A partial theory of sleep. A novel view of its phenomenology and organization.

The various stages of sleep are characterized by specific vigilance profiles across the universe of available behavioral systems. The induction and structuring of sleep and its adaptation to a variety of internal needs is the result of a general vigilance-controlling apparatus.

CNS-related (side-)effects of beta-blockers with special reference to mechanisms of action.

beta-Adrenoreceptor antagonists are liable to produce behavioural side-effects such as drowsiness, fatigue, lethargy, sleep disorders, nightmares, depressive moods, and hallucinations. These undesirable actions indicate that beta-blockers affect not only peripheral autonomic activity but also some central nervous mechanisms. In experimental animals beta-blockers have been found to reduce spontaneous motor activity, to counteract isolation-, lesion-, stimulation- and amphetamine-induced hyperactivity, and to produce slow-wave and paradoxical sleep disturbances.

[Biochemistry and pharmacology of vigilance: role of neurotransmitters within the framework of vigilance control].

Biochemical, pharmacological and neurophysiological research has produced an ever increasing amount of evidence that a variety of (putative) neurotransmitter (NT) mechanisms is implicated in the gross regulation of the many waking behaviours as well as in the organization of sleep. Yet, few of these experimental findings have yielded information as to the exact--specific and detailed--role played by anyone of these "wet" transmission systems in this whole regulatory and organizational function. Based on a new "Universal Concept of Vigilance" we were led to conclude that the actions and influences of at least some of these humoral transmission instruments are considerably better understood, if they are interpreted as being the main controlling instruments of the many local vigilances--the individual levels of responsiveness in the many behavioral systems that are responsible for the making of the many behavioral components.

Feedback control of noradrenaline release as a function of noradrenaline concentration in the synaptic cleft in cortical slices of the rat.

Cortical slices incubated with [3H]noradrenaline (NA) were used to study quantitatively the infelucne of the NA concentration in the synaptic cleft on electrically induced release of [3H]NA from adrenergic nerve terminals. Stimulation-induced [3H]-overflow was regarded to be proportional to the NA concentration in the synaptic cleft. High concentrations of piperoxan or clonidine were used to block, or maximally stimulate, respectively, the presynaptic alpha-receptors and thus to eliminate feedback control.

Epileptic phenomena induced in the cat by the antidepressants maprotiline, imipramine, clomipramine, and amitriptyline.

The epileptogenic properties of four tricyclic antidepressant drugs: maprotiline, imipramine, clomipramine, amitriptyline, were investigated in locally anesthetized cats immobilized with gallamine and supplied with neocortical, hippocampal, and reticular recording electrodes. The drugs were infused intravenously at a constant rate (0.5 or, in some cases, 0.

Inhibition of nigral and neocortical cells by gamma-hydroxybutyrate: a microiontophoretic investigation.

gamma-Hydroxybutyrate (GHB) and gamma-aminobutyrate (GABA) were applied microiontophoretically near spontaneously active cells in the substantia nigra and the neocortex of chloral hydrate-anaesthetized rats. Whereas GABA in "low doses" (i.e.

The biological activity of d- and l-baclofen (Lioresal).

Racemic d,l-baclofen and l-baclofen depressed the patellar, flexor, linguo-mandibular (0.1--30 mg/kg i.v.

Activation of an inhibitory noradrenergic pathway projecting from the locus coeruleus to the cingulate cortex of the rat.

Repetitive stimulation of the locus coeruleus evoked strong inhibition of the firing rate of about 50% of cells of the cingulate rat cortex. Forty per cent of the cells were not affected and 9% were excited by stimulation of the locus coeruleus. Pretreatment of the rats with reserpine and alpha-methyl-p-tyrosine drastically reduced the percentage of cells inhibited by locus coeruleus stimulation.

Influence of vincamine and piracetam on sleep--waking pattern of the cat.

The effect of Vincamine and Piracetam, two geriatric drugs, on sleep behavior of the laboratory cat was studied. The animals were chronically prepared for recording of the EEG of the cerebral cortex, the lateral geniculate body, and the hippocampus, and for recording of eye movements, the muscular tonus and respiration. During the experiment, sleep and waking behavior were monitored by the above mentioned telemetrically transmitted indicators and also through observation via closed-circuit television.

The effect of some neuroleptics on the interaction of cortically and nigrally evoked potentials in the rat striatum.

The interaction of cortico- and nigrofugal inputs to the striatum of the rat was investigated using the technique of evoked potentials. Repetitive, unilateral stimulation of the substantia nigra inhibited potentials which were evoked from the ipsilateral rostral cortex and recorded from the ipsilateral striatum. The inhibition was antagonized by low doses of various intraperitoneally administered neuroleptics such as: pimozide (0.

Rotational behavior induced in rats by intranigral application of GABA-related drugs and GABA antagonists.

GABA and GABA-related drugs such as muscimol, gamma-hydroxybutyric acid and baclofen injected unilaterally into the substantia nigra of rats elicited contraversive turning. Unilateral injections of picrotoxin and bicuculline produced either ipsi- or contraversive turning depending on the volume of vehicle. I.