The antidepressants fluoxetine, idazoxan and phenelzine alter corticotropin-releasing hormone and tyrosine hydroxylase mRNA levels in rat brain: therapeutic implications

Brady, Linda S.; Gold, Philip W.; Herkenham, Miles; Lynn, Allison B.; Whitfield, Harvey J.

doi:10.1016/0006-8993(92)90459-m

Cited by 230 publications

(130 citation statements)

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“…The same results were found with several other antidepressant drugs selected for their distinctly different primary pharmacological actions (Brady et al, 1992). Based on these data, we studied the effects of short-term (2 weeks) and long-term (8 weeks) administration of a methanolic SJW extract, hypericin and imipramine on the expression of genes that may be involved in the regulation of the HPA axis (Butterweck et al, 2001b).…”

Section: Introductionsupporting

confidence: 60%

“…Previous work validated the long-term drug administration protocol applied to unstressed eucortisolemic rats as an appropriate model for assessing the therapeutic efficacy of antidepressant drugs (Brady et al, 1991(Brady et al, , 1992. The changes in mRNA expression levels of genes involved in the HPA axis control served to correct imbalances created in these 100 7 4 100 7 3 9 77 2 101 7 3 101 7 4 9 97 2 9 27 4 9 87 2 9 77 2 105 7 2 DG 100 7 4 100 7 2 100 7 4 118 7 2* 100 7 5 112 7 2 9 77 5 110 7 3 100 7 3 110 7 2 GR CA1 100 7 5 100 7 2 101 7 3 108 7 4 104 7 3 104 7 4 9 67 3 9 67 3 9 77 5 9 97 3 CA3 100 7 3 100 7 1 100 7 2 108 7 3 100 7 2 103 7 2 9 77 2 9 77 1 9 97 4 108 7 5 DG 100 7 4 100 7 2 9 97 3 119 7 2* 101 7 5 104 7 5 9 77 3 101 7 2 9 47 4 104 7 3 5-HT 1A CA1 100 7 4 100 7 3 102 7 7 121 7 3* 101 7 5 107 7 4 104 7 4 105 7 5 108 7 4 102 7 3 CA3 100 7 5 100 7 3 9 87 7 122 7 3* 96 7 5 102 7 5 9 87 6 9 67 4 103 7 6 111 7 6 DG 100 7 4 100 7 5 9 57 6 106 7 6 9 87 5 102 7 5 9 47 4 9 67 5 100 7 3 108 7 4 POMC Ant.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperforin and the HPA axis V Butterweck et al neurochemical systems by chronic immobilization stress (Butterweck et al, 2001b). Brady et al (1991Brady et al ( , 1992 showed that long-term treatment with imipramine, fluoxetine, idazoxan, and phenelzine reduces HPA axis activity and regulates gene transcription levels in relevant structures with delayed onset, resembling the delayed onset of therapeutic efficacy of these drugs when given to patients for treatment of depression. In the current study, using in situ hybridization histochemistry, we have examined the effect of chronic administration of the SSRI fluoxetine, the antipsychotic drug haloperidol, a lipophilic SJW extract prepared with supercritical CO 2 , and hyperforin-TMB on these same genes.…”

Section: Discussionmentioning

confidence: 99%

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Hyperforin-Containing Extracts of St John's Wort Fail to Alter Gene Transcription in Brain Areas Involved in HPA Axis Control in a Long-Term Treatment Regimen in Rats

Butterweck

Winterhoff²,

Herkenham

2003

Neuropsychopharmacol

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We previously showed that a methanolic extract of St John's wort (SJW) (Hypericum) and hypericin, one of its active constituents, both have delayed regulation of genes that are involved in the control of the hypothalamic-pituitary-adrenal (HPA) axis. Hyperforin, another constituent of SJW, is active in vitro and has been proposed to be the active constituent for therapeutic efficacy in depression. We therefore examined if hyperforin has delayed effects on HPA axis control centers similar to those of Hypericum and hypericin. We used in situ hybridization histochemistry to examine in rats the effects of short-term (2 weeks) and long-term (8 weeks) oral administration of two hyperforin preparations, fluoxetine (positive control), and haloperidol (negative control) on the expression of genes involved in the regulation of the HPA axis. Fluoxetine (10 mg/kg) given daily for 8 weeks, but not 2 weeks, significantly decreased levels of corticotropinreleasing hormone (CRH) mRNA by 22% in the paraventricular nucleus (PVN) of the hypothalamus and tyrosine hydroxylase (TH) mRNA by 23% in the locus coeruleus. Fluoxetine increased levels of mineralocorticoid (MR) (17%), glucocorticoid (GR) (18%), and 5-HT 1A receptor (21%) mRNAs in the hippocampus at 8, but not 2, weeks. Comparable to haloperidol (1 mg/kg), neither the hyperforinrich CO 2 extract (27 mg/kg) nor hyperforin-trimethoxybenzoate (8 mg/kg) altered mRNA levels in brain structures relevant for HPA axis control at either time point. These data suggest that hyperforin and hyperforin derivatives are not involved in the regulation of genes that control HPA axis function.

