Natalia Rybalko

Threshold shifts and enhancement of cortical evoked responses after noise exposure in rats.

The effect of exposure to various types of noise (broadband, high-frequency or low-frequency) was studied in adult pigmented rats. Thresholds and amplitudes of middle latency responses (MLR) recorded from electrodes implanted on the surface of the auditory cortex were analyzed before and after noise exposure. Exposure to noise with intensities ranging from 105 to 120 dB for 1 h produced only temporary threshold shifts (TTS). Exposure to broadband noise produced TTS throughout the whole frequency range of the rats hearing, mostly expressed at frequencies of maximal hearing sensitivity (16-32 kHz). Hearing loss produced by high- or low-frequency noise exposure was related to the spectral characteristics of the noise. The exposure to high-intensity noise may also result in amplitude enhancement of the MLR. This phenomenon was seen mainly after broadband noise exposure and occurred in response to both low-frequency and high-frequency test stimuli. High-frequency and low-frequency noise produced amplitude enhancement mainly at frequencies which corresponded to the maximum exposure energy. In contrast to the relatively similar values of TTS obtained in different rats under the same conditions of noise exposure, great inter-individual variability was found in the MLR amplitude enhancement. In all rats the dynamics of recovery functions for amplitude enhancement were different from those for MLR thresholds. The data indicate that whereas post-exposure TTS are related to peripheral changes, the post-exposure MLR amplitude enhancement is most probably connected with a change in the processing of auditory information in the central nervous system.

Enhancement of the auditory cortex evoked responses in awake guinea pigs after noise exposure

In a previous paper [Popelár et al., Hear. Res. 26, 239-247 (1987)] we have shown that amplitudes of the auditory cortex evoked responses (AC-ER) in awake guinea pigs were enhanced for several hours after 1 h of noise exposure whereas amplitudes of the compound potential of the auditory nerve (CAP) and of the inferior colliculus evoked responses (IC-ER) declined. The present study demonstrates that the duration of the AC-ER amplitude increase is related to the intensity of the noise exposure (white noise, for 30 min or 1 h, intensity range 105-125 dB). The AC-ER amplitude as well as the threshold shift increased linearly with increasing intensity of the noise. The maximum AC-ER increase occurred when clicks served as stimuli; amplitude enhancement was smaller for 1 kHz tone pips and was absent when 20 kHz tone pips were used. The amplitude enhancement was specific for the auditory cortex since the amplitude of visually evoked responses, recorded in the occipital cortex, was unchanged after noise exposure. It is suggested that the postexposure amplitude enhancement of the AC-ER is produced by temporary exhaustion of inhibitory processes in the auditory cortex.

Effect of auditory cortex lesions on the discrimination of frequency‐modulated tones in rats

The lateralization of functions to individual hemispheres of the mammalian brain remains, with the exception of the human brain, unresolved. The aim of this work was to investigate the ability to discriminate between falling and rising frequency‐modulated (FM) stimuli in rats with unilateral or bilateral lesions of the auditory cortex (AC). Using an avoidance conditioning procedure, thirsty rats were trained to drink in the presence of a rising FM tone and to stop drinking when a falling FM tone was presented. Rats with a lesion of the AC were able to learn to discriminate between rising and falling FM tones; however, they performed significantly worse than did control rats. A greater deficit in the ability to discriminate the direction of frequency modulation was observed in rats with a right or bilateral AC lesion. The discrimination performance (DP) in these rats was significantly worse than the DP in rats with a left AC lesion. Animals with a right or bilateral AC lesion improved their DP mainly by recognizing the pitch at the beginning of the stimuli. The lesioning of the AC in trained animals caused a significant decrease in DP, down to chance levels. Retraining resulted in a significant increase in DP in rats with a left AC lesion; animals with a right lesion improved only slightly. The results demonstrate a hemispheric asymmetry of the rat AC in the recognition of FM stimuli and indicate the dominance of the right AC in the discrimination of the direction of frequency modulation.

