Short-term cotherapy with clonazepam and fluoxetine: anxiety, sleep disturbance and core symptoms of depression

Londborg, Peter D.; Smith, Ward T.; Glaudin, Vincent; Painter, John R.

doi:10.1016/s0165-0327(99)00195-0

Cited by 87 publications

(51 citation statements)

References 15 publications

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“…However, overall comparison of the respective effects of 5-HT 1B vs 5-HT 1A receptor inactivation on PS under baseline conditions as well as after citalopram treatment (see Table 1) clearly indicates that 5-HT 1A much 5-HT 1A/1B mediated paradoxical sleep inhibition by SSRI C Monaca et al more than 5-HT 1B receptors mediate the 5-HT inhibitory control of this sleep stage in the mouse. To conclude, given that insomnia, one cardinal symptom of depression, may be exacerbated by SSRIs, notably at initiation of the treatment (Levitan et al, 2000;Londborg et al, 2000), the present data provide further support to the therapeutic strategy consisting of the association of these antidepressants with 5-HT 1A antagonists (Artigas et al, 1994). Indeed, such combined treatments would simultaneously accelerate and/or augment the antidepressive action (Artigas et al, 1994Blier and Bergeron, 1995;Stahl, 1998;Adrien, 2002), and limit the sleep-inhibitory effect of of SSRIs (Thase, 2000).…”

Section: Discussionmentioning

confidence: 99%

5-HT1A/1B Receptor-Mediated Effects of the Selective Serotonin Reuptake Inhibitor, Citalopram, on Sleep: Studies in 5-HT1A and 5-HT1B Knockout Mice

Monaca

Boutrel

Hen

et al. 2002

Neuropsychopharmacol

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Selective serotonin reuptake inhibitors (SSRIs) are extensively used for the treatment of depression. Aside from their antidepressant properties, they provoke a deficit in paradoxical sleep (PS) that is most probably mediated by the transporter blockade-induced increase in serotonin concentration in the extracellular space. Such an effect can be accounted for by the action of serotonin at various types of serotonergic receptors involved in PS regulation, among which the 5-HT 1A and 5-HT 1B types are the best candidates. According to this hypothesis, we examined the effects of citalopram, the most selective SSRI available to date, on sleep in the mouse after inactivation of 5-HT 1A or 5-HT 1B receptors, either by homologous recombination of their encoding genes, or pharmacological blockade with selective antagonists. For this purpose, sleep parameters of knockout mice that do not express these receptors and their wild-type counterparts were monitored during 8 h after injection of citalopram alone or in association with 5-HT 1A or 5-HT 1B receptor antagonists. Citalopram induced mainly a dose-dependent inhibition of PS during 2-6 h after injection, which was observed in wild-type and 5-HT 1B À/À mice, but not in 5-HT 1A À/À mutants. This PS inhibition was fully antagonized by pretreatment with the 5-HT 1A antagonist WAY 100635, but only partially with the 5-HT 1B antagonist GR 127935. These data indicate that the action of the SSRI citalopram on sleep in the mouse is essentially mediated by 5-HT 1A receptors. Such a mechanism of action provides further support to the clinical strategy of antidepressant augmentation by 5-HT 1A antagonists, because the latter would also counteract the direct sleep-inhibitory side-effects of SSRIs.

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Section: Discussionmentioning

confidence: 99%

5-HT1A/1B Receptor-Mediated Effects of the Selective Serotonin Reuptake Inhibitor, Citalopram, on Sleep: Studies in 5-HT1A and 5-HT1B Knockout Mice

Monaca

Boutrel

Hen

et al. 2002

Neuropsychopharmacol

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“…Further, it is reported that SSRIs affect sleep patterns and reduce rapid eye movement (REM) sleep during early phases of treatment, as are reports of increased anxiety and nervousness. [47][48][49][50][51] A number of transcripts show up-and downregulation depending on brain region and/or treatment All three antidepressant treatments induced up-and downregulation of transcripts level. While upregulation was more frequent overall, downregulation was recorded with similar frequency in all brain regions following all three treatments.…”

