The power of delta and theta frequency bands of the EEG in the posterior hypothalamus of the rat fluctuates according to an
ultradian rhythm. To investigate, whether catecholamine receptor ligands influence the ultradian EEG rhythm, drugs were applied
intracerebroventricularly into the lateral ventricle of anaesthetized rats. Injection of the α
1-adrenoceptor agonist (±)-methoxamine (150nmol) abolished, while 25nmol of the compound prolonged the cycle duration of the
rhythmic changes in the delta and theta frequency bands. Injected into the lateral ventricle, the α
2-adrenoceptor agonists 6-ethyl-5,6,7,8-tetrahydro-4H-oxazol[4,5-d] azepin-2-amine (B-HT 933) or clonidine (150nmol each) prolonged
the duration of the cycles of both frequency bands. The β
1/2-receptor agonists (±)-orciprenaline (300nmol) and (R)-(–)-isoprenaline (150nmol) slowed down the cycle durations of both
frequency bands. The β
1-receptor agonist (±)-xamoterol (300nmol) also prolonged the cycle durations of the delta and theta frequency bands. The β
1-receptor antagonist (S)-(–)-atenolol was ineffective (150 and 300nmol). The β
2-receptor agonist (±)-salbutamol (300nmol) shortened the duration of the ultradian rhythm in the two frequency bands, while
the β
2-receptor antagonist (±)-1-[2,3(dihydro-7-methyl-1H-inden-4-yl) oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118,551) (300nmol)
exerted the opposite effect. On the other hand, the D
1 receptor agonist (±)-1-phenyl-2,3,4,5-tetrahydro-1H)-3-benzazepine-7,8-diol (SKF 38393) and the D
2 agonist (4aR,8aR)-(–)-quinpirole (150nmol each) slowed down the frequency of the ultradian rhythm. The powers of alpha
and beta frequency bands were not significantly influenced by the catecholamine receptor ligands used in this study.
The findings suggest that, in the posterior hypothalamus, the ultradian rhythm of the delta and theta frequency bands are
prolonged when β1-receptors are stimulated and shortened on stimulation of β2-adrenoceptors. Endogenous catecholamines released from their neurons seem to shorten the duration of the rhythmic fluctuations
by stimulating β2-receptors and to slow down the frequency of the cyclic fluctuations by stimulating α2-adrenoceptors. The ultradian rhythm is also slowed down on stimulation of D1 and D2 receptors by endogenous dopamine. Together with previous observations, the results indicate that the ultradian EEG rhythm
is susceptible to modulatory mechanisms mediated by catecholaminergic neurons.
Key words EEG spectral power analysis - Delta - Theta - Ultradian rhythm - Posterior hypothalamus - Adrenoceptor agonists - Adrenoceptor antagonists - Dopamine receptor agonists
Received: 14 March 1997 / Accepted: 24 October 1997