Resting-state EEG, impulsiveness, and personality in daily and nondaily smokers

OBJECTIVES: Resting EEG is sensitive to transient, acute effects of nicotine administration and abstinence, but the chronic effects of smoking on EEG are poorly characterized. This study measures the resting EEG profile of chronic smokers in a non-deprived, non-peak state to test whether differences in smoking behavior and personality traits affect pharmaco-EEG response. METHODS: Resting EEG, impulsiveness, and personality measures were collected from daily smokers (n=22), nondaily smokers (n=31), and non-smokers (n=30). RESULTS: Daily smokers had reduced resting delta and alpha EEG power and higher impulsiveness (Barratt Impulsiveness Scale) compared to nondaily smokers and non-smokers. Both daily and nondaily smokers discounted delayed rewards more steeply, reported lower conscientiousness (NEO-FFI), and reported greater disinhibition and experience seeking (Sensation Seeking Scale) than non-smokers. Nondaily smokers reported greater sensory hedonia than nonsmokers. CONCLUSIONS: Altered resting EEG power in daily smokers demonstrates differences in neural signaling that correlated with greater smoking behavior and dependence. Although nondaily smokers share some characteristics with daily smokers that may predict smoking initiation and maintenance, they differ on measures of impulsiveness and resting EEG power. SIGNIFICANCE: Resting EEG in non-deprived chronic smokers provides a standard for comparison to peak and trough nicotine states and may serve as a biomarker for nicotine dependence, relapse risk, and recovery

Neural correlates of performance monitoring in daily and intermittent smokers

OBJECTIVES: Despite efforts that have increased smoking regulation, cigarette taxation, and social stigma, cigarette smoking remains the leading cause of preventable death worldwide, and a significant personal and public economic burden. In the U.S., intermittent smokers comprise approximately 22% of all smokers and represent a stable, non-dependent group that may possess protective factors that prevent the transition to dependence. One possibility is that intermittent smokers have intact CNS frontal regulatory and control mechanisms that enable resistance to nicotine-induced changes. METHODS: The present study measured inhibitory control using a flanker task and a go-nogo continuous performance tasks in daily dependent smokers, intermittent non-dependent smokers, and nonsmokers. Event-related potential (ERP) measures of were concurrently recorded to measure performance monitoring via Event-Related Negativity (ERN) and error positivity (Pe) components during error trials for each task. RESULTS: In both tasks, behavioral and ERN measures did not differ between groups; however, amplitude of the Pe component was largest among intermittent smokers. CONCLUSIONS: Thus, intermittent smokers differed from both daily smokers and nonsmokers on error processing, potentially revealing neuroprotective cognitive processes in nicotine dependence. SIGNIFICANCE: A better understanding of factors that mediate behavioral regulation may provide novel treatment approaches that help individuals achieve controlled smoking or cessation

The auditory steady-state response (ASSR): a translational biomarker for schizophrenia

Electrophysiological methods have demonstrated disturbances of neural synchrony and oscillations in schizophrenia which affect a broad range of sensory and cognitive processes. These disturbances may account for a loss of neural integration and effective connectivity in the disorder. The mechanisms responsible for alterations in synchrony are not well delineated, but may reflect disturbed interactions within GABAergic and glutamatergic circuits, particularly in the gamma range. Auditory steady-state responses (ASSRs) provide a non-invasive technique used to assess neural synchrony in schizophrenia and in animal models at specific response frequencies. ASSRs are electrophysiological responses entrained to the frequency and phase of a periodic auditory stimulus generated by auditory pathway and auditory cortex activity. Patients with schizophrenia show reduced ASSR power and phase locking to gamma range stimulation. We review alterations of ASSRs in schizophrenia, schizotypal personality disorder, and first-degree relatives of patients with schizophrenia. In vitro and in vivo approaches have been used to test cellular mechanisms for this pattern of findings. This translational, cross-species approach provides support for the role of N-methyl-D-aspartate and GABAergic dysregulation in the genesis of perturbed ASSRs in schizophrenia and persons at risk