Gap detection threshold in the rat before and after auditory cortex ablation

Gap detection threshold (GDT) was measured in adult female pigmented rats (strain Long-Evans) by an operant conditioning technique with food reinforcement, before and after bilateral ablation of the auditory cortex. GDT was dependent on the frequency spectrum and intensity of the continuously present noise in which the gaps were embedded. The mean values of GDT for gaps embedded in white noise or low-frequency noise (upper cutoff frequency 3 kHz) at 70 dB sound pressure level (SPL) were 1.57+/-0.07 ms and 2.9+/-0.34 ms, respectively. Decreasing noise intensity from 80 dB SPL to 20 dB SPL produced a significant increase in GDT. The increase in GDT was relatively small in the range of 80-50 dB SPL for white noise and in the range of 80-60 dB for low-frequency noise. The minimal intensity level of the noise that enabled GDT measurement was 20 dB SPL for white noise and 30 dB SPL for low-frequency noise. Mean GDT values at these intensities were 10.6+/-3.9 ms and 31.3+/-4.2 ms, respectively. Bilateral ablation of the primary auditory cortex (complete destruction of the Te1 and partial destruction of the Te2 and Te3 areas) resulted in an increase in GDT values. The fifth day after surgery, the rats were able to detect gaps in the noise. The values of GDT observed at this time were 4.2+/-1.1 ms for white noise and 7.4+/-3.1 ms for low-frequency noise at 70 dB SPL. During the first month after cortical ablation, recovery of GDT was observed. However, 1 month after cortical ablation GDT still remained slightly higher than in controls (1.8+/-0.18 for white noise, 3.22+/-0.15 for low-frequency noise, P<0.05). A decrease in GDT values during the subsequent months was not observed.

Auditory frequency and intensity discrimination in pigmented rats

Auditory function was investigated in seven pigmented hooded rats (strain Long-Evans) with the aid of an operant conditioning procedure. Frequency difference limen was measured at frequencies from 0.5 to 64 kHz at 50 dB sensation level (SL). Weber ratios (frequency difference limen/frequency) in this range varied between 3.7 and 7.3%. The decline in the intensity of the stimulus from 50 to 10 dB SL was accompanied by a slight increase in the frequency difference limen. The frequency difference limen values were similar for frequency shifts upwards or downwards. Intensity discrimination was measured at 50 dB SL at frequencies of 2, 8 and 32 kHz. Intensity difference limen was frequency independent and amounted to 2.9 +/- 0.5 dB in conditions of upward intensity shift. The values of intensity difference limen measured in conditions of downward intensity shift were significantly larger and amounted to 6.5 +/- 1.6 dB. The characteristics of hearing function found in these experiments correspond with those described by other authors in albino rats and indicate that albinism in the rat has no significant influence on auditory frequency and intensity discrimination.

Comparison of noise-induced changes of auditory brainstem and middle latency response amplitudes in rats

Auditory brainstem responses (ABRs) and middle latency responses (MLRs) were compared after noise exposure to elucidate the specific effects of a loud sound on the central auditory system in rats. Rats were exposed twice for 1 h to broad-band noise (BBN) of 118 dB SPL (first exposure) and 122 dB SPL (second exposure) with an interval between the exposures of three weeks. The first noise exposure produced threshold shifts (TSs) amounting to 5-45 dB, and the second exposure resulted in 40-70 dB TSs. The slope of MLR amplitude-intensity functions (AIFs) increased significantly in correlation with the TS, resembling loudness recruitment. However, maximal MLR amplitudes measured at 8 kHz increased after the first and second noise exposures to almost equal values in individual animals regardless of the TS. In addition, maximum MLR amplitude enhancement was dependent on pre-exposure MLR voltage, probably reflecting the level of metabolic activity or neurotransmitter processes in individual animals. In contrast to MLR amplitudes, ABR amplitudes were suppressed after noise exposure without changing the slope of ABR AIFs. The MLR changes reflect the specific effects of noise exposure on the central auditory system.

Susceptibility to noise exposure during postnatal development in rats.

Susceptibility to noise-induced hearing loss was studied during maturation in 20 female pigmented rats (strain Long-Evans). Young rats, 3, 4, 5 and 6-7 weeks old, were exposed for 1 h to a broad-band noise with an intensity of 120 dB SPL. The thresholds and amplitudes of middle latency responses (MLR) recorded from electrodes implanted on the surface of the auditory cortex were analyzed before and after noise exposure. The results were compared with data from our previous study, in which the effects of broad-band noise exposure on MLR were investigated in adult rats [Syka, J. and Rybalko, N. (2000) Hear. Res. 139, 59-68]. The hearing thresholds of 3-7 week old rats before noise exposure were within the normal adult range. Noise exposure in young rats produced an adult-like pattern with an elevation of hearing thresholds. One-two weeks post-exposure a recovery of MLR thresholds was observed, though full recovery only occurred in the low frequency range. Recovery of hearing thresholds in the high frequency range depended on the age of the animal at the time of exposure. In all animals aged less that 6-7 weeks, exposure resulted in a permanent threshold shift in the range of 4-32 kHz. The mean values of permanent threshold shifts at 16 kHz (the frequency of maximal hearing loss) were 53.0+/-4.5, 47.6+/-9.6, 37.5+/-7.5 and 27+/-10 dB for rats exposed at 3, 4, 5 and 6-7 weeks of age, respectively. Similar to adult rats, young rats exposed to noise exhibited an enhancement of MLR amplitudes. This amplitude enhancement was more pronounced in the high frequency range. In several rats exposed at 3-5 weeks of age, the recovery period to normal amplitudes was substantially prolonged and lasted 4-8 weeks in comparison with 1-2 weeks in adult rats. These results demonstrate a greater susceptibility to noise exposure in rats during the first 5 postnatal weeks.

