Acute and Long‐Term Treatments with the Selective Serotonin Reuptake Inhibitor Citalopram Modulate the HPA Axis Activity at Different Levels in Male Rats

Jb, Jensen; Ds, Jessop; Ms, Harbuz; Mørk, Arne; Sanchéz, Connie; Jd, Mikkelsen

doi:10.1046/j.1365-2826.1999.00362.x

Cited by 92 publications

(65 citation statements)

References 38 publications

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“…Previous studies have reported that basal PVN CRF mRNA is decreased by 30 to 67% (Brady et al, 1991(Brady et al, , 1992Aubry et al, 1999) or is unchanged (Jensen et al, 1999) after chronic antidepressant treatment. Consistent with the latter study, we found that administration of a variety of antidepressant agents produced no effect on basal CRF hnRNA or mRNA expression in the PVN.…”

Section: Discussionmentioning

confidence: 89%

Regulation of Corticotropin-Releasing Factor Neuronal Systems and Hypothalamic-Pituitary-Adrenal Axis Activity by Stress and Chronic Antidepressant Treatment

Stout

Owens

Nemeroff

2002

J Pharmacol Exp Ther

108

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In a series of experiments, we tested the hypothesis that chronic antidepressant drug administration reduces the synaptic availability of corticotropin-releasing factor (CRF) through one or more effects on CRF gene expression or peptide synthesis. We also determined whether effects of acute or chronic stress on CRF gene expression or peptide concentration are influenced by antidepressant drug treatment. Four-week treatment with venlafaxine, a dual serotonin (5-HT)/norepinephrine (NE) reuptake inhibitor, and tranylcypromine, a monoamine oxidase inhibitor, resulted in an attenuation of acute stress-induced increases in CRF heteronuclear RNA (hnRNA) synthesis in the paraventricular nucleus (PVN). Trends toward the same effect were observed after treatment with the 5-HT reuptake inhibitor fluoxetine, or the NE reuptake inhibitor reboxetine.CRF mRNA accumulation in the PVN during exposure to chronic variable stress was attenuated by concurrent antidepressant administration. Basal CRF hnRNA and mRNA expression were not affected by antidepressant treatment in the PVN or in other brain regions examined. Chronic stress reduced CRF concentrations in the median eminence, but there were no consistent effects of antidepressant drug treatment on CRF, serum corticotropin, or corticosterone concentrations. CRF receptor expression and basal and stress-stimulated HPA axis activity were unchanged after antidepressant administration. These results suggest that chronic antidepressant administration diminishes the sensitivity of CRF neurons to stress rather than alters their basal activity. Additional studies are required to elucidate the functional consequences and mechanisms of this interaction.Corticotropin-releasing factor (CRF) is a 41 amino acid peptide that is synthesized and secreted in many regions of the brain, particularly in limbic-associated areas such as the hypothalamus, amygdala, and bed nucleus of the stria terminalis. There is extensive evidence that CRF functions as both a neurohormone and neurotransmitter in coordinating endocrine, autonomic, and behavioral aspects of the stress response (Owens and Nemeroff, 1991). Major depression is a condition that has been associated with a predisposing influence of major stressors, particularly early in life, and with neurochemical and neuroendocrine findings of CRF hypersecretion (Arborelius et al., 1999). On the basis of these observations, we hypothesized that antidepressant agents, whose ultimate therapeutic mechanism(s) of action are poorly understood, may act in part by reducing CRF synthesis or secretion, either tonically or in response to stress.There is clinical evidence that antidepressants exert effects on CRF systems. Hypothalamic-pituitary-adrenal (HPA) axis abnormalities, hypothesized to result at least in part from CRF hypersecretion and elevated cerebrospinal fluid (CSF) CRF concentrations in depressed patients, have been reported to normalize after antidepressant treatment or electroconvulsive therapy. However, in human studies it is currently impossi...

