I Lack of REM sleep increases somatostatin mRNA and lack of SWS increases GHRH mRNA in the rat hypothalamus. This together with the earlier pharmacological studies supports the hypothesis that endogenous somatostatin facilitates REM sleep and GHRH facilitates SWS.
Sleep deprivation affects mostly the somatostatin cells in the arcuate
nucleus and GHRH cells in the paraventricular nucleus, which are not the
main hypophysiotropic nuclei of these neuropeptides. Thus, it is possible
that sleep regulatory and GH-controlling functions in the hypothalamus
are partly mediated by different somatostatin and GHRH cell populations.
REM sleep deprivation increases galanin mRNA in the anterior hypothalamus
but injected galanin does not affect the sleep structure. It is possible
that galanin mediates the effects of REM sleep deprivation in the CNS but
does not itself affect sleep via the areas examined in the present work.
Intracerebroventricular and local microinjection of somatostatin antagonist
into the locus coeruleus decreases the amount of REM sleep, which supports
the hypothesis that the effect of somatostatin on REM sleep is at least
partly mediated by the locus coeruleus.