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Section: Introductionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Hyperforin-Containing Extracts of St John's Wort Fail to Alter Gene Transcription in Brain Areas Involved in HPA Axis Control in a Long-Term Treatment Regimen in Rats

Butterweck

Winterhoff²,

Herkenham

2003

Neuropsychopharmacol

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“…For example, following long (8 weeks), but not short (2 weeks) treatment with either fluoxetine or imipramine, CRH mRNA was decreased by 30-48% in the hypothalamic PVN (Brady et al 1991(Brady et al , 1992. Moreover, chronic treatment with fluoxetine, as well as other antidepressants, significantly elevated the levels of glucocorticoid receptors in the hippocampus (Brady et al 1991(Brady et al , 1992, which normally mediate the negative feedback response to stress-induced activation of the HPA axis (Sapolsky et al 1984). Finally, our results are in agreement with previous studies in experimental animals (Reul et al 1993) and in healthy humans (Michelson et al 1997), which reported that chronic treatment with antidepressants markedly attenuated the pituitary-adrenal response to stressful or pharmacological challenges.…”

Section: Discussionmentioning

confidence: 99%

“…Another system that is markedly altered following chronic antidepressant treatment is the HPA axis. For example, following long (8 weeks), but not short (2 weeks) treatment with either fluoxetine or imipramine, CRH mRNA was decreased by 30-48% in the hypothalamic PVN (Brady et al 1991(Brady et al , 1992. Moreover, chronic treatment with fluoxetine, as well as other antidepressants, significantly elevated the levels of glucocorticoid receptors in the hippocampus (Brady et al 1991(Brady et al , 1992, which normally mediate the negative feedback response to stress-induced activation of the HPA axis (Sapolsky et al 1984).…”

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confidence: 99%

Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Yirmiya

Pollak

Barak

et al. 2001

Neuropsychopharmacology

203

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Antidepressants produce various immunomodulatory effects, as well as an attenuation of the behavioral responses to immune challenges, such as lipopolysaccharide (LPS). To explore further the effects of antidepressants on neuroimmune interactions, rats were treated daily with either fluoxetine (Prozac) or saline for 5 weeks, and various behavioral, neuroendocrine, and immune functions were measured following administration of either LPS or saline. Chronic fluoxetine treatment significantly attenuated the anorexia and body weight loss, as well as the depletion of CRH-41 from the median eminence and the elevation in serum corticosterone levels induced by LPS. Chronic treatment with imipramine also attenuated LPS-induced adrenocortical activation. In rats and in mice, which normally display a biphasic body temperature response to LPS (initial hypothermia followed by hyperthermia), chronic treatment with fluoxetine completely abolished the hypothermic response and facilitated and strengthened the hyperthermic response. The effects of antidepressants on the responsiveness to LPS are probably not mediated by their effects on peripheral proinflammatory cytokine production, because LPS-induced expression of TNFSeveral lines of evidence indicate that antidepressants produce various immunomodulatory effects. In depressed patients, the effects of antidepressants are variable and seem to be related to the immune status of the patients at the initiation of the treatment. When depression was associated with immune activation, antidepressants reduced immune function and cytokine secretion. For example, the increased plasma levels of IL-6 during acute depression were normalized by 8-week treatment with fluoxetine (Sluzewska et al. 1995), the increased monocyte counts in depressed patients were reduced following 6-weeks treatment with tricyclic antidepressants (TCAs) (Seidel et al. 1996), and the increased numbers of leukocytes and neutrophils were also reduced by antidepressant treatment (Maes et al. 24 , NO . 5 1997). On the other hand, when immune functions were found to be normal, antidepressants had no immunological effects; for example, chronic moclobemide treatment had no effect on monocytes functions, TNF ␣ production or IFN ␥ levels (Landmann et al. 1997). Moreover, in a study of depressed patients who exhibited immune suppression before treatment, the TCA clomipramine increased the production of IL-1 ␤ , IL-2, and IL-3 (Weizman et al. 1994).In experimental animals, TCAs as well as selective serotonin reuptake inhibitors (SSRIs) produce mainly immune suppression and anti-inflammatory effects. For example, antidepressant treatment in vivo inhibited the increased acute phase response in olfactory bulbectomized rats, a useful animal model of depression (Song and Leonard 1994), reduced the production of interleukin-1 (IL-1) and IL-2 in a chronic mild stress model of depression (Kubera et al. 1996), inhibited immune activation in rats with experimental allergic neuritis (Zhu et al. 1994), and produced anti-inflammatory ...

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Changes in Cerebrospinal Fluid Neurochemistry During Treatment of Obsessive-compulsive Disorder With Clomipramine

Altemus¹

1994

Arch Gen Psychiatry

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These neuropeptide results coupled with evidence that central administration of corticotropin-releasing hormone, vasopressin, and somatostatin to laboratory animals increases arousal and acquisition of conditioned behaviors whereas central administration of oxytocin has opposite behavioral effects are consistent with a role for these neuropeptides in the pathophysiologic processes and pharmacologic treatment of obsessive-compulsive disorder.

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The antidepressants fluoxetine, idazoxan and phenelzine alter corticotropin-releasing hormone and tyrosine hydroxylase mRNA levels in rat brain: therapeutic implications

Cited by 230 publications

References 32 publications

Hyperforin-Containing Extracts of St John's Wort Fail to Alter Gene Transcription in Brain Areas Involved in HPA Axis Control in a Long-Term Treatment Regimen in Rats

Hyperforin-Containing Extracts of St John's Wort Fail to Alter Gene Transcription in Brain Areas Involved in HPA Axis Control in a Long-Term Treatment Regimen in Rats

Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Changes in Cerebrospinal Fluid Neurochemistry During Treatment of Obsessive-compulsive Disorder With Clomipramine

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