Article

Anesthesia suppresses nonsynchronous responses to repetitive broadband stimuli

University of Oklahoma, 865 Asp Avenue, Felgar Hall 210, Norman, OK 73019, USA.
Neuroscience (Impact Factor: 3.33). 04/2007; 145(1):357-69. DOI: 10.1016/j.neuroscience.2006.11.043
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ABSTRACT Although many aspects of sensory processing are qualitatively similar in awake and anesthetized subjects, important state-dependent differences are known to exist. To investigate the effects of anesthesia on temporal processing in rat auditory cortex, multi-unit neural responses to trains of broadband clicks were recorded prior to, 15 min following, and 5 h following the administration of a ketamine-based anesthetic. While responses to clicks in isolation were relatively stable between states, responses to subsequent clicks exhibited increases in latency, peak latency, response duration, and post-onset suppression under anesthesia. Ketamine anesthetic reduced the maximum rate at which multi-unit clusters entrained to repeated clicks. No multi-unit clusters entrained to stimulus presentation rates greater than 33 Hz under anesthesia, compared with 85% and 81% in the pre- and post-anesthetic condition, respectively. Anesthesia also induced oscillatory activity that was not present in awake subjects. Finally, ketamine anesthesia abolished all tonic excitatory and suppressive nonsynchronous responses to click trains. The results of this study suggest that ketamine-based anesthesia significantly alters neural coding of broadband click trains in auditory cortex.

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Available from: Sara E Anderson, Jan 13, 2014
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    • "Apart from its amplitude effects, ketamine robustly suppressed and delayed the latency of ERPs, especially at the first time point (~10 min post-injection), suggesting a relative slowing of signal processing and delay in peak synchrony of the neural oscillators generating the ERP response. Ketamine-induced slowing of ERPs has been reported both in clinical (30, 83) as well as in experimental subjects previously (56, 84, 85). Apart from its effects on N1 amplitude and latency, Ketamine impacted other ERP components as well. "
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    • "The difference in the persistence of adaptation in the results of Eggermont (2000) and our results may be due to the fact that Eggermont (2000) used anesthesia. Anesthesia would be expected to diminish or even abolish the ongoing response to the adapter (e.g., Cheung et al. 2001; Rennaker et al. 2007), allowing synapses to recover from depression and abolishing sAHP (Schwindt 1988a). Anesthesia may also be expected to affect the processes involved in the reuptake of neurotransmitter after its release into the synaptic cleft and thus shorten the recovery from synaptic depression (Richards 2002). "
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    • "To date, only one study used the awake rats to examine the ability of multi-unit clusters in A1 in response to click-trains. The results showed that anesthesia could significantly alter the temporal patterns of neural response, and suppress the non-synchronized response [11]. The neural response of AAF to temporal modulated stimuli has not been investigated under either anesthetized or awake condition. "
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