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

Citation
C. Sebban et al., Changes in EEG spectral power in the prefrontal cortex of conscious rats elicited by drugs interacting with dopaminergic and noradrenergic transmission, BR J PHARM, 128(5), 1999, pp. 1045-1054
Citations number
62
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BRITISH JOURNAL OF PHARMACOLOGY
ISSN journal
00071188 → ACNP
Volume
128
Issue
5
Year of publication
1999
Pages
1045 - 1054
Database
ISI
SICI code
0007-1188(199911)128:5<1045:CIESPI>2.0.ZU;2-#
Abstract
1 The electroencephalographic (EEG) effects of drugs interacting with dopam inergic and noradrenergic systems were studied in conscious rats. Power spe ctra (0-30 Hz) were recorded from electrodes implanted bilaterally in the p refrontal cortex. Drug effects on EEG power were calculated as the spectral power following drug administration divided by the spectral power after ve hicle administration. 2 Dopaminergic agonists at low doses, (apomorphine 0.01 mg kg(-1) s.c., qui npirole 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 t ransmission, induced an increase of EEG power. Conversely, dopaminergic ago nists at higher doses (apomorphine 0.5 mg kg(-1) s.c., quinpirole 0.5 mg kg (-1) i.p.) which increase activation of postsynaptic D-2 and D-3 receptors, induced a decrease of EEG power. 3 The alpha(1)-adrenoceptor antagonists (phenoxybenzamine 0.64 mg kg(-1) s. c., prazosin 0.32 mg kg(-1) s.c.) and the alpha(2)-adrenoceptor agonists (U K 14303 0.05 mg kg(-1) s.c., clonidine 0.025 mg kg(-1) i.p.), which decreas e noradrenergic transmission, induced an increase of EEG power. Conversely, the alpha(1)-adrenoceptor agonist, cirazoline (0.05 mg kg(-1) s.c.), the a drenergic agent modafinil (250, 350 mg kg(-1) i.p.) and alpha(2)-adrenocept or 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 pow er. The effects of prazosin (0.64 mg kg(-1) s.c.) were dose-dependently ant agonized by coadministration with modafinil and cirazoline, but not by apom orphine. 4 In conclusion, pharmacological modulation of dopaminergic and noradrenerg ic transmission may result in consistent EEG changes: decreased dopaminergi c or noradrenergic activity induces an increase of EEG spectral power; whil e increased dopaminergic or noradrenergic activity decreases EEG spectral p ower.