According to the literature GHRH may act as a slow wave sleep facilitating factor when injected systemically or i.c.v. Corresponding studies with somatostatin have demonstrated that somatostatin may facilitate REM sleep, but the results of the studies are divergent showing some discrepancy between the findings in experimental animals and humans. It should be noted that the effects of somatostatin receptor antagonist on sleep structure have not been studied. Further, there is no earlier knowledge about the effects of total sleep deprivation or selective REM sleep deprivation on the gene expression of GHRH and somatostatin in the hypothalamus. Furthermore the proposed sleep regulatory role of galanin, which is known to affect the hypothalamic GH-regulatory system, is almost completely unstudied. For these reasons this work concentrated on the present series of experiments:
I To measure the effects of selective REM sleep deprivation on somatostatin, GHRH and galanin mRNA expression in hypothalamic cells, and to measure the effect of recovery sleep on these neuropeptide mRNAs after REM sleep deprivation.
II To measure the effect of short term total sleep deprivation on somatostatin, GHRH and galanin mRNA expression in hypothalamic cells, and to compare the differences in the effects of REM sleep deprivation and total sleep deprivation on the mRNA expression of these neuropeptides.
III To study the effects of blocking endogenous somatostatin by administering a somatostatin antagonist on spontaneous sleep and rebound sleep after REM sleep deprivation, and to compare these effects with those observed after administrations of somatostatin and galanin.
To study the role of the locus coeruleus as one of the possible sites of
sleep modulation by administering somatostatin, somatostatin antagonist
and galanin locally into the cells of locus coeruleus.
-> MATERIALS AND METHODS