COMT polymorphism modulates the resting‐state EEG alpha oscillatory response to acute nicotine in male non‐smokers

Bowers, Hayley; Smith, Dylan M.; Choueiry, Joëlle; Impey, Danielle; Philippe, Tristan; Dort, H.; Millar, Anne; Daigle, Mireille; Albert, Paul R.; Beaudoin, Adrien R.; Knott, Verner

doi:10.1111/gbb.12226

Cited by 10 publications

(8 citation statements)

References 170 publications

(182 reference statements)

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“…A more recent study [55] investigated the modulatory role of the COMT genotype on nicotine effects in resting-state condition in nonsmokers. They found an increase in upper α power frontocentrally in Met/Met carriers.…”

Section: Discussionmentioning

confidence: 99%

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EEG Source Reconstruction in Male Nonsmokers after Nicotine Administration during the Resting State

Ranzi

Thiel²,

Herrmann³

2016

Neuropsychobiology

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Modern psychopharmacological research in humans focuses on how specific psychoactive molecules modulate oscillatory brain activity. We present state-of-the-art EEG methods applied in a resting-state drug study. Thirty healthy male nonsmokers were randomly allocated either to a nicotine group (14 subjects, 7 mg transdermal nicotine) or a placebo group (16 subjects). EEG activity was recorded in eyes-open (EO) and eyes-closed (EC) conditions before and after drug administration. A source reconstruction (minimum norm algorithm) analysis was conducted within a frequency range of 8.5-18.4 Hz subdivided into three different frequency bands. During EO, nicotine reduced the power of oscillatory activity in the 12.5- to 18.4-Hz frequency band in the left middle frontal gyrus. In contrast, in the EC condition, nicotine reduced the power in the 8.5- to 10.4-Hz frequency band in the superior frontal gyri and in the 10.5- to 12.4-Hz and 12.5- to 18.4-Hz frequency bands in the supplementary motor areas. In summary, nicotine reduced the power of the 12.5- to 18.4-Hz band in the left middle frontal gyrus during EO, and it reduced power from 8.5 to 18.4 Hz in a brain area spanning from the superior frontal gyri to the supplementary motor areas during EC. In conclusion, the results suggest that nicotine counteracts the phenomenon of anteriorization of α activity, hence potentially increasing the level of vigilance.

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Section: Discussionmentioning

confidence: 99%

“…Particularly, the COMT genotype seems to be important in determining the individual response to nicotine [55]. …”

Section: Discussionmentioning

confidence: 99%

EEG Source Reconstruction in Male Nonsmokers after Nicotine Administration during the Resting State

Ranzi

Thiel²,

Herrmann³

2016

Neuropsychobiology

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“…It has been reported that while muscarinic blockers like scopolamine diminish the resting parieto-occipital alpha oscillations (Sannita et al, 1987 ; Sloan et al, 1992 ; Ebert et al, 1998 , 2001 ; Kikuchi et al, 1999 ; Osipova et al, 2003 ; Ramos Reis et al, 2013 ), nicotinic administration produces the reverse effect (Gilbert et al, 2000 ; Knott et al, 2000 , 2012 ; Walker et al, 2001 ; Bowers et al, 2015 ; Smith et al, 2016 ) but see (Knott and Fisher, 2007 ; Balsters et al, 2011 ; Fisher et al, 2012b ). Acetylcholine enhancers tend to increase posterior alpha power during visuospatial attentional modulations (Bauer et al, 2012 ) Figure 1c and frontal alpha during working memory tasks (Fisher et al, 2012a , 2013 ) but see (Eckart et al, 2016 ).…”

Section: Parieto-occipital Alpha Oscillations Are Modulated By a Myrimentioning

confidence: 99%

On the Physiological Modulation and Potential Mechanisms Underlying Parieto-Occipital Alpha Oscillations

Lozano-Soldevilla

2018

Front. Comput. Neurosci.

