning the efferents also suggests that inter-animal variations in susceptibility to noise trauma may be a consequence of differing tonic activity of the efferents, and/or a variation in the sensitivity of the efferent pathway.

Action Potentials↗

PubMed1991

Electrical responses from the chicken basilar papilla.

A surgical approach to the basilar papilla of the chicken cochlea has been developed which allows recordings from within the hair cells and supporting cells in vivo. The frequency tuning curves for the AC receptor potentials measured in extracellular space immediately outside hair cells, within the hair cells and in adjacent supporting cells were similar, with best frequencies ranging from 600 Hz to 2000 Hz, and Q10 dB values between 0.6 and 2.5. In cells classified as hair cells there was no evidence of spontaneous oscillations in the membrane potentials, nor of ringing of the membrane potential in response to injected current pulses. Moreover, displacement of the papilla with the microelectrodes could modulate the hair cell membrane potential over the range 0 to -90 mV, suggesting that the current-voltage relationship in these cells was essentially linear. This view was supported by preliminary investigations of cell properties with current injection. We interpret these observations as evidence that the hair cells impaled were not electrically tuned under our experimental conditions, unlike the hair cells of the turtle cochlea. These observations, taken together with the electrode angles used, fluorescent dye-marking and previous measurements of chicken hair cells in vitro [Fuchs, P.A., Nagai, T. and Evans, M.G. (1988) J. Neuro. Sci. 8, 2460-2467], suggest that the hair cells we have impaled were the short hair cells of the papilla, and that the tuning of the AC receptor potentials we have observed was due solely to a tuned mechanical drive to their hair bundles.

Acoustic Stimulation↗

PubMed1990

Saturation of outer hair cell receptor currents causes two-tone suppression.

Zwicker [Biol. Cybern. 35, 243-250, (1979); J. Acoust. Soc. Am. 80, 163-176 (1986)] has previously proposed that many nonlinear phenomena in the mammalian cochlea can be explained by saturation of a positive feedback process which enhances mechanical sensitivity, although the site of the nonlinearity producing this saturation has so far remained obscure. In this paper we present evidence suggesting that the nonlinearity of mechano-electrical transduction in the outer hair cells is the dominant nonlinearity producing two-tone suppression in the mammalian cochlea. In particular, we show that: (i) suppression of the extracellular summating potential (SP), recorded from a particular place within the organ of Corti, has characteristics similar to the suppression of activity in the auditory-nerve; (ii) that SP suppression occurs at approximately constant basilar membrane displacement, inferred from the SP iso-response contours; and that (iii) the onset of SP suppression with suppressor tones on the tail of the frequency tuning curve closely parallels the onset of nonlinearity in the local cochlear microphonic. Since previous studies (Patuzzi et al., 1989) have demonstrated that the vibration of the basilar membrane at its characteristic frequency is very sensitive to changes in outer hair cell receptor current, we consider that interference in outer hair cell currents caused by nonlinearity in mechano-electrical transduction is an adequate explanation of two-tone suppression. This requires that outer hair cell receptor currents deviate from linearity at a suppressor tone level below that required to produce a significant DC receptor potential within the inner hair cells, and that the active process within the cochlea is distributed along a local region of the cochlea, basal of the vibration peak.

Acoustic Stimulation↗

PubMed1989

The origin of the low-frequency microphonic in the first cochlear turn of guinea-pig.

Low-frequency microphonic potentials (100 Hz to 2000 Hz) have been measured in the first turn of the guinea pig cochlea before and after a variety of manipulations of the cochlea. These included ablation of the apical turns, iontophoresis of streptomycin, dc current injection into the first turn, acoustic trauma and two-tone interference with pure tones. These manipulations indicate that the low-frequency microphonic measured in the first turn and at the round window is generated predominantly by the hair cells of this region. It is a convenient and relatively uncomplicated indicator of the integrity of the mechano-electrical transduction process of these cells.

Acoustic Stimulation↗

PubMed1989

Changes in cochlear microphonic and neural sensitivity produced by acoustic trauma.

The low-frequency (200 Hz) microphonic potentials at the round window and in the organ of Corti of the first turn of the guinea pig cochlea have been measured before and after acoustic overstimulation. Reductions in the amplitude of this microphonic after loud sound are highly correlated with neural threshold elevation in this region. The fall in the microphonic amplitude appears due to an inactivation of mechano-electrical transduction channels at the apex of the outer hair cells into a closed state. These results are consistent with the idea that the current through the outer hair cells controls the mechanical sensitivity of the organ of Corti, and that the temporary loss of mechanical and neural sensitivity following loud sound is due to a simple inactivation of the mechano-electrical transduction channels.

Action Potentials↗

PubMed1989

Outer hair cell receptor current and sensorineural hearing loss.

It is argued in this paper that many nonlinear phenomena in audition and many types of sensorineural hearing loss can be explained by a disruption of the mechano-electrical transduction process at the apex of the outer hair cells. This is done using experimental data and a simple model of the active role of outer hair cells in cochlear mechanics based on our previous experiments with acoustic trauma. The causes of sensorineural loss addressed include acoustic trauma, aminoglycoside ototoxicity, intoxication with loop diuretics, hypoxia and Meniere's disease. The nonlinear phenomena discussed include loudness compression, two-tone suppression and modulation of cochlear sensitivity by very low-frequency tones. In every case considered the reduction in neural sensitivity was related to the reduction in outer hair cell receptor current in a quantitatively similar way. We conclude that the link is causal.

Animals↗

PubMed1988

Post-stimulatory effects of direct current stimulation of the cochlea on auditory nerve activity.

Glass micro-electrode recordings from the spiral ganglion of the basal turn of the guinea pig cochlea have been obtained before, during and after negative (cathodic) current injection into scala tympani. Electrical stimulation with currents between 100 microA and 900 microA produced a marked increase in firing rate of the afferent neurons for the first 3 min of electrical stimulation. This was followed by a fall in firing rate to rates near or below the pre-stimulatory spontaneous rate if stimulation continued. Continuous electrical stimulation lasting 5 or 10 min reduced neural sensitivity to acoustic stimulation. Although threshold elevation was greatest for sound frequencies near the characteristic frequency of each neuron, thresholds could also be elevated at lower frequencies on the tail of the frequency-threshold tuning curve. After electrical stimulation a fall in the amplitude of the low-frequency microphonic recorded at the round window was also observed, indicating a disruption of the outer hair cell transduction. These effects were highly localized in the basal turn near the site of current injection, and were not associated with any significant structural changes in the organ of Corti, except after stimulation with very high current intensities.

Acoustic Stimulation↗