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Changes in EEG spectral power in the prefrontal cortex of conscious rats elicited by drugs interacting with dopaminergic and noradrenergic transmission
Author(s) -
Sebban C,
Zhang X Q,
TesolinDecros B,
Millan M J,
Spedding M
Publication year - 1999
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0702894
Subject(s) - prazosin , dopaminergic , idazoxan , apomorphine , quinpirole , chemistry , haloperidol , medicine , agonist , endocrinology , pharmacology , dopamine , antagonist , receptor
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. 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 D 2 and D 3 receptors, induced a decrease of EEG power. The α 1 ‐adrenoceptor antagonists (phenoxybenzamine 0.64 mg kg −1  s.c., prazosin 0.32 mg kg −1  s.c.) and the α 2 ‐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 α 1 ‐adrenoceptor agonist, cirazoline (0.05 mg kg −1  s.c.), the adrenergic agent modafinil (250, 350 mg kg −1  i.p.) and α 2 ‐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. 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.British Journal of Pharmacology (1999) 128 , 1045–1054; doi: 10.1038/sj.bjp.0702894

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