title: 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) effects 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 effects on EEG power were calculated as the spectral power following drug administration divided by the spectral power after vehicle administration. 2. Dopaminergic agonists at low doses, (apomorphine 0. 01 mg kg-1 s.c., quinpirole 0.01 mg kg-1 i.p.) and dopaminergic antagonists (haloperidol 1 mg kg-1 i.p., raclopride 2.5 mg kg-1 s.c. ), which decrease dopaminergic transmission, induced an increase of EEG power. Conversely, dopaminergic agonists at higher doses (apomorphine 0.5 mg kg-1 s.c., quinpirole 0.5 mg kg-1 i.p.) which increase activation of postsynaptic D2 and D3 receptors, induced a decrease of EEG power. 3. The alpha1-adrenoceptor antagonists (phenoxybenzamine 0.64 mg kg-1 s.c., prazosin 0.32 mg kg-1 s.c.) and the alpha2-adrenoceptor agonists (UK 14304 0.05 mg kg-1 s.c., clonidine 0.025 mg kg-1 i.p.), which decrease noradrenergic transmission, induced an increase of EEG power. Conversely, the alpha1-adrenoceptor agonist, cirazoline (0.05 mg kg-1 s.c.), the adrenergic agent modafinil (250, 350 mg kg-1 i.p.) and alpha2-adrenoceptor antagonists (RX 821002 0.01 mg kg-1 s.c., yohimbine 0.5 mg kg-1 i.p.), which increase noradrenergic transmission, induced a decrease of EEG power. The effects of prazosin (0.64 mg kg-1 s.c.) were dose-dependently antagonized by co-administration with modafinil 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.
authors.affiliation: Laboratoire de Biologie du Vieillissement, Hopital Charles Foix, 7 avenue de la République, 94205 Ivry sur Seine cedex, France.
authors.forename: C
authors.initials: C
authors.lastname: Sebban
authors.forename: X Q
authors.initials: XQ
authors.lastname: Zhang
authors.forename: B
authors.initials: B
authors.lastname: Tesolin-Decros
authors.forename: M J
authors.initials: MJ
authors.lastname: Millan
authors.forename: M
authors.initials: M
authors.lastname: Spedding
mesh_terms: D018663:Adrenergic Agents / Q000494:pharmacology*; D058646:Adrenergic alpha-1 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001143:Arousal / Q000187:drug effects; D001559:Benzhydryl Compounds / Q000494:pharmacology; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D003243:Consciousness; D015259:Dopamine Agents / Q000494:pharmacology*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004569:Electroencephalography / Q000187:drug effects*; D007839:Functional Laterality / Q000502:physiology; D008297:Male; D000077408:Modafinil; D009638:Norepinephrine / Q000502:physiology*; D011224:Prazosin / Q000494:pharmacology; D017397:Prefrontal Cortex / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000187:drug effects*
chemical_list: D018663:Adrenergic Agents; D058646:Adrenergic alpha-1 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D001559:Benzhydryl Compounds; D000697:Central Nervous System Stimulants; D015259:Dopamine Agents; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D000077408:Modafinil; D009638:Norepinephrine; D011224:Prazosin