Disturbed resting state EEG synchronization in bipolar disorder: A graph-theoretic analysis

AbstractDisruption of functional connectivity may be a key feature of bipolar disorder (BD) which reflects disturbances of synchronization and oscillations within brain networks. We investigated whether the resting electroencephalogram (EEG) in patients with BD showed altered synchronization or network properties. Resting-state EEG was recorded in 57 BD type-I patients and 87 healthy control subjects. Functional connectivity between pairs of EEG channels was measured using synchronization likelihood (SL) for 5 frequency bands (δ, θ, α, β, and γ). Graph-theoretic analysis was applied to SL over the electrode array to assess network properties. BD patients showed a decrease of mean synchronization in the alpha band, and the decreases were greatest in fronto-central and centro-parietal connections. In addition, the clustering coefficient and global efficiency were decreased in BD patients, whereas the characteristic path length increased. We also found that the normalized characteristic path length and small-worldness were significantly correlated with depression scores in BD patients. These results suggest that BD patients show impaired neural synchronization at rest and a disruption of resting-state functional connectivity

Phencyclidine Disrupts the Auditory Steady State Response in Rats

The Auditory Steady-State Response (ASSR) in the electroencephalogram (EEG) is usually reduced in schizophrenia (SZ), particularly to 40 Hz stimulation. The gamma frequency ASSR deficit has been attributed to N-methyl-D-aspartate receptor (NMDAR) hypofunction. We tested whether the NMDAR antagonist, phencyclidine (PCP), produced similar ASSR deficits in rats. EEG was recorded from awake rats via intracranial electrodes overlaying the auditory cortex and at the vertex of the skull. ASSRs to click trains were recorded at 10, 20, 30, 40, 50, and 55 Hz and measured by ASSR Mean Power (MP) and Phase Locking Factor (PLF). In Experiment 1, the effect of different subcutaneous doses of PCP (1.0, 2.5 and 4.0 mg/kg) on the ASSR in 12 rats was assessed. In Experiment 2, ASSRs were compared in PCP treated rats and control rats at baseline, after acute injection (5 mg/kg), following two weeks of subchronic, continuous administration (5 mg/kg/day), and one week after drug cessation. Acute administration of PCP increased PLF and MP at frequencies of stimulation below 50 Hz, and decreased responses at higher frequencies at the auditory cortex site. Acute administration had a less pronounced effect at the vertex site, with a reduction of either PLF or MP observed at frequencies above 20 Hz. Acute effects increased in magnitude with higher doses of PCP. Consistent effects were not observed after subchronic PCP administration. These data indicate that acute administration of PCP, a NMDAR antagonist, produces an increase in ASSR synchrony and power at low frequencies of stimulation and a reduction of high frequency (> 40 Hz) ASSR activity in rats. Subchronic, continuous administration of PCP, on the other hand, has little impact on ASSRs. Thus, while ASSRs are highly sensitive to NMDAR antagonists, their translational utility as a cross-species biomarker for NMDAR hypofunction in SZ and other disorders may be dependent on dose and schedule

Acute Phencyclidine Alters Neural Oscillations Evoked by Tones in the Auditory Cortex of Rats

