Suppression of desynchronized sleep through microinjection of the alpha 2-adrenergic agonist clonidine in the dorsal pontine tegmentum of the cat.

The relationships between sleep-waking states and the activity of the noradrenergic system are controversial. In particular, according to an influential model of desynchronized sleep (DS) generation, the arrest of firing of noradrenergic neurons in the locus coeruleus should enhance DS, due to the release from inhibition of executive neurons located in the nearby pontine tegmentum. Since locus coeruleus neurons are strongly inhibited by alpha 2-adrenergic agonists like clonidine, this agent would be expected to increase DS. Yet clonidine powerfully decreases DS when injected systemically in several species. In this study, clonidine was microinjected locally into the dorsal pontine tegmentum of the cat, a region which comprises anatomically the whole locus coeruleus complex and which plays a key role in the generation of DS. In accord with the results of systemic experiments, bilateral injections of clonidine almost suppressed DS and unilateral injections consistently reduced it. The effects were dose dependent and site specific. It is suggested that clonidine may suppress DS by acting additionally on non-noradrenergic cell groups located in the dorsal pontine tegmentum.