Changes in EEG spectral power in the prefrontal cortex of conscious rats elicited by drugs interacting with dopaminergic and noradrenergic transmission

Abstract

1 The electroencephalographic (EEG) eects of drugs interacting with dopaminergic and noradrenergic systems were studied in conscious rats. Power spectra (0 ± 30 Hz) were recorded from electrodes implanted bilaterally in the prefrontal cortex. Drug eects on EEG power were calculated as the spectral power following drug administration divided by the spectral power after vehicle administration. were dose-dependently antagonized by coadministration with moda®nil and cirazoline, but not by apomorphine. 4 In conclusion, pharmacological modulation of dopaminergic and noradrenergic transmission may result in consistent EEG changes: decreased dopaminergic or noradrenergic activity induces an increase of EEG spectral power; while increased dopaminergic or noradrenergic activity decreases EEG spectral power.

Power Fluctuations in Beta and Gamma Frequencies in Rat Globus Pallidus: Association with Specific Phases of Slow Oscillations and Differential Modulation by Dopamine D1and D2Receptors

“…Both D 1 and D 2 antagonists acutely increased low-beta power in the GP. This is consistent with some previous acute studies (Sebban et al, 1999;Dejean et al, 2009) and with the idea that beta power is linked to akinetic states, although increases in beta power appear to be much more robust in chronic lesion rat models of Parkinson's disease (Sharott et al, 2005).…”

Decreased Production of Reactive Oxygen Species by Blood Monocytes Caused by Clozapine Correlates with EEG Slowing in Schizophrenic Patients

“…MO may be used as a model for microglia and brain macrophages, since they share numerous functions, including the production of ROS and cytokines [24,25]. Cytokines have also been reported to affect the production of biogenic amines in the CNS [36], which affect the arousal EEG spectral power as well as the EEG patterns during sleep in animal studies [37,38]. In the present study, this mechanism would provide an explanatory link between the activation of microglia and the slowing in EEG.…”

Essential Role of Dopamine D2Receptor in the Maintenance of Wakefulness, But Not in Homeostatic Regulation of Sleep, in Mice

“…First, the use of D 2 R agonist drugs has been found in patients with Parkinson's disease to cause sudden sleep attacks, but in humans these are mainly during the active (light) phase (Tan, 2003). Of course D 2 R agonists are a two-edged sword, because they activate postsynaptic D 2 R, but also reduce dopamine release via presynaptic D 2 R (Monti et al, 1988;Ongini et al, 1993;Sebban et al, 1999), and thus may actually decrease dopamine availability at D 1 R. Second, the flipflop switch model of sleep regulation predicts that when either side of the sleep-arousal circuit is weakened (Saper et al, 2005;Lu et al, 2006), there should be an increase in the instability in both states (i.e., that we would see an increase in both wake to NREM transitions, but also in NREM to wake transition, a result that is counter-intuitive if one thinks of the D 2 R effect as only being to promote arousal). Our results not only support that model, but also suggest that the dopamine system is an important part of the arousal side of the wake-sleep flip-flop switch.…”

“…To clarify the roles of D 2 R in sleep-wake regulation, researchers have often used the pharmacological approach. Systemic administration of a D 2 R antagonist increases NREM sleep and the electroencephalogram (EEG) power density in the low-frequency bands (Monti et al, 1988;Ongini et al, 1993;Sebban et al, 1999). Under conditions of low arousal, the D 2 R agonist quinpirole promotes wakefulness after an intracerebroventricular administration (Isaac and Berridge, 2003).…”