152

Electroencephalography and Clinical Neurophysiology, 1979, 46:452--459 © Elsevier/North-Holland Scientific Publishers, Ltd.

DIFFERENTIAL CHANGES OF AUDITORY NERVE AND BRAIN STEM SHORT LATENCY EVOKED POTENTIALS IN THE L A B O R A T O R Y MOUSE

KENNETH R. HENRY Department of Psychology, University of California, Davis, Calif. 95616 (U.S.A.) (Accepted for publication: August 14, 1978)

The laboratory mouse (Mus musculus) has been underutilized in electrophysiological studies of the auditory system. Although the inbred mouse has advantages in terms of reduced genetic variability {Green 1966), rapid postnatal auditory development (Alford and Ruben 1963; Mlonyeni 1967), and sensitivity to acoustic stress (Henry 1967), its small size has restricted studies of its auditory periphery and brain stem. Recent studies have also shown that auditory psychophysical measures can be assessed in the mouse with a precision which rivals those obtained from cats and humans (Ehret 1975a, b, 1977). The present paper describes volume-conducted evoked potentials from the subcollicular auditory system of the mouse, quantifying their changes in response to environmental and developmental factors. A series of short latency evoked potentials can be recorded from the scalp, reflecting activity which is volume-conducted from the auditory nerve and brain stem (Jewett 1970; Sohmer and Feinmesser 1970). Latencies of locally recorded evoked potentials (Jewett 1970; Lev and Sohmer 1972) and of a subpopulation of single units (Huang and Buchwald 1977), as well as lesions (Buchwald and Huang 1975) have provided evidence concerning their sources in the cat. The vertexpositive peaks in this animal appear to originate primarily or exclusively at or near the following structures: P~, the auditory nerve; P,~, the cochlear nucleus; PI~, the superior olivary complex; Piv, the vicinity of the preolivary and lateral lemniscal nuclei. Limited

data from the rat (Jewett and Romano 1972) and man (Starr and Hamilton 1976) suggest similar sources in these species. More recently (Henry 1979), lesions and local recordings have shown that these responses have essentially the same origins in the mouse. In addition, the small brain and thin skull enhance volume-conducted responses in the mouse (Henry et al. 1977). These short latency, volume-conducted potentials have several characteristics in common with single unit and gross evoked potentials which are locally recorded from the auditory nerve and brain stem. As stimulus intensity increases, latencies decrease and amplitudes increase (Jewett and Williston 1971; Hecox and Galambos 1974). Latencies are inversely related to the stimulus frequency (Brama and Sohmer 1977). Amplitudes and latencies also show adaptation with increasing repetition rate (Jewett and Romano 1972). In addition, latencies decrease with maturation (Jewett and Romano 1972; Schulman-Galambos and Galambos 1975). Although many of these brain stem latency and amplitude changes appear to merely reflect auditory nerve activity, several studies have shown this is not always the case. While binaural summation has been observed for P I - l I l , it was not seen with Piv (Huang and Buchwald 1978) in the cat. Noise trauma also has a greater effect on P~ than on subsequent responses in man (Sohmer and Pratt 1975). Maturational factors and high frequency hearing loss also differentially affect these

A U D I T O R Y N E R V E A N D B R A I N S T E M P O T E N T I A L S IN M O U S E

responses in mouse and man (Salamy et al. 1975; Coats and Martin 1977; Henry and H a y t h o r n 1978). One disadvantage of the laboratory mouse for such studies is the large change in body temperature attendant to physical restraint and to pentobarbital anesthesia. Since hypothermia is known to affect the latency of the auditory nerve action potential (Fernandez et al. 1958), b o d y temperature was varied in the mouse in order to evaluate its effects on P~-P~v. This information was then used to provide a more detailed analysis of age-related changes than was previously possible in the mouse (Henry and H a y t h o r n 1978). Noise exposure and the m e t h o d of reducing physical movement during the recording session were also found to differentially affect the first 4 early auditory evoked potentials from the laboratory mouse.

