NEONATAL TREATMENTS WITH THE SEROTONIN UPTAKE INHIBITORS CLOMIPRAMINEAND ZIMELIDINE, BUT NOT THE NORADRENALINE UPTAKE INHIBITOR DESIPRAMINE, DISRUPT SLEEP PATTERNS IN ADULT RATS

Citation
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
Citations number
31
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
768
Issue
1-2
Year of publication
1997
Pages
287 - 293
Database
ISI
SICI code
0006-8993(1997)768:1-2<287:NTWTSU>2.0.ZU;2-U
Abstract
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.