Effects of acute and chronic treatment with trazodone, an antidepressant, on the sleep-wake activity in rats

Lelkes, Z.; Obál, F.; Alföldi, P.; Erdös, A.; Rubicsek, György; Benedek, György

doi:10.1016/1043-6618(94)80002-2

Cited by 17 publications

(9 citation statements)

References 20 publications

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“…Interestingly, trazodone also increased theta power relative to caffeine alone in the combination group, which could not have been predicted by the effect of either drug alone. At present there is only a single study of the effects of trazodone on sleep EEG in rats, which also reported increases in total sleep time, NREM sleep and SWA (Lelkes, et al, 1994). Like us, they showed that delta activity was increased in response to trazodone, but they also reported decreases in higher frequencies (6-20 Hz), a finding that we did not observe.…”

Section: Effects Of Zolpidem and Trazodone On Caffeine-induced Sleep Disruptioncontrasting

confidence: 58%

Characterisation of the effects of caffeine on sleep in the rat: a potential model of sleep disruption

et al. 2009

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Caffeine is known to disrupt sleep and its administration to human subjects has been used to model sleep disruption. We previously showed that its effects on sleep onset latency are comparable between rats and humans. This study evaluated the potential use of caffeine as a model of sleep disruption in the rat, by assessing its effects on sleep architecture and electroencephalogram (EEG) frequency spectrum, and using sleep-promoting drugs to reverse these effects. Rats were implanted with radiotelemetry devices for body temperature, EEG, electromyogram and locomotor activity. Following recovery, animals were dosed with caffeine (10 mg/kg) alone or in combination with zolpidem (10 mg/kg) or trazodone (20 mg/kg). Sleep was scored for the subsequent 12 h using automated analysis software. Caffeine dose-dependently disrupted sleep: it increased WAKE time, decreased NREM (non-REM) sleep time and NREM bout duration (but not bout number), and decreased delta activity in NREM sleep. It also dose-dependently increased locomotor activity and body temperature. When given alone, zolpidem suppressed REM whilst trazodone increased NREM sleep time at the expense of WAKE, increased NREM bout duration, increased delta activity in NREM sleep and reduced body temperature. In combination, zolpidem attenuated caffeine's effects on WAKE, whilst trazodone attenuated its effects on NREM sleep, NREM bout duration, delta activity, body temperature and locomotor activity. Caffeine administration produced many of the signs of insomnia that were improved by two of its most successful current treatments. This model may therefore be useful in the study of new drugs for the treatment of sleep disturbance.

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Section: Effects Of Zolpidem and Trazodone On Caffeine-induced Sleep Disruptioncontrasting

confidence: 58%

Characterisation of the effects of caffeine on sleep in the rat: a potential model of sleep disruption

et al. 2009

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“…*P<0.05 compared with vehicle **P<0.05 compared with caffeine ***P=0.06 compared with caffeine alone determine whether this trend was real at this dose. Only one paper has been published on the effects of trazodone in sleep in rats, and SOL was not measured (Lelkes et al 1994).…”

Section: Discussionmentioning

confidence: 99%

A translational, caffeine-induced model of onset insomnia in rats and healthy volunteers

et al. 2007

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“…Pharmacological doses, which were determined in previous studies, were chosen as the study doses of TRZ. 16 –21 Furthermore, the clinical dose of TRZ for the treatment of depression is 250–600 mg per day and the proper dose for the treatment of insomnia is 25–100 mg before sleep. 22 The doses studied were also in accordance with the guidelines extrapolating human doses to animal doses.…”

Section: Methodsmentioning

confidence: 99%

Assessment of trazodone-induced cardiotoxicity after repeated doses in rats

et al. 2018

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Trazodone (TRZ) is an antidepressant drug commonly used in the treatment of depression, anxiety, and insomnia. Although some studies demonstrated the adverse effects of TRZ related to cardiovascular system, the conflicting results were observed in these studies. Therefore, we aimed to investigate the cardiac adverse effects of TRZ in rats at repeated doses in our study. In accordance with this purpose, TRZ was administered orally to rats at 5, 10, and 20 mg/kg doses for 28 days. Electrocardiogram records, serum aspartate aminotransferase (AST), lactate dehydrogenase, creatine kinase-myoglobin band, cardiac troponin-T (cTn-T) levels, DNA damage in cardiomyocytes, and histologic view of heart tissues were evaluated. In addition, glutathione (GSH) and malondialdehyde (MDA) levels were measured to determine the oxidative status of cardiac tissue after TRZ administration. Heart rate was decreased, PR interval was prolonged, and QRS and T amplitudes were decreased in 20 mg/kg TRZ-administered group compared to the control group. Serum AST and cTn-T levels were significantly increased in 10 and 20 mg/kg TRZ-administered rats with respect to control rats. DNA damage was significantly increased in these groups. Additionally, degenerative histopathologic findings were observed in TRZ-administered groups. Although there was no difference in MDA levels between groups, GSH levels were significantly decreased in 10 and 20 mg/kg TRZ-administered groups compared to the control group. Our results have shown that TRZ induced cardiotoxicity in rats dose-dependently. It is assumed that oxidative stress related to GSH depletion may be accompanied by these adverse effects.

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Effects of acute and chronic treatment with trazodone, an antidepressant, on the sleep-wake activity in rats

Cited by 17 publications

References 20 publications

Characterisation of the effects of caffeine on sleep in the rat: a potential model of sleep disruption

Characterisation of the effects of caffeine on sleep in the rat: a potential model of sleep disruption

A translational, caffeine-induced model of onset insomnia in rats and healthy volunteers

Assessment of trazodone-induced cardiotoxicity after repeated doses in rats

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