Coding of communication calls in the subcortical and cortical structures of the auditory system.

The processing of species-specific communication signals in the auditory system represents an important aspect of animal behavior and is crucial for its social interactions, reproduction, and survival. In this article the neuronal mechanisms underlying the processing of communication signals in the higher centers of the auditory system--inferior colliculus (IC), medial geniculate body (MGB) and auditory cortex (AC)--are reviewed, with particular attention to the guinea pig. The selectivity of neuronal responses for individual calls in these auditory centers in the guinea pig is usually low--most neurons respond to calls as well as to artificial sounds; the coding of complex sounds in the central auditory nuclei is apparently based on the representation of temporal and spectral features of acoustical stimuli in neural networks. Neuronal response patterns in the IC reliably match the sound envelope for calls characterized by one or more short impulses, but do not exactly fit the envelope for long calls. Also, the main spectral peaks are represented by neuronal firing rates in the IC. In comparison to the IC, response patterns in the MGB and AC demonstrate a less precise representation of the sound envelope, especially in the case of longer calls. The spectral representation is worse in the case of low-frequency calls, but not in the case of broad-band calls. The emotional content of the call may influence neuronal responses in the auditory pathway, which can be demonstrated by stimulation with time-reversed calls or by measurements performed under different levels of anesthesia. The investigation of the principles of the neural coding of species-specific vocalizations offers some keys for understanding the neural mechanisms underlying human speech perception.

Fast tonotopy mapping of the rat auditory cortex with a custom-made electrode array.

We present a custom-made multielectrode array for the recording of evoked potentials during acute experiments in rats, which offers a quick and reliable estimation of the cortical tonotopy. The array consists of electrodes represented by insulated copper wires of 0.09 mm diameter fixed in epoxy resin in a 3 x 5 arrangement, with final impedances of 410-800 kOhm. The array was placed on the brain surface of anesthetized rats approximately at the location of the auditory cortex (AC) and the cortical evoked potentials (middle-latency responses, MLR) were elicited by a series of tone pips of different frequencies at 50 dB of sound pressure level (SPL) intensity. The frequency that evoked the highest MLR amplitude (best frequency, BF) was identified for each electrode. The obtained distribution of the BFs characterized the cortical tonotopy, and it correlated with the frequency selectivity of neurons recorded at the same positions by an extracellular microelectrode. Although the space resolution of the array did not allow for the identification of AC sub regions, the array proved to be a reliable tool for a quick estimation and prediction of areas of interest for the subsequent measurements of neurons by more precise techniques.

The absence of brain-specific link protein Bral2 in perineuronal nets hampers auditory temporal resolution and neural adaptation in mice.

Brain-specific link protein Bral2 represents a substantial component of perineuronal nets (PNNs) enwrapping neurons in the central nervous system. To elucidate the role of Bral2 in auditory signal processing, the hearing function in knockout Bral2(-/-) (KO) mice was investigated using behavioral and electrophysiological methods and compared with wild type Bral2(+/+) (WT) mice. The amplitudes of the acoustic startle reflex (ASR) and the efficiency of the prepulse inhibition of ASR (PPI of ASR), produced by prepulse noise stimulus or gap in continuous noise, was similar in 2-week-old WT and KO mice. Over the 2-month postnatal period the increase of ASR amplitudes was significantly more evident in WT mice than in KO mice. The efficiency of the PPI of ASR significantly increased in the 2-month postnatal period in WT mice, whereas in KO mice the PPI efficiency did not change. Hearing thresholds in 2-month-old WT mice, based on the auditory brainstem response (ABR) recordings, were significantly lower at high frequencies than in KO mice. However, amplitudes and peak latencies of individual waves of click-evoked ABR did not differ significantly between WT and KO mice. Temporal resolution and neural adaptation were significantly better in 2-month-old WT mice than in age-matched KO mice. These results support a hypothesis that the absence of perineuronal net formation at the end of the developmental period in the KO mice results in higher hearing threshold at high frequencies and weaker temporal resolution ability in adult KO animals compared to WT mice.

Influence of increasing doses of pentobarbital on the mesencephalic reticular formation in rats. Spontaneous firing of neuronal pairs and activity evoked by polarization.

