K. Gerozissis et al., CHANGES IN HYPOTHALAMIC PROSTAGLANDIN E(2) MAY PREDICT THE OCCURRENCEOF SLEEP OR WAKEFULNESS AS ASSESSED BY PARALLEL EEG AND MICRODIALYSISIN THE RAT, Brain research, 689(2), 1995, pp. 239-244
Prostaglandin (PG) E(2) is produced by mammalian hypothalamus and when
administered exogenously prolongs wakefulness. In order to study the
relation of endogenous hypothalamic PGE(2) to sleep and wakefulness, w
e have used microdialysis in freely moving rats associated with EEG re
cording. Male Wistar rats were implanted with three cortical electrode
s and with a guide cannula for microdialysis in the space between the
paraventricular nucleus (PVN) and the ventromedial hypothalamus (VMH).
PGE(2) was measured by RIA in 3-or 6-min dialysates 15 days after sur
gery, when sleep patterns were normal again and PGE(2) production stab
ilised. PGE(2) levels were significantly higher during wakefulness (60
1 +/- 35 pg/ml, 5 experiments, 35 samples) than during slow-wave sleep
(487 +/- 24 pg/ml, 5 experiments, 49 samples). Samples corresponding
to paradoxical sleep showed a tendency towards higher PGE(2) values co
mpared to slow-wave sleep but lower compared to wakefulness. In epochs
of wakefulness or sleep lasting at least 12 min, high PGE(2) levels i
n the middle of wakefulness regularly dropped, thus announcing the occ
urrence of sleep. During sleep, PGE(2) first went on dropping and then
reincreased towards the values that characterize early periods of wak
efulness. In its turn, this reincrease in PGE(2) announced the end of
sleep and the imminent occurrence of wakefulness. It is the first stud
y to our knowledge showing that the evolvement in endogenous PG profil
e may predict the occurrence of sleep or wakefulness.