The present study was aimed to compare in detail the distribution within the rostral ventromedial medulla of Methionin-Enkephalin-immunoreactive neurons with efferent projections to the facial or trigeminal motor nuclei, using a double immunostaining technique in colchicine-treated cats.

Following cholera toxin B subunit injections in the facial or trigeminal motor nuclei, we found that respectively 55% and 65% of the medium to large-sized retrogradely labeled cells in the lateral part of the nucleus reticularis magnocellularis were Methionin-Enkephalin-positive. For both motor nuclei, the double-labeled neurons had similar morphology and size and were located exactly in the same area. They could therefore belong to the same population of reticular enkephalinergic neurons. Based on these and previous anatomical and electrophysiological data, we propose that these enkephalin-containing neurons could participate in the hyperpolarization of brainstem and spinal somatic motoneurons during paradoxical sleep.

Sleep Research Online

Prolactin administered systemically, intracerebroventricularly or locally into the lateral hypothalamus enhances rapid eye movement sleep (REM) when given diurnally and decreases REM when given nocturnally. The amygdala is being recognized as an important modulator of behavioral state, and the central nucleus of the amygdala (CNA) has a high concentration of prolactin fibers and receptors. We microinjected prolactin (10, 100, 250 ng/0.2 µl saline) or saline alone into CNA of rats and measured the effect on behavioral state. Prolactin produced a dose-dependent decrease in non-REM (NREM), with the effect becoming significant at the high (250 ng) dose. REM was not significantly affected at any dosage. The results indicate a role for prolactin in CNA in the control of NREM. The results are discussed in terms of the amygdala having a broad role in the regulation of behavioral state.

Sleep Research Online

Melatonin treatment has been shown to induce sleepiness and promote sleep in humans. In order to understand the mechanisms by which melatonin acts on human sleep and behavior, it would be useful to have an animal model in which the physiological nocturnal increase in melatonin secretion correlated with nocturnal sleep, i.e., a diurnal species. In this pilot study the oral administration of melatonin to two Pigtail macaques (Macaca Nemestrina) at different times of the day significantly decreased motor activity and promoted earlier sleep onset, as measured actigraphically. The decline in the animals' motor activity occurred within 25-40 min after melatonin ingestion. The duration of motor inhibition was dose dependent. Administration of a 0.05 mg dose induced serum melatonin levels comparable to the peak physiologic concentrations reported in untreated humans and the non-human primates. These data suggest that melatonin may modulate motor activity and sleep pattern in certain diurnally-active primates.

Sleep Research Online

Adenosine is currently being investigated as a possible mediator of a homeostatic sleep need. Reports from different laboratories suggest that both adenosine A₁ agonists and selective serotonin reuptake inhibitors (SSRI) increase deep slow wave sleep (SWS-2) after an interval. In this study, the sleep-wake effects of the adenosine A₁ agonist N⁶-cyclopentyladenosine (CPA) and the SSRI zimeldine are directly compared in the same animals. Since the SWS-2 increase following SSRIs may be secondary to increased adenosine levels during the initially increased waking, it was also investigated whether the adenosine A₁ antagonist 8-cyclopentyltheofylline (CPT) would inhibit the SWS-2 increase following the serotonin reuptake inhibitor. Both the adenosine A₁ agonist CPA and the SSRI zimeldine increased SWS-2 after an interval. Both drugs increased slow wave activity and decreased 9-20 Hz activity during SWS-2. Both the adenosine A₁ antagonist CPT, zimeldine and the two drugs combined initially increased waking and subsequently increased SWS-2 after 2 or 4 h. All treatments increased 2-6 Hz activity in SWS-2 after 2h. Thus, CPT did not antagonize the SWS-2 increase of zimeldine. Based on the sleep and power spectral effects it is suggested that the adenosine A₁ antagonist potentiated the zimeldine effect, possibly due to antagonism of adenosine A₁ inhibition of serotonin release. The data indicate that the delayed SWS-2 and slow wave activity increases following zimeldine are not due to increased stimulation of adenosine A₁ receptors following the initial sleep loss.

Sleep Research Online