In rats immobilized by D-tubocurarine the spontaneous activity in pairs of mesencephalic reticular neurons was recorded by means of one microelectrode and differentiated by amplitude discriminators. Spontaneous activity of neuronal pairs and activity evoked by electrical polarization of cells (5-235 nA) through the recording microelectrode was evaluated in the curarized state and after cumulative doses of 15 mg/kg pentobarbital. No correlation between mean interspike interval duration in pairs of adjacent neurons was found in the unanesthetized state. After pentobarbital a slight dependence was observed between the values. Furthermore, it is probable that adjacent neurons will both cease firing at the same dose of pentobarbital. Cross-correlation of the spike trains of two adjacent neurons was found in the range of minus 10 msec to plus 10 msec (which is probably an expression of direct interaction or of a common input) in 6 of 50 pairs analyzed in the unanesthetized state. This dependence fully disappeared after 15-30 mg/kg of pentobarbital. After 15 mg/kg of pentobarbital in 17 recorded pairs (out of 50 analyzed) peaks in the cross-correlograms appeared in a range of about 100 msec and at a distance of 150-300 msec. Such a relationship was already present in 4 pairs of neurons in the unanesthetized state. The similarity of autocorrelation and cross-correlation histograms in this case favors the hypothesis that spontaneous activity of many mesencephalic reticular neurons is synchronized after pentobarbital administration. In many reticular neurons the firing may be evoked by direct cell polarization through the recording microelectrode even at cumulative doses of pentobarbital much higher than those sufficient to block spontaneous activity.

Inferior colliculus in the rat: neuronal responses to stimulation of the auditory cortex.

Responses to electrical stimulation of the auditory cortex (silver ball bipolar electrodes, single pulses, duration 0.2 ms, current 0.1-1.5 mA) were recorded in neurones in the inferior colliculus of rats anaesthetized with pentobarbital. Excitatory or inhibitory effects were obtained in 84 out of 162 recorded neurones. The majority of neurones responded with a short excitatory burst (with a latency from 3 to 15 ms); in some of them the initial excitation was followed by inhibition lasting from 30 to 150 ms. Few neurones only reacted to electrical stimulation by inhibition, which occurred 3-10 ms after the stimulus and lasted up to 300 ms. The inhibition either suppressed the spontaneous activity or the acoustically evoked response. Neurones reacting to stimulation of the auditory cortex were found mainly in the caudal and dorsal parts of the inferior colliculus.

Middle latency responses to electrical stimulation of the auditory nerve in unanaesthetized guinea pigs.

Middle latency responses (MLR) to sinusoidal and pulsatile electrical stimulation (ES) of the cochlea and to acoustical stimulation (AS) were evaluated in awake guinea pigs with chronically implanted electrodes. The ear, which was later electrically stimulated, was deafened by local intracochlear application of gentamicin, the opposite ear was left intact. Waveforms and P1-P2 interpeak intervals of the electrically evoked MLR (ES-MLR) were similar to those evoked by acoustical stimulation of the intact ear (AS-MLR) and the latencies of the ES-MLR were shorter by about 1-3 ms. Thresholds of ES-MLR in the frequency range 0.5-32 kHz increased with increasing ES frequency (slope 3.2 dB/octave), thresholds were 3.5-9.5 dB lower for intracochlear than for extracochlear ES. Dynamic ranges for ES-MLR varied between 6-20 dB. MLR amplitude-intensity functions for ES were steeper (slope 2-12 microV/dB) than those for AS (slope 0.2-2 microV/dB). Maximal ES-MLR amplitudes exceeded usually 1.5-3 times the amplitudes of the acoustically evoked MLR. Both types of stimulations evoked larger MLR amplitudes to contralateral stimulation than to ipsilateral stimulation (average ratio = 4.1 +/- 2.2 for AS and 3.3 +/- 2.2 for ES). Because of the relatively long latency and therefore insensitivity to electrical artifact, the ES-MLR can be used for the evaluation of different strategies of the electrical stimulation of the cochlea in awake guinea pig.

Noise impairment in the guinea pig. I. Changes in electrical evoked activity along the auditory pathway.

