Catecholaminergic function and P300 amplitude in major depressive disorder (P300 and catecholamines)

Hansenne, Michel; Pitchot, William; Moreno, A. González; Papart, Patrick; Timsit‐Berthier, M.; Ansseau, Marc

doi:10.1016/0168-5597(94)00317-8

Cited by 45 publications

(25 citation statements)

References 10 publications

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“…This finding is similar to the report that P200 amplitude was greater in depressive patients than in normal controls [15]. It is suggested that neurotransmitters, such as serotonin, catecholamines, and GABA, play a role in the generation of AERPs [16][17][18], and hence that disturbances in these neurotransmitter systems could be involved in the alterations in AERPs in SD. Another interesting finding from the present study is the significant interactive effects or interactive tendencies between order of days (SD) and TD on sleepiness, fatigue, and negative mood.…”

Section: Discussionsupporting

confidence: 80%

Auditory Event-Related Potentials and Psychological Changes during Sleep Deprivation

Lee¹,

Kim²,

Suh³

et al. 2004

Neuropsychobiology

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This study investigated the psychophysiological effects of sleep deprivation on auditory event-related potentials (AERPs) and their relationship with psychological parameters. Twenty-four subjects remained awake for 37 h under continuous surveillance. In the mornings and the evenings of 2 consecutive study days, AERPs were recorded and 4 self-rated scales (sleepiness, fatigue, anxiety, and mood) were quantified. The latencies of P300 and N200 were significantly prolonged (p < 0.001) and their amplitudes decreased (p < 0.05) as a consequence of sleep deprivation. However, the only significant change in N100 and P200 was an increase in the P200 amplitude (p < 0.05). The increase in the latencies of P300 and N200 were correlated with increased sleepiness (p < 0.05), and the increase in P200 amplitude was correlated with negative mood, anxiety, and fatigue (p < 0.05). Although the changes in P300 and N200 induced by sleep deprivation are due to sleepiness, which may slow cognitive processing and decrease the efficiency of mental processing, the increase in P200 may be related with increased anxiety, negative mood, and fatigue.

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Section: Discussionsupporting

confidence: 80%

Auditory Event-Related Potentials and Psychological Changes during Sleep Deprivation

Lee¹,

Kim²,

Suh³

et al. 2004

Neuropsychobiology

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“…Like other substances of abuse, nicotine activates the mesolimbic dopamine system, and this effect appears to be essential for the reinforcing properties of nicotine (Ashton and Golding 1989;Nisell et al 1995). Vulnerability to both smoking and alcoholism may be mediated by common alterations of brain neurotransmission systems that influence P300 amplitude, a conclusion supported by evidence that dopamine is involved in the neu-rophysiological mechanisms which generate and/or modulate P300 (Stanzione et al 1991;Hansenne et al 1995).…”

Section: Discussionmentioning

confidence: 71%

The P300 brain potential is reduced in smokers

Anokhin¹,

Vedeniapin²,

Sirevaag³

et al. 2000

Psychopharmacology

117

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Rationale: Tobacco smoking is the most prevalent type of substance abuse, yet its biobehavioral etiology is little understood. Identification of differences between smokers and non-smokers on basic characteristics of neurocognitive functioning may help to elucidate the mechanisms of tobacco dependence. Objectives: This study assessed the relationship between smoking status and the P300 component of event-related potential (ERP) while controlling for potential confounders such as alcoholism, drug abuse, and psychopathology. Methods: The ERP responses elicited by a visual oddball task were measured at the mid-parietal site in 905 current smokers, 463 ex-smokers, and 979 never smokers. Results: P300 amplitude was significantly lower in current cigarette smokers compared to never-smokers. Exsmokers did not differ significantly from never-smokers. P300 reduction was also associated with alcoholism, drug dependence, and family density of alcoholism. However, after controlling for smoking, only family density of alcoholism remained a significant predictor of P300 amplitude. Conclusions: The results indicate a significant effect of smoking status on P300 amplitude which is additive to family history of alcoholism and suggest that either (1) long-term tobacco smoking may produce a reversible change in brain function, or (2) reduced P300 may be a marker of risk for nicotine dependence.

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“…(2) The dopamine antagonist sulpiride increases P300 in low-amplitude subjects and decreases it in high-amplitude subjects (Takeshita and Ogura, 1994). (3) Pharmacological studies have found dopaminergic mediation of P300 amplitude and latency (Hansenne et al, 1995;Wang et al, 2000). (4) Children at elevated risk for alcoholism demonstrate dopamine-related genetic differences and P300 amplitude deficits (Hill et al, 1998), which may be associated with an "endophenotype of alcoholism" that likely originate from externalizing disorders (cf.…”

Section: Dual-transmitter Hypothesismentioning

confidence: 99%

Updating P300: An integrative theory of P3a and P3b

Polich

2007

Clinical Neurophysiology

6,455

458

6,265

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The empirical and theoretical development of the P300 event-related brain potential (ERP) is reviewed by considering factors that contribute to its amplitude, latency, and general characteristics. The neuropsychological origins of the P3a and P3b subcomponents are detailed, and how target/ standard discrimination difficulty modulates scalp topography is discussed. The neural loci of P3a and P3b generation are outlined, and a cognitive model is proffered: P3a originates from stimulusdriven frontal attention mechanisms during task processing, whereas P3b originates from temporalparietal activity associated with attention and appears related to subsequent memory processing. Neurotransmitter actions associating P3a to frontal/dopaminergic and P3b to parietal/norepinephrine pathways are highlighted. Neuroinhibition is suggested as an overarching theoretical mechanism for P300, which is elicited when stimulus detection engages memory operations.

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Catecholaminergic function and P300 amplitude in major depressive disorder (P300 and catecholamines)

Cited by 45 publications

References 10 publications

Auditory Event-Related Potentials and Psychological Changes during Sleep Deprivation

Auditory Event-Related Potentials and Psychological Changes during Sleep Deprivation

The P300 brain potential is reduced in smokers

Updating P300: An integrative theory of P3a and P3b

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