Inactivation of the left auditory cortex impairs temporal discrimination in the rat

The left auditory cortex (AC) in humans is involved in the processing of the temporal parameters of acoustical signals, specifically in speech perception, whereas the right AC plays the dominant role in pitch and melody perception. The hemispheric lateralization of acoustical signal processing in non-human mammals is less explored. The present study examined the ability of rats to detect or discriminate a series of gaps in continuous noise under conditions of unilateral or bilateral reversible inactivation of the AC. The results showed that muscimol-induced reversible inactivation of the left AC suppresses the ability of rats to discriminate between acoustical stimuli of different temporal parameters (duration or repetition rate), whereas inactivation of the right AC results in no change or only a mild decrease in discrimination ability. Hemispheric asymmetry was observed only in the case of gap discrimination tasks, but not in a gap detection task. Our findings demonstrate that, similarly as in humans, the left AC in the rat plays the dominant role in temporal discrimination. These data provide further evidence for the functional asymmetry of the mammalian brain, which appears in a relatively early phase of evolution.

Effect of noise exposure on gap detection in rats

The effects of intense (110-120 dB) noise exposure (broadband noise for one hour) on temporal resolution was estimated in rats by measuring the behavioural gap detection threshold (GDT). Changes in GDT after 120 dB noise exposure were compared with changes in the threshold and amplitude of middle latency responses (MLR) recorded in response to tone stimuli. GDT values increased from 1.6 to 4.3 or 7.8 ms after exposure to 110 or 115 dB SPL, respectively; GDT recovered to pre-exposure values in 3-7 days. Three main types of noise-induced changes were observed after 120 dB SPL exposure: (I) GDT changes similar to those following noise exposure to 115 dB SPL and maximal hearing threshold shifts (TSs) at high frequencies of about 45 dB; (II) more pronounced changes in GDT (up to 60 ms) with maximal hearing threshold shifts of about 65 dB and (III) a lack of reliable responses to gap during the first weeks post-exposure with maximal hearing threshold shifts of about 80 dB. An increased GDT was present two months after noise exposure in animals with types II and III post-exposure changes; enhanced MLR amplitudes were also found in most of these in the first post-exposure week. The pronounced deficit in gap detection in some rats after 120 dB SPL noise exposure may signal the presence of a noise-induced tinnitus.

Noise exposure during early development influences the acoustic startle reflex in adult rats

Noise exposure during the critical period of postnatal development in rats results in anomalous processing of acoustic stimuli in the adult auditory system. In the present study, the behavioral consequences of an acute acoustic trauma in the critical period are assessed in adult rats using the acoustic startle reflex (ASR) and prepulse inhibition (PPI) of ASR. Rat pups (strain Long-Evans) were exposed to broad-band noise of 125 dB SPL for 8 min on postnatal day 14; at the age of 3-5 months, ASR and PPI of ASR were examined and compared with those obtained in age-matched controls. In addition, hearing thresholds were measured in all animals by means of auditory brainstem responses. The results show that although the hearing thresholds in both groups of animals were not different, a reduced strength of the startle reflex was observed in exposed rats compared with controls. The efficacy of PPI in exposed and control rats was also markedly different. In contrast to control rats, in which an increase in prepulse intensity was accompanied by a consistent increase in the efficacy of PPI, the PPI function in the exposed animals was characterized by a steep increase in inhibitory efficacy at low prepulse intensities of 20-30 dB SPL. A further increase of prepulse intensity up to 60-70 dB SPL caused only a small and insignificant change of PPI. Our findings demonstrate that brief noise exposure in rat pups results in altered behavioral responses to sounds in adulthood, indicating anomalies in intensity coding and loudness perception.