Changes in the cochlear microphonics (CM), auditory nerve action potential (AP), and evoked responses from the inferior colliculus (IC-ER) and auditory cortex (AC-ER) of the guinea pig were assessed after exposure to white noise of 115 dB for 30 min. Both continuous and intermittent (200 ms noise and 200 ms pause) exposures were used. In comparison with the pre-exposure level, CM isopotential curves were shifted by 1.1 +/- 0.5 dB (means +/- S.E.) on the average in the range of 0.5-8 kHz (recorded at the round window). The amplitude-intensity function of the click-evoked auditory nerve action potential decreased by 8.4 +/- 1.2 dB, that of the inferior colliculus evoked response by 20.9 +/- 3.7 dB, and the amplitude-intensity function of the auditory cortex evoked potential decreased by 6.2 +/- 4.7 dB. A similar reduction in the amplitude was found after both continuous and intermittent noise exposure. In contrast to the decrease in amplitudes of evoked potentials, the latency-intensity functions of the individual waves of potentials evoked along the auditory pathway did not change when compared at the same click intensity before and after the exposure. The results suggest that individual auditory nuclei are impaired by the noise to different extents and that the impairment does not increase linearly up to the auditory cortex.

Noise impairment in the guinea pig. II. Changes of single unit responses in the inferior colliculus.

Spontaneous and evoked activity of neurons in the inferior colliculus of guinea pigs was recorded before and after exposure to noise (continuous or intermittent white noise, 115 dB SPL for 30 min). A single unit was investigated in each animal, and its activity was monitored for several hours. Exposure to noise elevated the threshold of the tip of the tuning curve, resulting in a broadening of the tuning curve. Threshold elevation at the characteristic frequency was greater after exposure to intermittent noise (200 ms noise and 200 ms pause), reaching values of 22.8 +/- 3.7 dB (means +/- S.E.) than it was after exposure to continuous noise (threshold elevation of 13.1 +/- 1.7 dB). The average threshold shift was 17.1 +/- 2 dB. Neither the shape of the poststimulus histograms nor the slope of the spike-intensity curves changed with the noise exposure. The total number of spikes during the response was, however, reduced, and the reduction was in proportion to the threshold elevation. Monaural noise exposure had no effect on the neuronal activity evoked by stimulation of the opposite, nonexposed ear. The latencies of responses recorded after exposure to noise were also longer than the latencies at the same absolute intensity recorded before the exposure. Thus the latencies during the original pre-exposure and acquired postexposure thresholds were practically identical.

Modulation of thresholds to acoustical and electrical stimulation of the intact ear in guinea pig by furosemide and noise.

Middle latency responses (MLR) to acoustical stimulation (AS) and to electrical stimulation (ES) of the intact inner ear were recorded in guinea pigs. ES threshold curve decreased in the frequency range 2-16 kHz with a slope 5.4 dB/octave. Immediately after 50 mg/kg intravenous injection of the furosemide, which resulted in a temporary suppression of the cochlear function, the ES thresholds increased and resembled thresholds found in gentamicin-treated animals. Whereas temporary threshold shift (TTS) at 1 kHz ES was negligible at this time, maximum TTS at 8 kHz and 20 kHz ES was limited to 27 dB and 37 dB resp. TTS to acoustical stimulation was larger than TTS to ES (in some cases exceeded 50 dB) and it was similar at all frequencies. Amplitude-intensity functions (AIF) to high-frequency ES stimuli (20 kHz) consisted of two parts--a flat part at low intensities and a steep part at high intensities of the ES. High-frequency noise exposure (third-octave band noise, centered at 16 kHz, intensity 105 dB for 1 h) reduced or abolished only the flat part of the AIF, the steep part, as well as the responses to low-frequency ES, were not substantially changed. TTS at high frequencies, elicited by the noise exposure, were similar for ES and AS. However, amplitudes of acoustically evoked MLR significantly increased after the noise exposure while MLR amplitudes to ES did not change. The results characterize the frequency-intensity domain of the electrophonic effect in the guinea pig and its changes after influencing the inner ear function by furosemide and noise.

Hearing threshold shifts from prolonged exposure to noise in guinea pigs.

