Gyorsan ható antidepresszánsok hatása az alvás-ébrenlétre
Koncz Szabolcs
Pharmaceutical Sciences
Dr. Zelkó Romána
NET 21.emelet Johan Béla konferencia terem
2024-11-22 13:00:00
Experimental and Clinical Pharmacology
Dr. Szökő Éva
Dr. Bagdy György
Dr. Bódizs Róbert
Dr. Hernádi István
Dr. Gyires Klára
Dr. Timár Júlia
Dr. Jakus Rita
Major depressive disorder is a debilitating psychiatric disorder affecting many people
worldwide and is often associated with sleep disturbance. Patients with depression show
characteristic alterations in sleep, including shortened REM sleep latency, increased time
spent in REM sleep, and decreased delta power during NREM sleep. Most conventional
antidepressants demonstrate specific effects on these parameters. The vast majority of
reuptake inhibitor antidepressants influence REM sleep parameters, namely prolong
REM sleep latency and reduce REM sleep duration. Chronic administration of
antidepressants with serotonin-2 (5-HT2) receptor antagonist properties increase delta
EEG power during NREM sleep. Limited data are available on the effects of rapid acting
or potentially rapid acting antidepressants on sleep-wakefulness, particularly in the cases
of (S)- and (R)-ketamine, as well as tramadol. This new group of antidepressants have
favourable therapeutic effects compared to classic antidepressants due to their fast clinical
actions.
In our behavioural study, we investigated the effects of 15 mg/kg i.p. (R)- and (S)-
ketamine enantiomers on depression-like behaviours induced by chronic restraint stress.
The antidepressant-like effects of each enantiomer were evaluated in the rat forced
swimming test. In our EEG experiments we investigated the effects of 15 mg/kg i.p. doses
of ketamine enantiomers and 5, 15, and 45 mg/kg i.p. doses of tramadol treatments on
sleep-wake parameters.
We showed that (S)-ketamine but not (R)-ketamine reversed the depression-like
behaviours induced by chronic stress. Both (S)-ketamine and tramadol treatments
exhibited REM-suppressing and REM latency increasing properties similar to those of
reuptake inhibitor antidepressants, and both compounds increased NREM sleep EEG
delta power, an effect that is primarily characteristic of antidepressants with 5-HT2
receptor antagonist properties.
Taken together, it can be concluded that the characteristic REM suppression and NREM
delta power increasing effects described for conventional antidepressants are also
characteristic of rapid acting antidepressants. Furthermore, the acute effects of tramadol
on EEG and sleep parameters suggest a potential antidepressant effect.