Section: Number Of Transcripts Affected By Single and Multiple Treatmmentioning

confidence: 99%

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

et al. 2006

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The significant proportion of depressed patients that are resistant to monoaminergic drug therapy and the slow onset of therapeutic effects of the selective serotonin reuptake inhibitors (SSRIs)/serotonin/noradrenaline reuptake inhibitors (SNRIs) are two major reasons for the sustained search for new antidepressants. In an attempt to identify common underlying mechanisms for fast-and slow-acting antidepressant modalities, we have examined the transcriptional changes in seven different brain regions of the rat brain induced by three clinically effective antidepressant treatments: electro convulsive therapy (ECT), sleep deprivation (SD), and fluoxetine (FLX), the most commonly used slow-onset antidepressant. Each of these antidepressant treatments was applied with the same regimen known to have clinical efficacy: 2 days of ECT (four sessions per day), 24 h of SD, and 14 days of daily treatment of FLX, respectively. Transcriptional changes were evaluated on RNA extracted from seven different brain regions using the Affymetrix rat genome microarray 230 2.0. The gene chip data were validated using in situ hybridization or autoradiography for selected genes. The major findings of the study are:1. The transcriptional changes induced by SD, ECT and SSRI display a regionally specific distribution distinct to each treatment. 2. The fast-onset, short-lived antidepressant treatments ECT and SD evoked transcriptional changes primarily in the catecholaminergic system, whereas the slow-onset antidepressant FLX treatment evoked transcriptional changes in the serotonergic system. 3. ECT and SD affect in a similar manner the same brain regions, primarily the locus coeruleus, whereas the effects of FLX were primarily in the dorsal raphe and hypothalamus, suggesting that both different regions and pathways account for fast onset but short lasting effects as compared to slow-onset but long-lasting effects. However, the similarity between effects of ECT and SD is somewhat confounded by the fact that the two treatments appear to regulate a number of transcripts in an opposite manner. 4. Multiple transcripts (e.g. brain-derived neurotrophic factor (BDNF), serum/glucocorticoidregulated kinase (Sgk1)), whose level was reported to be affected by antidepressants or behavioral manipulations, were also found to be regulated by the treatments used in the present study. Several novel findings of transcriptional regulation upon one, two or all three treatments were made, for the latter we highlight homer, erg2, HSP27, the proto oncogene ret, sulfotransferase family 1A (Sult1a1), glycerol 3-phosphate dehydrogenase (GPD3), the orphan receptor G protein-coupled receptor 88 (GPR88) and a large number of expressed sequence tags (ESTs). 5. Transcripts encoding proteins involved in synaptic plasticity in the hippocampus were strongly affected by ECT and SD, but not by FLX.The novel transcripts, concomitantly regulated by several antidepressant treatments, may represent novel targets for fast onset, long-duration antidepressants.

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“…47 Anticonvulsants have also been used to treat anxiety and nervousness, with some success, as have buspirone and atypical antipsychotics.…”

Section: Common Side Effects Of Antidepressant Treatmentmentioning

confidence: 99%

Managing Depression in Primary Care

2006

Prim. Care Companion CNS Disord.

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Short-term cotherapy with clonazepam and fluoxetine: anxiety, sleep disturbance and core symptoms of depression

Cited by 87 publications

References 15 publications

5-HT1A/1B Receptor-Mediated Effects of the Selective Serotonin Reuptake Inhibitor, Citalopram, on Sleep: Studies in 5-HT1A and 5-HT1B Knockout Mice

5-HT1A/1B Receptor-Mediated Effects of the Selective Serotonin Reuptake Inhibitor, Citalopram, on Sleep: Studies in 5-HT1A and 5-HT1B Knockout Mice

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

Managing Depression in Primary Care

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