Research reportSleep–waking discharge patterns of ventrolateral preoptic/anterior hypothalamic neurons in rats
Section snippets
Introductions
There is extensive experimental evidence that the rostral hypothalamus is involved in sleep regulation, functioning to promote sleep induction and maintenance. Electrolytic or chemical lesions of the preoptic/anterior hypothalamus (POA) result in persistent insomnia 18, 27, 33, 37. Chemical stimulation of the POA with microinjected benzodiazepines [19], prostaglandin D2[39]and adenosine [38]promote sleep. Local warming of the POA in cats promotes sleep [26]and enhances EEG delta power in the
Subjects and surgical procedures
Subjects were 15 male, Sprague–Dawley rats weighing between 300–350 g at the time of surgery. They were housed individually on a 12:12 light:dark cycle (lights-on at 0700 h) at ambient temperatures of 23±2°C. Food and water were continuously available.
Surgical preparation for chronic sleep-wake and extracellular vlPOA neuronal recordings were performed under anesthesia (Ketamine, 80 mg/kg plus Xylazine, 10 mg/kg, i.p.) using aseptic techniques. Details of the methods are described elsewhere [3]
Distribution of cells with sleep- and wake- related discharge patterns in the lateral preoptic/anterior hypothalamic area
The nonREM/waking discharge ratio was determined for 105 cells recorded from dorsal to ventral microwire passes through the lateral preoptic area of 7 rats. The most frequently encountered cells (27% of the sample) had much higher discharge rates in waking compared to nonREM sleep (ratios between 0.01–0.39) Another large group (24%) had similar rates in waking and nonREM sleep (ratios between 0.80–1.19), and 22% were moderately waking–related (ratios between 0.40–0.79). Seventeen of 105 neurons
Discussion
We found that within the lateral preoptic/anterior hypothalamic area of rats, cells with sleep-related discharge were localized primarily to the vlPOA. A majority of vlPOA sleep-related cells displayed elevated discharge rates in both nonREM and REM sleep, compared to waking. Discharge of vlPOA neurons varied with sleep depth. As EEG delta power increased from the early to late portions of a nonREM sleep episode, discharge rate of vlPOA neurons increased. Following sleep deprivation, increased
Acknowledgements
Supported by the Department of Veterans Affairs Medical Research Service and NIMH MH 474780.
References (41)
- et al.
Preoptic/anterior hypothalamic neurons: thermosensitivity in wakefulness and non rapid eye movement sleep
Brain Res.
(1996) - et al.
Effect of sleep deprivation on sleep and EEG power spectra in the rat
Behav. Brain Res.
(1984) - et al.
Activity of identified cortically projecting and other basal forebrain neurons during large slow waves and cortical activation in anesthetized rats
Brain Res.
(1987) Sleep–wake regulation by prostaglandins D2 and E2
J. Biol. Chem.
(1988)- et al.
C-fos and related immediate early gene products as markers of activity in neuroendocrine systems
Front Endocrinol.
(1993) Preoptic area unit activity during sleep and wakefulness in the cat
Exp. Neurol.
(1984)- et al.
Photic and circadian regulation of c-fos gene expression in the hamster suprachiasmatic nucleus
Neuron
(1990) - et al.
Firing of neurons in the preoptic/anterior hypothalamic area in rat: its possible involvement in slow wave sleep and paradoxical sleep
Neurosci. Res.
(1994) - et al.
Keeping cool: a hypothesis about the mechanisms and functions of slow wave sleep
Trends Neurosci.
(1990) - et al.
Preoptic/anterior hypothalamic warming increases EEG delta frequency activity within non-rapid eye movement sleep
Brain Res.
(1994)