BACKGROUND/AIMS: The onset response to a single tone as measured by electroencephalography (EEG) is diminished in power and synchrony in schizophrenia. Because neural synchrony, particularly at gamma frequencies (30-80 Hz), is hypothesized to be supported by the N-methyl-D-aspartate receptor (NMDAr) system, we tested whether phencyclidine (PCP), an NMDAr antagonist, produced similar deficits to tone stimuli in rats. METHODS: Experiment 1 tested the effect of a PCP dose (1.0, 2.5, and 4.5 mg/kg) on response to single tones on intracranial EEG recorded over the auditory cortex in rats. Experiment 2 evaluated the effect of PCP after acute administration of saline or PCP (5 mg/kg), after continuous subchronic administration of saline or PCP (5 mg/kg/day), and after a week of drug cessation. In both experiments, a time-frequency analysis quantified mean power (MP) and phase locking factor (PLF) between 1 and 80 Hz. Event-related potentials (ERPs) were also measured to tones, and EEG spectral power in the absence of auditory stimuli. RESULTS: Acute PCP increased PLF and MP between 10 and 30 Hz, while decreasing MP and PLF between approximately 50 and 70 Hz. Acute PCP produced a dose-dependent broad-band increase in EEG power that extended into gamma range frequencies. There were no consistent effects of subchronic administration on gamma range activity. Acute PCP increased ERP amplitudes for the P16 and N70 components. CONCLUSIONS: Findings suggest that acute PCP-induced NMDAr hypofunction has differential effects on neural power and synchrony which vary with dose, time course of administration and EEG frequency. EEG synchrony and power appear to be sensitive translational biomarkers for disrupted NMDAr function, which may contribute to the pathophysiology of schizophrenia and other neuropsychiatric disorders

Examining the role of menthol cigarettes in progression to established T smoking among youth

Background: Menthol, a flavoring compound added to cigarettes, makes cigarettes more appealing to youth and inexperienced smokers and increases cigarettes\u27 abuse liability. However, limited studies are available on menthol\u27s role in smoking progression. Methods: To assess the association between menthol in cigarettes and progression to established smoking, we used five waves of data from the Evaluation of Public Education Campaign on Teen Tobacco Cohort Study, a nationally representative longitudinal survey of U.S. youth conducted as part of “The Real Cost” evaluation. We used discrete time survival analysis to model the occurrence of two event outcomes—progression to established, current smoking and progression to established, frequent smoking—using a logit model with a menthol use indicator as the key explanatory variable. Based on this framework, we estimated the effect of prior menthol use on the odds of smoking progression. Results: In the progression to established, current smoking model, prior menthol use was significantly associated with progression [adjusted odds ratio (aOR) = 1.80, p \u3c .05, confidence interval (CI) = (1.03–3.16)]. While results were in a similar direction for the model of progression to established, frequent smoking, the association between prior menthol use and this progression model did not reach significance [aOR=1.56, CI = (0.80–3.03)]. Conclusion: The results suggest a relationship between using menthol cigarettes and progression from experi- mental to established, current smoking among youth. This study adds to a growing literature base that supports that menthol cigarettes, compared to nonmenthol cigarettes, put youth at increased risk for regular cigarette use

Examining the role of menthol cigarettes in progression to established T smoking among youth

Background: Menthol, a flavoring compound added to cigarettes, makes cigarettes more appealing to youth and inexperienced smokers and increases cigarettes\u27 abuse liability. However, limited studies are available on menthol\u27s role in smoking progression. Methods: To assess the association between menthol in cigarettes and progression to established smoking, we used five waves of data from the Evaluation of Public Education Campaign on Teen Tobacco Cohort Study, a nationally representative longitudinal survey of U.S. youth conducted as part of “The Real Cost” evaluation. We used discrete time survival analysis to model the occurrence of two event outcomes—progression to established, current smoking and progression to established, frequent smoking—using a logit model with a menthol use indicator as the key explanatory variable. Based on this framework, we estimated the effect of prior menthol use on the odds of smoking progression. Results: In the progression to established, current smoking model, prior menthol use was significantly associated with progression [adjusted odds ratio (aOR) = 1.80, p \u3c .05, confidence interval (CI) = (1.03–3.16)]. While results were in a similar direction for the model of progression to established, frequent smoking, the association between prior menthol use and this progression model did not reach significance [aOR=1.56, CI = (0.80–3.03)]. Conclusion: The results suggest a relationship between using menthol cigarettes and progression from experi- mental to established, current smoking among youth. This study adds to a growing literature base that supports that menthol cigarettes, compared to nonmenthol cigarettes, put youth at increased risk for regular cigarette use