Auditory thresholds were assessed in three guinea pigs with a conditioning procedure based on the positive reinforcement paradigm. Thereafter, the guinea pigs were exposed for 5 days to third octave band noise centred at 2 kHz at 100 dB SPL. Thresholds at 0.5, 2 and 4 kHz were controlled during the exposure and up to 120 days after exposure. After 6 h of exposure, the threshold shift at 4 kHz reached 40 dB and increased slowly to 45 dB by the fifth day. The quasi-asymptotic shift was less expressed at 2 kHz, where the initial threshold shift amounted to 20 dB and rose to 40 dB by the fifth day. Thresholds recovered in the time course of 5 days after exposure and a significant permanent threshold shift was present 120 days after exposure. It amounted to 35 dB at 4 kHz and to 20 dB at 2 kHz. Auditory thresholds were dependent upon the duration of the stimulus: the decrease in duration of a tone from 200 ms to 2 ms caused a rise in threshold of about 10 dB before as well as after the exposure. The effects of prolonged noise exposure upon guinea pigs are similar to those found in chinchillas with the exception of the permanent threshold shift, which is more marked in guinea pigs.

Effects of electrical stimulation of the inferior colliculus on 2f1-f2 distortion product otoacoustic emissions in anesthetized guinea pigs.

The effects of electrical stimulation of the inferior colliculus (IC) on the activation of olivocochlear nerve fibers were investigated in guinea pigs in which the 2f1-f2 distortion product otoacoustic emissions (DPOAE) were recorded. Animals were anesthetized with ketamine (33 mg/kg) and xylazine (6.6 mg/kg). Bipolar electrical stimulation of the IC by a train of pulses with currents less than the threshold for evoking muscle twitches resulted in a small depression of the DPOAE amplitude by 0.1-2 dB. The maximal effect was observed when the stimulating electrodes were located in the rostro-medial or ventral parts of the IC. The suppression of electrically evoked DPOAE was similar to the DPOAE suppression produced by acoustical stimulation of the contralateral ear by a broad-band noise. Suppression of DPOAE amplitude in response to both acoustical and electrical stimulation was abolished 1-2 h after a single intramuscular injection of gentamicin (210-250 mg/kg). The results indicate that electrical stimulation of the IC can activate the efferent system and produce DPOAE changes by similar mechanisms as does acoustical stimulation of the contralateral ear.

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.

Acoustically and electrically evoked contralateral suppression of otoacoustic emissions in guinea pigs.

It is generally accepted that stimulation of the efferent auditory system results in changes of cochlear activity. A simple method of activating the olivocochlear pathway by contralateral electrical stimulation of the round window (ES-RW) was used in this study with the aim of comparing the efficacy of acoustically and/or electrically evoked contralateral suppression. The suppression of transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs) was elicited by contralateral acoustic stimulation (AS) (61 dB SPL continuous white noise), and/or by electrical stimulation of an electrode implanted at the contralateral round window (monopolar rectangular pulses 0.1 ms, repetition rate 300 Hz, intensity 50-100 PA) in 12 guinea pigs. The average value of contralateral suppression of TEOAEs amounted to 1.04 +/- 0.48 dB for acoustic stimulation and 0.97 +/- 0.53 dB for round window electrical stimulation. The simultaneous presentation of both acoustic and electrical stimulation had only a slight additive effect and resulted in 1.27 +/- 0.79 dB diminution of TEOAEs. The suppression of DPOAEs during contralateral acoustic and electrical stimulation was evident mainly at low and middle frequencies (14 kHz). In two guinea pigs the maximum DPOAE suppression was present at high frequencies. The average values of contralateral suppression measured at individual f2 frequencies of DPOAEs were similar to those calculated from 1/4 octave power spectrum analysis of the TEOAEs in half of the animals. The results demonstrated that contralateral ES-RW had a similar suppressive effect on TEOAEs and DPOAEs as did contralateral AS and simultaneous AS+(ES-RW). The results of spectral analysis suggested that both modes of contralateral stimulation excited similar sensory cochlear elements and induce comparable suppression of both TEOAEs and DPOAEs.

Effect of noise on auditory evoked responses in awake guinea pigs.

