Antidepressant-induced regulation of 5-HT1b mRNA in rat dorsal raphe nucleus reverses rapidly after drug discontinuation

Anthony, Joanne; Sexton, Timothy J.; Neumaier, John F.

doi:10.1002/1097-4547(20000701)61:1<82::aid-jnr10>3.0.co;2-e

Cited by 66 publications

(24 citation statements)

References 26 publications

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“…of imipramine, but did not observe any significant change in the number of escape failures (10 mg/kg of fluoxetine, 5.071.0 (n ¼ 3); 50 mg/kg of imipramine, 2.071.3 (n ¼ 3)) between the two doses. In addition, Anthony et al 21 showed that 5 mg/kg of fluoxetine, the same dose as used in the present study, was enough to elicit monoaminergic perturbation such as a reduced 5-hydroxytryptamine receptor 1B expression in the dorsal raphe of rats. Bristow et al 22 also demonstrated the validity and efficacy of 5 mg/kg of fluoxetine in ameliorating depressive behavior in rats.…”

Section: Effectiveness Of Antidepressants In Learned Helplessnesssupporting

confidence: 50%

Comprehensive expression analysis of a rat depression model

et al. 2004

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Herein we report on a large-scale analysis of gene expression in the 'learned helplessness' (LH) rat model of human depression, using DNA microarrays. We compared gene expression in the frontal cortex (FC) and hippocampus (HPC) of untreated controls, and LH rats treated with saline (LH-S), imipramine or fluoxetine. A total of 34 and 48 transcripts were differentially expressed in the FC and HPC, respectively, between control and LH-S groups. Unexpectedly, only genes for NADH dehydrogenase and zinc transporter were altered in both the FC and HPC, suggesting limited overlap in the molecular processes from specific areas of the brain. Principal component analysis revealed that sets of upregulated metabolic enzyme genes in the FC and downregulated genes for signal transduction in the HPC can distinguish clearly between depressed and control animals, as well as explain the responsiveness to antidepressants. This comprehensive data could help to unravel the complex genetic predispositions involved in human depression.

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Section: Effectiveness Of Antidepressants In Learned Helplessnesssupporting

confidence: 50%

Comprehensive expression analysis of a rat depression model

et al. 2004

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“…Both 5-HT 1A and 5-HT 1B receptors serve as autoreceptors in serotonergic cells and heteroreceptors in other neurons. 5-HT 1B autoreceptors are selectively regulated by fluoxetine [1,30] and chemical axotomy with 5,7-dihydroxytryptamine [31]. 5-HT 1A receptors are also regulated in a cell specific manner.…”

Section: Discussionmentioning

confidence: 99%

Corticosteroids regulate 5-HT1A but not 5-HT1B receptor mRNA in rat hippocampus

Neumaier

Sexton

Hamblin

et al. 2000

Molecular Brain Research

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The role of mineralocorticoid and glucocorticoid receptors (MR and GR, respectively) in the regulation of serotonin receptors has not been clearly delineated. There is no consensus regarding the regulation of 5-HT 1A receptors, and corticosteroid regulation of 5-HT 1B mRNA has not been previously studied. We compared the effects of long-term (two week) adrenalectomy (no MR or GR activation) and several hormone replacement protocols designed to stimulate MR selectively (ALDO), MR and GR (HCT), and continuous MR with cyclical GR activation (SHAM adrenalectomy). 5-HT 1A and 5-HT 1B mRNAs were measured by in situ hybridization in hippocampus and raphe nuclei. None of the experimental manipulations altered 5-HT 1B mRNA levels in the hippocampus or dorsal raphe, and also had no effect on 5-HT 1A mRNA in dorsal or median raphe. However, 5-HT 1A mRNA levels were regulated in a complex manner in the different subfields of hippocampus. We conclude that both MR and GR play an integrated role in regulating 5-HT 1A mRNA levels in hippocampus while having no effect on 5-HT 1B mRNA levels under these conditions.

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“…Investigations of the effects of SSRIs on expression or ligand binding activity of the serotonin transporter have reported increases (Hrdina and Vu, 1993;Lopez et al, 1994), decreases (Lesch et al, 1993;Benmansour et al, 1999), or no change (Spurlock et al, 1994). Long-term antidepressant treatment is reported to down-regulate the presynaptic serotonin autoreceptors (Neumaier et al, 1996;Anthony et al, 2000) and to enhance the electrically evoked release of serotonin (Blier and Bouchard, 1994), whereas others have reported that the autoreceptors remain functional (Hjorth and Auerbach, 1999).…”

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Up-Regulation of Tryptophan Hydroxylase Expression and Serotonin Synthesis by Sertraline

2002

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The neurotransmitter serotonin is involved in a variety of brain functions, and abnormal changes in serotonin neurotransmission are associated with an array of psychiatric disorders, including depression. Sertraline is a selective serotonin reuptake inhibitor (SSRI) and an effective antidepressant. Sertraline increases the serotonin concentration in the synaptic cleft by a short-term action; however, clinical improvement is observed only after several weeks, suggesting that the therapeutic effect may be caused by long-term alterations in serotonin transmission. We determined the effects of sertraline on serotonin synthesis in vivo and in vitro. Long-term treatment of rats with sertraline up-regulated mRNA and protein levels of the serotonin-synthesizing enzyme tryptophan hydroxylase (TPH), as determined by in situ hybridization and immunocytochemistry, respectively. In vitro studies using RBL-2H3 cells also showed an increase in mRNA and protein levels of TPH by sertraline, as determined by Northern blot and immunoblot analyses, respectively. This was accompanied by increases in the levels of TPH enzymatic activity and total serotonin. These data demonstrate that in addition to the known short-term action as an uptake blocker, sertraline also exerts a long-term effect on the serotonin neurotransmission by enhancing serotonin synthesis. A similar effect was observed with another SSRI, fluoxetine, but not with the non-SSRI chlorpromazine. The up-regulation of TPH gene expression by sertraline was attenuated by the protein kinase A (PKA) inhibitor N-[2-(p-bromocinnamylamine)-ethyl]-5-isoquinolinesulfonamine, suggesting that a mechanism involving the PKA signaling pathway might at least in part mediate the long-term therapeutic action.

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Antidepressant-induced regulation of 5-HT1b mRNA in rat dorsal raphe nucleus reverses rapidly after drug discontinuation

Cited by 66 publications

References 26 publications

Comprehensive expression analysis of a rat depression model

Comprehensive expression analysis of a rat depression model

Corticosteroids regulate 5-HT1A but not 5-HT1B receptor mRNA in rat hippocampus

Up-Regulation of Tryptophan Hydroxylase Expression and Serotonin Synthesis by Sertraline

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