NEONATAL TREATMENTS WITH THE SEROTONIN UPTAKE INHIBITORS CLOMIPRAMINEAND ZIMELIDINE, BUT NOT THE NORADRENALINE UPTAKE INHIBITOR DESIPRAMINE, DISRUPT SLEEP PATTERNS IN ADULT RATS
Mg. Frank et Hc. Heller, NEONATAL TREATMENTS WITH THE SEROTONIN UPTAKE INHIBITORS CLOMIPRAMINEAND ZIMELIDINE, BUT NOT THE NORADRENALINE UPTAKE INHIBITOR DESIPRAMINE, DISRUPT SLEEP PATTERNS IN ADULT RATS, Brain research, 768(1-2), 1997, pp. 287-293
Chronic postnatal exposure to clomipramine (CMI), a monoamine uptake i
nhibitor, results in persistent alterations in adult rat REM sleep. Th
ese effects have been ascribed to CMI's ability to block neonatal acti
ve sleep (AS). However, these effects have not been obtained with othe
r anti-depressants which also block neonatal AS. We compared the long-
term effects on adult rat sleep after postnatal treatments (P8-P21) wi
th either CMI or zimelidine (ZMI, a selective serotonin uptake inhibit
or) or desipramine (DMI, a selective noradrenaline uptake inhibitor).
ZMI and CMI: increased the frequency and decreased the duration of REM
sleep bouts, increased the number of nonREM-RER transitions, and incr
eased sigma power in REM and nonREM sleep EEGs in adulthood. In contra
st, DMI had no effect on any adult sleep parameters. Since ZMI, DMI an
d CMI all reduce AS to similar levels, these results suggest that neon
atal AS suppression is not responsible for the sleep deficits followin
g CMI: or ZMI treatment. However, since ZMI and CMI, but not DMI, incr
ease synaptic concentrations of serotonin, elevated serotonin levels d
uring development may instead be responsible for the long-lasting slee
p deficits. (C) 1997 Elsevier Science B.V.