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Acoustic stimuli were presented through a PC-controlled an auditory neurophysiology workstation (Tucker-Davis Technologies, USA). The hardware of the workstation for presenting acoustic stimuli included a multifunction processor (RX6-A5), a stereo power amplifier (SA1), and two multi-field magnetic speakers (MF1). The acoustic stimuli were delivered to the ears of the rats via a close-field system similar to our previous studies (Liu et al., 2021). Briefly, the MF1 speakers were incorporated internal parabolic cones and coupled to the ears through PVC plastic tubes (9.5 cm long, 1/16 inch ID, 1/8 inch OD, and 1/32 inch wall thickness) leading to the ear canals. Adaptable plastic tubes were used when necessary to couple the ear canals of infant rats. The distance from the end of the tube in the ear canal to the tympanic membrane was approximately 5 mm. The output of each MF1 speaker was calibrated from 2.0 to 44.0 kHz (sampling rate, 100 kHz) using a 1/4 inch condenser microphone (model 7,016, ACO Pacific Inc.) coupled to the end of the plastic tube (with 5 mm distance to the microphone) with a suitable latex tube. The calibration data from the MF1 speakers were stored in computer and used for obtaining the desired sound pressure levels in decibel (dB SPLs, re: 20 μPa) within frequency ranging from 2.0 to 44.0 kHz. This close-field sound delivery system was used to precisely control the acoustic stimulus parameters presented in the two ears.

The acoustic stimuli were either pure tones (100 ms duration, 5 ms rise-fall time) or noise bursts (broadband white noise, 4.0–44.0 kHz, 100 ms duration) shaped with linear rise and fall functions (1 ms rise time and 1 ms fall time). The tone bursts were used to search the characteristic frequency (CF) of the inferior collicular neurons, and the noise bursts were used to measure the GDTs of rat inferior collicular neurons. The acoustic stimuli were presented monaurally to either ear, or binaurally to both ears simultaneously.

Gap stimuli (i.e., pairs of noise bursts with varying durations of silent gaps) were used to measure the GDT of each neuron. The two noise bursts were identical and separated by a silent gap between them. The gap durations were varied from 0 ms to 200 ms (i.e., 0, 2, 4, 6, 8, 10, 15, 20, 30, 40, 50, 100, 150, and 200 ms). Under the condition of the 0 ms gap duration, the downward ramp of the leading noise burst (noise burst 1, NB1) and the upward ramp of the lagging noise burst (noise burst 2, NB2) abutted each other without a true silent gap between NB1 and NB2. To create a gap between NB1 and NB2, the onset of NB2 related to the recording epoch was held constant at 400 ms, whereas the silent interval (gap duration) between NB1 and NB2 was varied. The inter-trial interval for successive stimulus trials of stimuli was 1,200 ms.

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