Methods Inbred C57BL/6 laboratory mice were used for these experiments. Eleven subjects were tested when awake and restrained with a head stock and b o d y h a m m o c k , while the remainder were anesthetized (pentobarbital, 60 mg/kg, i.p.). All subjects were placed in a stereotaxic instrument which did n o t utilize earbars. The head was immobilized by a muzzle clamp similar to that used by Jones et al. (1977), with lidocaine applied to pressure points in the awake mice. The m o u t h bar was pressed against the soft palate, and a wire from this bar was connected to the negative input of a preamplifier, while a wire from a wound clip applied to the scalp vertex was attached to the positive preamplifier input. With the exception of the hypothermic experiment, both awake and anesthetized mice were actively maintained at a temperature of 37.5 (+0.1)°C. Acoustic click stimuli were produced by an amplified 0.1 msec duration square wave, at a rate of 20/sec, and transduced by an Altec 802A tweeter. The sounds were channeled to

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a single ear of the mouse via a 't' tube, one end of whi'ch terminated at a Briiel and Kjaer No. 4145 1" calibrated microphone. The voltage o u t p u t of the B and K NO: 2209 impulse SPL meter was displayed ~on an oscilloscope, and these values were used to determine peak energy SPL at the level of the mouse's ear. Because of resonance and other non-linearities of the sound delive~y:'s'ysteml the acoustic click had a measured duration of approximately 2 msec, and a spectral peak at 2 kHz, with a 25 dB drop at 1 K and 10 kHz. The acoustic stressing stimulus was an asynchronous 120 dB noise, with peak energy at 5 k H z and a 2 8 d B rolloff at 1 K and 30 kHz. (These spectral analyses were determined at 80 dB with the use of a B and K No. 4135 1/4" calibrated microphone, a B and K No. 2209 SPL meter, and a Krohn-Hite No. 3500 bandpass filter in series w i t h the meter circuit. Measurements were taken as the bandpass was varied in quarter octave Steps.) All SPLs were measured in peak energy dB (re 0.0002 dynes/cm 2) at the level o f the mouse's ear. Click polarities were alternated to eliminate cochlear microphonics and electromechanical artifacts. All testing w a s performed in an electrically shielded and acoustically insulated chamber (Industrial Acoustics Company). The bioelectrical signals were amplified l 0 s by adjacent, cascaded Grass P15 amplifiers, with frequency settings of 100 and 10,000 Hz. They were processed at 15--30psec per address, with 256--1024 responses per average. Prior to collecting experimental data, each subject was presented with a series o f 80 dB rarefaction clicks in order to obtain cochlear microphonics (CM). The latency of the CM for each mouse was n o t observed to change over the range of experimental conditions in this paper (within the 15 gsec resolution of the computer), in agreement with others (Fernandez et al. 1958). Therefore, subsequently obtained P~--P~v latencies were measured from the time of appearance of the CM to the positive peak of :the relative wave. Amplitude measurements were the average of

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the rising and falling legs of each positive peak. The PI response often had subpeaks (corresponding to NIN2 of the gross action potential), and latency values were measured from the most prominent of these. Latency values were evaluated in terms of absolute or differential values (in /~sec), whereas amplitudes are discussed in terms of relative values (per cent change).

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Results A typical response from the anesthetized mouse at 37.5°C appears in Fig. 1. P[ through P~v were reliably obtained under all the experimental variations, while Pv showed much greater variability of amplitude and latency. Therefore, measurements were confined to the first 4 peaks. Eleven mice were allowed to become hypothermic (approx. 3 0 ° C ) f o l l o w i n g injection with pentobarbital ( 6 0 m g / k g , i.p.). Their temperatures were then slowly elevated, and recordings were made at every 2°C change of ear temperature, as determined by a microthermistor resting against bulla of the stimulated ear. Hypothermia increased the latencies of all components, with the effect being most pronounced at higher brain stem levels (Fig. 2). Pre-weanling (16

Differential changes of auditory nerve and brain stem short latency evoked potentials in the laboratory mouse.

152 Electroencephalography and Clinical Neurophysiology, 1979, 46:452--459 © Elsevier/North-Holland Scientific Publishers, Ltd. DIFFERENTIAL CHANGES...
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