Sound-attenuated Booth Research Articles

The effects of nembutal anesthesia on the auditory steady-state response (ASSR) from the inferior colliculus and auditory cortex of the chinchilla

We examined the effects of nembutal anesthesia on the amplitude of the auditory steady-state response (ASSR) in the inferior colliculus (IC) and auditory cortex (AC) of the chinchilla. Tungsten electrodes were chronically implanted following anesthesia with ketamine/acepromazine. After a recovery period, the chinchillas were placed in a passive restraining device and put in a sound-attenuating booth. Recordings were made from the right IC and AC simultaneously, while a two-tone stimulus was presented to the left ear. The stimuli consisted of two equal-level tones (F1 and F2) that were mixed acoustically; F1 remained constant at 2000 Hz, while F2 varied between 2029 and 2249 Hz, in steps of ∼20 Hz. The stimuli decreased in 10 dB steps from 80 to 30 dB pSPL. Animals were evaluated when unanesthetized, as well as when anesthetized with nembutal (on separate days). In the IC, the administration of nembutal resulted in either no change in ASSR amplitude or an amplitude increase for difference tone (DT) frequencies below 90 Hz, while an amplitude decrease was typically seen for DT frequencies at or above 90 Hz. In the AC, a decrease in amplitude was seen across DT frequencies and stimulus levels after the administration of nembutal anesthesia. Our results suggest that both the AC and IC may contribute to the scalp-recorded ASSR in the awake state. However, in the nembutal-anesthetized state, it seems unlikely that the AC contributes substantially to the surface-recorded ASSR, as the AC response was greatly attenuated under nembutal anesthesia. In contrast, the IC ASSR responses remained robust, which makes it a likely contributor to the surface-recorded responses under nembutal anesthesia.

Onset and offset responses from inferior colliculus and auditory cortex to paired noisebursts: inner hair cell loss

Thirteen adult chinchillas were anesthetized with ketamine/acepromazine and tungsten electrodes were placed in the right inferior colliculus (IC) and auditory cortex (AC). A reference electrode was implanted in the anterior cranium. Following a recovery period, AC and IC responses to left ear stimulation were obtained from unanesthetized animals resting in a passive restraint inside a sound-attenuating booth. After the first recording, the animals were injected with carboplatin (75 mg/kg). Four to five weeks later, a second recording was made. Stimuli were 50 ms duration (0 ms rise and fall time), 80 dB SPL noiseburst pairs. In one group of seven animals, the gap time varied from 1 to 64 ms. In a second group of six animals, the gap time ranged from 0.25 to 64 ms in order to determine gap threshold. The responses were amplified (10 000×) and filtered from 10 to 3000 Hz. Each response was the average of 100 stimulus presentations. The dependent variables were the latency of the initial positive peak and the amplitude of the response from initial positive peak to the following negativity. Following the second recording, all animals were sacrificed, the cochleas harvested, and cochleograms were obtained by counting outer hair cells (OHCs) and inner hair cells (IHCs). For the onset response to the second noiseburst of each pair, response amplitudes decreased and latencies increased with decreasing gap time. For a 64 ms gap time, the IC response approached the latencies and amplitudes seen for the onset response to the single noiseburst or first noiseburst in the pair (herein called ‘baseline’ values), while the AC response latency approached baseline values, but AC amplitude did not. Interestingly, the offset responses to the first noiseburst were not present at gaps of less than 8 ms, while the onset responses to the second noiseburst were typically present at gaps of 1–2 ms. Cochleograms revealed a normal (or near-normal) complement of OHCs, and IHC loss averaging roughly 30–40% in apical regions and increasing to 60–70% in more basal regions (compared to normative data). Following carboplatin, the latencies of IC onset responses were delayed by several tenths of a millisecond, with the greatest pre- versus post-carboplatin latency shift occurring at short noiseburst gaps. AC response latencies were largely unaffected by carboplatin. IC onset response amplitudes were reduced following carboplatin, while AC onset responses were similar to pre-carboplatin values. IC offset response latencies to the first noiseburst were increased post-carboplatin, while AC offset response latencies varied little from pre-carboplatin values. IC and AC offset response amplitudes to the first noiseburst were decreased post-carboplatin.

363. Test-retest reliability of brain SPECT studies in normals

Brain HMAO SPECT studies are used to evaluate brain activity in clinical populations. SPECT studies are also conducted in protocols comparing the brain’s resting state with that seen during an activation procedure. However, no data are available to evaluate the stability of these measures over time. We conducted HMPAO-SPECT studies of 6 normal control subjects (3 males age 32 ± 6.5 years and 3 females age 31 ± 14.5 years) on two occasions at least one week apart. Conditions of each study were maintained constant. To minimize the effects of ambient sound and light, subjects were injected while reclining in a relaxed mode in a sound-attenuating booth with eyes covered. To reduce anxiety, the HMPAO was injected via a previously-prepared I.V. line which passed out of the booth. The SPECT images were obtained by triple-headed gamma camera one-hour post-injection of the standard dose of 25 mCi of Tc-99m HMPAO. The analysis of images involved coregistration in space and intensity normalization. Two methods of analysis were used. One, involved the analysis of regions of interest identified by MRI. Method two involved voxel-by-voxel evaluation based on Statistical Parametric Mapping (SPM). The results of these analyses showed that there were no significant differences between the two studies. The range of differences in the ROI analysis was 1–2.5%. The SPM analysis resulted in no detectable difference at the level of p < 0.05. These data provide evidence that brain perfusion studies by HMPAO SPECT under well-controlled conditions are a stable and useful tool for the evaluation of brain function over time.

Clinical Application of Sustained Auditory Evoked Potentials

This chapter discusses clinical application of sustained auditory evoked potentials. Clinical applications of evoked potentials range from the investigation of the effects of psychoactive compounds in normals to the search for neurophysiologic alterations that might accompany psychopathology. The chapter presents the results of 3 separate clinical studies designed to investigate the central nervous system (CNS) alterations seen: (1) in normal aging, (2) in schizophrenia, and (3) after long-term excessive consumption of alcohol. In each study, a similar paradigm is employed, allowing comparison among the results of the 3 studies. In each study evoked potentials were obtained during the presentation of sustained auditory stimuli 500 msec in duration. The stimulus series consisted of 500 Hz tones delivered at 4 different intensities above sensation threshold. The inter-stimulus interval (ISI) is 1500 msec and the stimuli were presented in a pseudo-random sequence with intensity following every other with equal frequency. The subjects received the stimuli through stereo headphones while sitting in a sound-attenuating booth.