Abstract
Systemic nicotine enhances neural processing in primary auditory cortex (A1) as determined using tone-evoked, current-source density (CSD) measurements. For example, nicotine enhances the characteristic frequency (CF)-evoked current sink in layer 4 of A1, increasing amplitude and decreasing latency. However, since presenting auditory stimuli within a stream of stimuli increases the complexity of response dynamics, we sought to determine the effects of nicotine on CSD responses to trains of CF stimuli (one-second trains at 2–40 Hz; each train repeated 25 times). CSD recordings were obtained using a 16-channel multiprobe inserted in A1 of urethane/xylazine-anesthetized mice, and analysis focused on two current sinks in the middle (layer 4) and deep (layers 5/6) layers. CF trains produced adaptation of the layer 4 response that was weak at 2 Hz, stronger at 5–10 Hz and complete at 20–40 Hz. In contrast, the layer 5/6 current sink exhibited less adaptation at 2–10 Hz, and simultaneously recorded auditory brainstem responses (ABRs) showed no adaptation even at 40 Hz. Systemic nicotine (2.1 mg/kg) enhanced layer 4 responses throughout the one-second stimulus train at rates ≤10 Hz. Nicotine enhanced both response amplitude within each train and the consistency of response timing across 25 trials. Nicotine did not alter the degree of adaptation over one-second trials, but its effect to increase amplitudes revealed a novel, slower form of adaptation that developed over multiple trials. Nicotine did not affect responses that were fully adapted (20–40 Hz trains), nor did nicotine affect any aspect of the layer 5/6 current sink or ABRs. The overall effect of nicotine in layer 4 was to enhance all responses within each train, to emphasize earlier trials across multiple trials, and to improve the consistency of timing across all trials. These effects may improve processing of complex acoustic streams, including speech, that contain information in the 2–10 Hz range.
Highlights
MATERIALS AND METHODSActivation of nicotinic acetylcholine receptors increases neural excitability due to the influx of cations through the receptor ion channel (Dani and Bertrand, 2007; Albuquerque et al, 2009)
Since repetitive stimulation produces strong adaptation in A1 and systemic nicotine enhances cortical responses, here we examined the effects of nicotine on response adaptation during characteristic frequency (CF) stimulus trains
We examined the effects of systemic nicotine on currentsource density (CSD) responses to CF stimulus trains of 2–40 Hz in urethane/xylazineanesthetized mice
Summary
MATERIALS AND METHODSActivation of nicotinic acetylcholine receptors (nAChRs) increases neural excitability due to the influx of cations through the receptor ion channel (Dani and Bertrand, 2007; Albuquerque et al, 2009). In primary auditory cortex (A1) of rodents, for example, nicotine enhances the characteristic frequency (CF)-evoked thalamocortical response (layer 4 current sink), increasing peak amplitude and decreasing both onset and peak latencies (Intskirveli and Metherate, 2012; Askew et al, 2017).
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