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The parieto-occipital alpha (8–13 Hz) rhythm is by far the strongest spectral fingerprint in the human brain. Almost 90 years later, its physiological origin is still far from clear. In this Research Topic I review human pharmacological studies using electroencephalography (EEG) and magnetoencephalography (MEG) that investigated the physiological mechanisms behind posterior alpha. Based on results from classical and recent experimental studies, I find a wide spectrum of drugs that modulate parieto-occipital alpha power. Alpha frequency is rarely affected, but this might be due to the range of drug dosages employed. Animal and human pharmacological findings suggest that both GABA enhancers and NMDA blockers systematically decrease posterior alpha power. Surprisingly, most of the theoretical frameworks do not seem to embrace these empirical findings and the debate on the functional role of alpha oscillations has been polarized between the inhibition vs. active poles hypotheses. Here, I speculate that the functional role of alpha might depend on physiological excitation as much as on physiological inhibition. This is supported by animal and human pharmacological work showing that GABAergic, glutamatergic, cholinergic, and serotonergic receptors in the thalamus and the cortex play a key role in the regulation of alpha power and frequency. This myriad of physiological modulations fit with the view that the alpha rhythm is a complex rhythm with multiple sources supported by both thalamo-cortical and cortico-cortical loops. Finally, I briefly discuss how future research combining experimental measurements derived from theoretical predictions based of biophysically realistic computational models will be crucial to the reconciliation of these disparate findings.

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“…The EO condition was considered ideal for testing the effect of nicotine, because nicotine appears to target attentional networks [13,14]. The EC condition was also considered important since nicotine impacts this condition as well [15]. Lastly, a mixed-effects design was employed in which subjects were randomly allocated to a drug or placebo and each subject was tested before and after their administration.…”

Section: Introductionmentioning

confidence: 99%

“…We chose to investigate 3 frequency bands in accordance with the previous literature about EEG and nicotine during EO and EC activity [15,18,19]. The selected frequency bands used here were: α 1 , 8.5-10.4 Hz; α 2 , 10.5-12.4 Hz, and β 1 , 12.5-18.4 Hz.…”

Section: Introductionmentioning

confidence: 99%

Encephalography Connectivity on Sources in Male Nonsmokers after Nicotine Administration during the Resting State

Ranzi

Freund²,

Thiel³

et al. 2016

Neuropsychobiology

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We present an encephalography (EEG) connectivity study where 30 healthy male nonsmokers were randomly allocated either to a nicotine group (14 subjects, 7 mg of transdermal nicotine) or to a placebo group. EEG activity was recorded in an eyes-open (EO) and eyes-closed (EC) condition before and after drug administration. This is a reanalysis of a previous dataset. Through a source reconstruction procedure, we extracted 13 time series representing 13 sources belonging to a resting-state network. Here, we conducted connectivity analysis (renormalized partial directed coherence; rPDC) on sources, focusing on the frequency range of 8.5-18.4 Hz, subdivided into 3 frequency bands (α₁, α₂, and β₁) with the hypothesis that an increase in vigilance would modulate connectivity. Furthermore, a phase-amplitude coupling (mean resultant vector length; VL) analysis, was performed investigating whether an increase of vigilance would modulate phase-amplitude coupling. In the VL analysis we estimated the coupling of the phases of 3 low frequencies (α₁, α₂, and β₁), respectively, with the amplitude of high-frequency oscillations (30-40 Hz, low γ). With rPDC we found that during the EC condition, nicotine decreased feedback connectivity (from the precentral gyrus to precuneus, angular gyrus, cuneus and superior occipital gyrus) at 10.5-12.4 Hz. The VL analysis showed nicotine-induced increases in coupling at 10.5-18.4 Hz in the precuneus, cuneus and superior occipital gyrus during the EC condition. During the EO condition, no significant results were found in connectivity or phase-amplitude coupling measures at any frequency range. In conclusion, the results suggest that nicotine potentially increases the level of vigilance in the EC condition.

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COMT polymorphism modulates the resting‐state EEG alpha oscillatory response to acute nicotine in male non‐smokers

Abstract: Performance improvements in cognitive tasks requiring executive functions are evident with nicotinic acetylcholine receptor (nAChR) agonists, and activation of the underlying neural circuitry supporting these cognitive effects is thought to involve dopamine neu-

Cited by 10 publications

References 170 publications

EEG Source Reconstruction in Male Nonsmokers after Nicotine Administration during the Resting State

EEG Source Reconstruction in Male Nonsmokers after Nicotine Administration during the Resting State

On the Physiological Modulation and Potential Mechanisms Underlying Parieto-Occipital Alpha Oscillations

Encephalography Connectivity on Sources in Male Nonsmokers after Nicotine Administration during the Resting State

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