Influence of catecholamine receptor agonists and antagonists on the ultradian rhythm of the EEG in the posterior hypothalamus

Abstract

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 α₁-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 α₂-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 β₁-receptor agonist (±)-xamoterol (300nmol) also prolonged the cycle durations of the delta and theta frequency bands. The β₁-receptor antagonist (S)-(–)-atenolol was ineffective (150 and 300nmol). The β₂-receptor agonist (±)-salbutamol (300nmol) shortened the duration of the ultradian rhythm in the two frequency bands, while the β₂-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 D₁ receptor agonist (±)-1-phenyl-2,3,4,5-tetrahydro-1H)-3-benzazepine-7,8-diol (SKF 38393) and the D₂ 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.