Modulation of auditory deviance detection by acute nicotine is baseline and deviant dependent in healthy nonsmokers: a mismatch negativity study

Abstract

These findings provide preliminary support for the role of nicotinic neurotransmission in sensory memory processing of auditory change and suggest that nicotinic receptor modulation can both enhance and diminish change detection, depending on baseline MMN and its eliciting stimulus feature.

An acute dose, randomized trial of the effects of CDP-Choline on Mismatch Negativity (MMN) in healthy volunteers stratified by deviance detection level

“…In general, the findings parallel our earlier report of the dual actions of the broad spectrum nAChR agonist, nicotine, on MMN in groups of healthy surrogates exhibiting relatively compromised and efficient deviance detection (Knott et al 2014). Increases in auditory change detection in individuals with diminished MMNs are of particular importance for SZ.…”

“…In line with previous suggestions of an inverted U-shaped response characterizing cognitive effects of nicotinic stimulation (Newhouse et al 2004), and based on our recent study with the prototypical nAChR agonist, nicotine, which enhanced auditory deviance detection in individuals with small amplitude MMNs and attenuated deviance detection in those with higher amplitude MMNs (Knott et al 2014), we hypothesized that both doses of CDP-choline (vs. placebo) would increase deviance detection (MMN) in individuals exhibiting relatively diminished detection ability (i.e. low baseline MMN amplitudes) and exert negative or diminishing effects in those with relatively moderate, optimal, or above optimal detection ability (i.e., medium or high baseline MMN amplitudes).…”

“…Frequently shown in animal models and in human studies, baseline-dependent differences have influenced behavioural, cognitive, and subjective mood responses to nicotine (Perkins 1999). More recently, baseline-dependent neural responses to nicotine have been evidenced with two widely used biomarkers of SZ, namely, P50-indexed auditory sensory gating (Knott et al , 2013 and MMN-indexed auditory sensory discrimination (Knott et al 2014), with both biomarkers being enhanced by acute nicotine, but only in individuals with relatively diminished, SZ-like P50 gating and MMN baseline responses. In individuals with high baseline gating and discriminability, P50 suppression and MMN amplitude were either not affected, or were attenuated by single dose nicotine treatment.…”

Stimulus-specific adaptation in the inferior colliculus: The role of excitatory, inhibitory and modulatory inputs

“…In humans, cholinergic manipulation affects auditory novelty detection (Klinkenberg, Blokland, Riedel, & Sambeth, 2013;Knott et al, 2014;Moran et al, 2013). Likewise, diverse studies in animals support the notion that ACh release is necessary for the induction of auditory plasticity (Bjordahl, Dimyan, & Weinberger, 1998;Edeline, 2012;Leach, Nodal, Cordery, King, & Bajo, 2013;Metherate & Weinberger, 1989).…”

“…Schizophrenia has been associated with alterations in neurotransmission as the one mediated by the NMDA (N-methyl-d-aspartate) receptor (Matsuno et al, 2015). Moreover, several studies have showed that acoustic MMN is sensitive to cholinergic modulation (Dunbar et al, 2007;Knott et al, 2014;Mathalon et al, 2014;Moran, Campo, Symmonds, Stephan, Dolan, & Friston, 2013) or to nitrous oxide (N 2 O) (e.g., Pang & Fowler, 1999). In autism spectrum disorders, larger amplitudes and earlier latencies relative to control subjects have been observed in children and adults diagnosed with these disorders (Kujala et al, 2007;Lepisto et al, 2008).…”