Changes in the auditory nerve action potential (AP), evoked responses from the inferior colliculus (IC-ER) and auditory cortex (AC-ER) were assessed after exposure to white noise of 120 dB SPL for 1 h in awake guinea pigs. Auditory thresholds were estimated with the aid of averaged AP, IC-ER and AC-ER, besides the threshold shifts also the changes in amplitude-intensity functions were evaluated. Auditory thresholds for tone pips and clicks increased by 20-30 dB 1 h after exposure and were similar in all the three investigated structures. The maximum threshold shifts for tone pips were observed at 8 kHz and were 33.2 +/- 12.9 dB for AP, 30.4 +/- 12.7 dB for IC-ER and 30.8 +/- 13.0 dB for AC-ER (n = 20). The thresholds recovered to preexposure levels within one week. Reduction in AP and IC-ER amplitudes 1 h after exposure was similar, the amplitude-intensity functions were shifted by 20-40 dB. In contrast, the amplitude-intensity functions in the auditory cortex 1 h after exposure were steeper than before exposure and this amplitude enhancement was present for 24 h after exposure. The enhancement of the AC-ER which resembles recruitment and which may be a sign of hypersensitivity of the animal to auditory stimuli was present only when the animals exposed to noise were awake. The noise exposure in animals anaesthetized with urethane reduced the amplitude-intensity functions of all three recorded potentials.

Middle latency responses to acoustical and electrical stimulation of the cochlea in cats.

The middle latency responses (MLR) to acoustical stimulation (A-MLR) as well as to electrical stimulation (E-MLR) of the inner ear were recorded in pentobarbital-anaesthetised cats. Monopolar and bipolar MLR recordings were performed with electrodes located at different places on the primary auditory cortex (AI). The cochlea was electrically stimulated (ES) through a single round-window electrode or through a multichannel intracochlear implant. The slope of amplitude-intensity functions of the A-MLR was steeper when the stimulus frequency of the acoustical stimuli corresponded to the tonotopical recording place on the auditory cortex. Other response properties (waveshape, thresholds and latencies) were related to the recording site and stimulus frequency in only two-thirds of animals. Parameters of E-MLRs evoked by high-frequency ( > 4 kHz) and low-intensity ES in hearing cats, which produced an electrophonic effect, were similar to parameters of acoustically evoked MLRs. In deafened cats, the properties of responses to extracochlear ES were different from those recorded to acoustical stimulation and they were almost uniform in all cortical places. Variations in thresholds, in latencies and in the slope of the amplitude-intensity functions of the E-MLRs recorded in individual tonotopical cortical places were observed when the auditory nerve was stimulated with different configurations of electrodes through a multichannel intracochlear implant.

Deterioration of hearing function in mice with neural crest defect.

Cochlear potentials were recorded in black-eyed white-mutant mice (strains W/Wv and S1/S1d) during the first months of postnatal life. In these animals melanocytes from the neural crest do not reach the stria vascularis. Hearing thresholds indicated by the compound action potential of the auditory nerve progressively increased. Hearing loss in comparison with the control CBA mice amounted 40 dB six weeks after birth, at eight months practically all mutants were deaf. Endocochlear potential was near zero already in the majority of 6 week-old animals. Abnormalities were observed also in intracellular potentials of the stria vascularis cells which were recorded in vitro and dye-marked. While in marginal cells of CBA mice positive potentials of about 10 mV were recorded, potentials of marginal cells in mutants were near zero. Basal cell potentials were negative in CBA mice (approximately -25 mV) and positive in young mutants (approximately +12 mV). However, in mutants older than 3 months the intracellular potentials of basal cells changed to negativity (approximately -10 mV). The results demonstrate gradual deterioration of hearing function observed in both W/Wv and S1/S1d mutants during first months of the postnatal life. In addition to the dysfunction of stria vascularis, where intermediate cells are missing, also the function of receptors progressively deteriorates.

Plastic changes in ipsi-contralateral differences of auditory cortex and inferior colliculus evoked potentials after injury to one ear in the adult guinea pig.

In normal adult guinea pigs, evoked potentials recorded at the ipsilateral auditory cortex to monaural high-frequency acoustic stimuli present higher thresholds and lower amplitudes than at the contralateral cortex; in the inferior colliculus, such ipsi-contralateral differences (ICDs) are smaller than in the auditory cortex. Changes in the ICDs were studied after opposite ear injury. Following quasi-complete hair cell destruction induced by sisomicin injection into the contralateral inner ear, threshold ICDs almost disappeared after about two to six days and ipsilateral amplitudes progressively increased in two to three weeks. The occurrence of ICDs at higher auditory centers revealed in this study, indicates peculiar processing of high frequency stimuli in normal guinea pigs. The alteration of ICDs after opposite ear impairment provides a new possibility to study the auditory plasticity in adult animals.

