Abstract
Auditory steady state response (ASSR) and inhibitory gating (IG) are electrophysiological examinations commonly used to evaluate the sensory and cognitive functions of the brain. In some clinic examinations and animal experiments, general anesthesia is necessary to conduct electrophysiological recordings. However, the effects of anesthesia on ASSR and IG remain unclear. For this reason, we recorded local field potentials though electrodes implanted in different brain areas of rats: the auditory cortex (AC), hippocampus (HC), amygdala (AMY), and prefrontal cortex (PFC), and compared the characteristics of ASSR and IG under anesthetized and conscious conditions. We found that ASSR signals were the strongest in the AC, and decreased sequentially in the HP, AMY, and PFC. Chloral hydrate anesthesia significantly reduced the power and phase-locking of ASSR in the AC, HP, and AMY. In contrast, the extent of IG in the AC was weakest and it increased sequentially in the HP, AMY, and PFC. Anesthesia had less effect on the extent of IG. Our results suggest that ASSR and IG may originate from different neural circuits and that IG is more resistant to general anesthesia and therefore better suited to examining the functioning of non-auditory brain regions.
Highlights
Auditory steady state response (ASSR) and inhibitory gating (IG) are commonly used to evaluate the sensory and cognitive functions of the central nervous system
mean trial power (MTP) reveals the amplitude of the evoked local field potentials (LFPs), and phase-locking factor (PLF) examines the trial-to-trial dynamics of the phase-locked response
The mean MTP and PLF of the conscious and anesthetized conditions are presented in Fig. 1F and G, and indicate that the MTP and PLF were obviously reduced by anesthesia
Summary
Auditory steady state response (ASSR) and inhibitory gating (IG) are commonly used to evaluate the sensory and cognitive functions of the central nervous system. IG is estimated using evoked response potential (ERP) techniques in which identical pairs of auditory stimuli (tones, white noises or clicks) are presented and ERP responses to the stimuli are elicited and compared. Because general anesthesia is required in some cases of clinical examination and animal experimentation, the effects of anesthesia on ASSR and IG warrant investigation. We designed this study to examine the effects of anesthesia on ASSR and IG recorded from different www.nature.com/scientificreports/. We implanted microelectrodes in the auditory cortex (AC), hippocampus (HC), amygdala (AMY), and prefrontal cortex (PFC) of rats and recorded the local field potentials (LFPs) evoked by auditory stimuli (click-trains and noise pairs) under conscious and chloral hydrate anesthetized conditions. By comparing the LFPs recorded from the auditory and non-auditory regions, we found different anatomical distributions of ASSR and IG, and different effects of anesthesia on ASSR and IG
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