Nine neonatal Long-Evans rats had continuous (24 h/day) polysomnography for
2 weeks, from age 14 days through age 27 days. A new finding was that six
more or less independent measures of REM sleep occurrence decreased in para
llel from age 14 days to age 27 days. The measures included parallel decrea
ses of four measures of 24-h REM duration (tonic REM sleep, phasic REM slee
p, mean REM period duration, and number of REM periods) along with parallel
increases of two measures of REM delay (REM latency and percent of nonslee
p onset REM periods). A parsimonious interpretation of the correlated chang
es is that a common developmental REM sleep inhibitory process accounts for
the six parallel changes over time. This hypothesis can be tested empirica
lly by studying inhibitory processes that operate on the pedunculopontine t
egmental/latero-dorsal tegmental nuclei, the generators of REM sleep. The s
tudy also noted that compared with (same species) normal adults, endogenous
depressives had the same distinctive REM sleep characteristics as neonatal
rats. The similarity suggests that an underdeveloped, relatively weak REM
sleep inhibitory process may account for the REM sleep peculiarities of end
ogenous depression. This hypothesis can be tested in adult rats made "depre
ssed" by neonatal treatment with antidepressant drugs. Thus, the ontogeny o
f REM sleep suggests a developmental process that may be altered in humans
predisposed to endogenous depression, and may account for the (life-long) R
EM sleep abnormalities of the disorder. (C) 2000 Elsevier Science Inc. All
rights reserved.