Effects of contralateral acoustical stimulation on three measures of cochlear function in the guinea pig.

The magnitudes of suppression of the click-evoked compound action potential of the auditory nerve (CAP), transient click-evoked otoacoustic emissions (TEOAEs) and ensemble background activity of the auditory nerve (EBA), elicited by contralateral acoustical stimulation, were compared in awake or lightly sedated guinea pigs. The contralateral ear was stimulated either by continuous broad-band noise or by low-pass or high-pass noise (intensity 41-62 dB SPL) with cut-off frequencies of 2, 8 and 12 kHz. The maximal suppression of TEOAEs was achieved by contralateral noise containing mainly low frequencies, whereas for suppression of the CAP it was necessary for middle frequencies to be present in the contralateral noise (less than 8 kHz). In contrast to this, EBA was suppressed mainly by high-frequency noise (higher than 8 kHz) whereas low- and middle-frequency noise was ineffective in suppressing EBA. Evaluation of the root mean square voltage of the EBA (filtered in frequency range 0.75-1.25 kHz) enabled the evaluation of fast and slow components of olivocochlear activation. Both fast and slow effects were proportionally suppressed by individual types of contralateral stimulation. The mechanisms of TEOAEs and CAP generation has been confirmed in many earlier studies, but the origin of EBA has yet to be fully elucidated. The obtained data support the hypothesis that a large part of EBA is formed by spontaneous activity of high-frequency-tuned auditory nerve fibres. Suppression of the EBA magnitude during contralateral stimulation may be caused either by a reduced spontaneous firing rate or by a decrease in possible synchronised neuronal firing.

Discharge properties of neurons in subdivisions of the medial geniculate body of the guinea pig.

The activity of 194 neurons was recorded in three subdivisions of the medial geniculate body (74 neurons in the ventral, 62 in the medial and 44 neurons in the dorsal subdivision, i.e. vMGB, mMGB and dMGB) of guinea pigs anesthetized with ketamine-xylazine. The discharge properties of neurons were evaluated by means of peristimulus time histograms (PSTHs), interval histograms (INTHs) and auto-correlograms (ACGs). In the whole MGB, the most frequent PSTH responses to pure tone stimuli were onset (43%) or chopper (32%). The onset responses were mostly present in the vMGB, whereas chopper responses dominated in the dMGB. In the whole MGB Poisson-like and bimodal INTHs were found in 46% and 40% of neurons, respectively. The mMGB revealed fewer bimodal and more symmetrical types of INTH. In the whole MGB, 60% of units were found to have ACGs typical for short bursts (<100 ms), 23% for long bursts (>100 ms) and 15% of units fired without bursts. Neurons in the vMGB were characterized by short bursting, whereas those in the mMGB and dMGB expressed more activity in the long bursts. The results demonstrate that the type of information processing in the vMGB, which belongs to the "primary" auditory system, is different from that in two other subdivisions of the MGB.

Changes in neuronal activity of the inferior colliculus in rat after temporal inactivation of the auditory cortex.

The role of cortico-tectal pathways in auditory signal processing was studied in anesthetized rats by comparing the extracellular single unit activity in the inferior colliculus (IC) before and after functional ablation of the auditory cortex (AC) by tetrodotoxin (TTX). The responses of several IC neurons to sound stimuli were simultaneously recorded with a 16-channel electrode probe introduced into the IC. Click-evoked middle latency responses (MLR) recorded from the AC were suppressed for several hours after TTX injection. During AC inactivation the firing rate of IC neurons increased (40 % of neurons), decreased (44 %) or did not change (16 %) in comparison with control conditions. In several IC neurons, TTX injection resulted in alterations in the shape of the rate-level functions. Response thresholds, tuning properties and the type of discharge pattern of IC neurons were not altered during AC inactivation. However, in one-third of the neurons, the initial part of the response was less altered than the later, sustained part. In two-thirds of neuronal pairs, functional decortication resulted in a change in the cross-correlation coefficient. The results reveal the complex changes that appear in IC neuronal activity after functional ablation of the ipsilateral auditory cortex.