Activity and onset of action of reboxetine and effect of combination with sertraline in an animal model of depression

Harkin, Andrew; Kelly, John; McNamara, Mairéad G.; Connor, Thomas J.; Dredge, Keith; Redmond, A. M.; Leonard, Brian E.

doi:10.1016/s0014-2999(98)00838-3

Cited by 90 publications

(44 citation statements)

References 28 publications

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“…The present study also investigated using the TST as a model to detect depression-like behavior (39), whether BS treatment affects emotional deficits that are distinctively observed in OBX animals (10,40). The vehicle-treated OBX mice showed significantly prolonged immobility time in a manner reversible by imipramine treatment in the TST.…”

Section: Discussionmentioning

confidence: 95%

Butea superba–Induced Amelioration of Cognitive and Emotional Deficits in Olfactory Bulbectomized Mice and Putative Mechanisms Underlying Its Actions

et al. 2014

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Abstract. This study investigated the effects of alcoholic extract of Butea superba (BS) on cognitive deficits and depression-related behavior using olfactory bulbectomized (OBX) mice and the underlying molecular mechanisms of its actions. OBX mice were treated daily with BS (100 and 300 mg/kg, p.o.) or reference drugs, tacrine (2.5 mg/kg, i.p.) and imipramine (10 mg/kg, i.p.) from day 3 after OBX. OBX impaired non-spatial and spatial cognitive performances, which were elucidated by the novel object recognition test and modified Y maze test, respectively. These deficits were attenuated by tacrine and BS but not imipramine. OBX animals exhibited depressionlike behavior in the tail suspension test in a manner reversible by imipramine and BS but not tacrine. OBX down-regulated phosphorylation of synaptic plasticity-related signaling proteins: NMDA receptor, AMPA receptor, calmodulin-dependent kinase II, and cyclic AMP-responsive element-binding protein. OBX also reduced choline acetyltransferase in the hippocampus. BS and tacrine reversed these neurochemical alterations. Moreover, BS inhibited ex vivo activity of acetylcholinesterase in the brain. These results indicate that BS ameliorates not only cognition dysfunction via normalizing synaptic plasticity-related signaling and facilitating central cholinergic systems but also depression-like behavior via a mechanism differing from that implicated in BS amelioration of cognitive function in OBX animals.

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Section: Discussionmentioning

confidence: 95%

Butea superba–Induced Amelioration of Cognitive and Emotional Deficits in Olfactory Bulbectomized Mice and Putative Mechanisms Underlying Its Actions

et al. 2014

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“…In addition, locomotor activity and rearing counts in single-housed OBX mice were not significantly affected by pretreatment with diazepam, 8-OH-DPAT, or SNC80, in contrast to the results regarding head-dipping behavior. Previously, it was reported that the increased locomotor activity in OBX rats is significantly attenuated by chronic, but not acute, treatment with antidepressants (36,39). Therefore, chronic treatment with antidepressants may be required to attenuate the increased locomotor activity and rearing counts in OBX mice.…”

Section: Discussionmentioning

confidence: 97%

Changes in Emotional Behavior of Mice in the Hole-Board Test After Olfactory Bulbectomy

et al. 2006

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Abstract. The most consistent behavioral change caused by olfactory bulbectomy (OBX) is a hyperemotional response to novel environmental stimuli. The aim of this study was to characterize the emotional behavior of OBX mice using the hole-board test. After the olfactory bulbs were lesioned, sham and OBX mice were housed in single cages for 14 days. The number of head-dips in the hole-board test in single-housed OBX mice was significantly greater than that in single-housed sham mice. The head-dipping behaviors in single-housed sham and OBX mice were reversed by treatment with diazepam, a typical benzodiazepine anxiolytic. (±)-8-Hydroxy-2-(di-n-propylamino) tetraline hydrobromide (8-OH-DPAT), a selective 5-HT 1A -receptor agonist that has a non-benzodiazepine anxiolytic-like effect, and (+)-4-[(aR)-a-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethyl benzamide (SNC80), a δ-opioid-receptor agonist, also significantly reversed the number of head-dips in single-housed sham and OBX mice. In conclusion, we suggest that the single-housed OBX mice showed heightened emotional behavior (e.g., increase in head-dipping behavior) in the hole-board test. In addition, we suggest that the hyperemotional behavior characterized by head-dipping behavior in OBX mice was selectively reversed by benzodiazepine and non-benzodiazepine anxiolytics.

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“…For example, subacute simultaneous treatment of RBX and sertraline made recovery from both 8-OH-DPAT and clonidine-induced responses more rapidly than the time course of recovery with either treatment alone, suggesting that the two drugs together accelerated changes to the responsiveness of 5- HT 1A and a 2 -adrenoceptors (Harkin et al, 1999). Chronic coadministration of desipramine and fluoxetine caused desipramine-mediated downregulation of b adrenergic receptors to occur more rapidly (Baron et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Regulatory Effects of Reboxetine Treatment Alone, or Following Paroxetine Treatment, on Brain Noradrenergic and Serotonergic Systems

Gould

Pardon

Morilak

et al. 2003

Neuropsychopharmacol

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When patients do not respond to an initial antidepressant, one clinical approach is to switch to an agent in a different pharmacological class. However, few studies have examined the neurochemical consequences of this practice. To study this, we examined changes in binding sites in rat brain for norepinephrine (NET) and serotonin transporters (SERT), a 1 , a 2 , and b 1 adrenergic receptors after chronic administration of paroxetine (PRX), reboxetine (RBX), or PRX followed by RBX. We also examined the effects of these treatments on mRNA expression for tyrosine hydroxylase (TH). RBX treatment for 3 weeks reduced NET binding significantly, by B40% in terminal field areas, and 6 weeks of RBX reduced it even more, by B60%. RBX treatment for 3 and 6 weeks reduced b 1 adrenergic receptorbinding sites equally, by 50-60%. At no time did RBX treatment reduce SERT-binding sites. PRX treatment had no effect on b 1 adrenergic or NET-binding sites, but reduced SERT-binding sites by 75-80%. Neither treatment altered mRNA for TH, a 1 , or a 2 adrenergic receptor-binding sites. When 3 weeks of RBX treatment followed 3 weeks of PRX treatment, NET-binding sites were reduced to the same extent as measured after 6 weeks of RBX treatment alone, indicating that PRX pretreatment may have 'primed' the subsequent regulatory effect of RBX on the NET. Thus, pretreatment of rats with PRX actually enhanced at least one regulatory effect of RBX treatment on the noradrenergic system, and did not interfere with any other pharmacological effect caused by RBX treatment.

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Activity and onset of action of reboxetine and effect of combination with sertraline in an animal model of depression

Cited by 90 publications

References 28 publications

Butea superba–Induced Amelioration of Cognitive and Emotional Deficits in Olfactory Bulbectomized Mice and Putative Mechanisms Underlying Its Actions

Butea superba–Induced Amelioration of Cognitive and Emotional Deficits in Olfactory Bulbectomized Mice and Putative Mechanisms Underlying Its Actions

Changes in Emotional Behavior of Mice in the Hole-Board Test After Olfactory Bulbectomy

Regulatory Effects of Reboxetine Treatment Alone, or Following Paroxetine Treatment, on Brain Noradrenergic and Serotonergic Systems

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