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Section: Discussionmentioning

confidence: 89%

Regulation of Corticotropin-Releasing Factor Neuronal Systems and Hypothalamic-Pituitary-Adrenal Axis Activity by Stress and Chronic Antidepressant Treatment

Stout

Owens

Nemeroff

2002

J Pharmacol Exp Ther

108

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“…Larson and Summers (2001) showed that a 1-week treatment with the SSRI, setralin, reduces aggressive behaviour and reverses dominant social status in the lizard Anolis carolinensis. As seen with elevated dietary intake of TRP, short-term treatment with SSRI activates the HPA axis, whereas long-term treatment has the opposite effect, desensitising the HPA axis in rats (Jensen et al, 1999). An effect on the densities and transduction mechanisms of postand/or pre-synaptic 5-HT receptors, resulting in a delayed elevation of 5-HT post-synaptic effects in certain brain regions, has been suggested as a mechanism involved in mediating the effects of long-term SSRI treatment (Mongeau et al, 1997;Nutt et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Time-course of the effect of dietaryl-tryptophan on plasma cortisol levels in rainbow troutOncorhynchus mykiss

Lepage

Vílchez

Pottinger³

et al. 2003

Journal of Experimental Biology

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SUMMARYIsolated juvenile rainbow trout were fed a feed supplemented with l-tryptophan (TRP) for 3, 7 or 28 days, after which they were either sampled directly (undisturbed) or subjected to a standardised stressor prior to sampling. Controls (stressed and undisturbed) received the same feed but without any supplementary TRP. Stress resulted in a significant elevation of plasma [cortisol] in fish fed control feed and in fish fed TRP-supplemented feed for 3 and 28 days. However, fish fed TRP-supplemented feed for 7 days did not show any significant elevation of plasma [cortisol] in response to stress. Plasma levels of adrenocorticotropin followed the same general pattern as cortisol. Plasma and brain [TRP] were elevated in fish fed TRP-supplemented feed. The amino acid TRP is the precursor of the monoamine neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) and the brain 5-HT system is known to be involved in the control of the hypothalamic-pituitary-interrenal (HPI) axis. Fish fed TRP-supplemented feed showed elevated levels of 5-hydroxyindoleacetic acid (5-HIAA, a major 5-HT metabolite) in the hypothalamus and optic tectum. However, TRP treatment did not appear to result in any effects on brain dopaminergic activity and the effects on brain norepinephric activity do not support a role of norepinephrine in mediating the effects of TRP on HPI axis reactivity in rainbow trout.

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“…Preclinical studies on the effects of the chronic administration of different antidepressants demonstrate that a decrease of the HPA-axis activity is a final common pathway of antidepressant effects, but that the different antidepressants unfold their specific pharmacological efficacy on varying HPA-axis levels and receptor subsystems. Tricyclic antidepressants as well as the SSRI fluoxetine are likely to increase either GR m-RNA or MR m-RNA expression in the hippocampus, depending on the type of drug (Barden et al, 1995;Brady et al, 1992;DeRijk et al, 2001;Holsboer and Barden, 1996;Jensen et al, 1999;Okugawa et al, 1999;Seckl and Fink, 1992). Owing to the increase of hippocampal MRs and GRs, they are thought to regain their balance re-establishing the inhibitory tone on the PVN in the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

Fluvoxamine Reduces Responsiveness of HPA Axis in Adult Female BPD Patients with a History of Sustained Childhood Abuse

Rinne

Kloet

Wouters

et al. 2003

Neuropsychopharmacol

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The aim of the study is to test whether fluvoxamine affects the function of the hypothalamic pituitary adrenal (HPA) axis in female borderline (borderline personality disorder, BPD) patients with and without a history of sustained childhood abuse. Special attention is given to the presence of comorbid major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). The HPA axis of 30 female BPD patients with (n ¼ 17) and without (n ¼ 13) a history of sustained childhood abuse was challenged with a combined dexamethasone and corticotropin releasing hormone test (DEX/CRH test) before and after 6 (n ¼ 14) and 12 (n ¼ 16) weeks of fluvoxamine treatment (150 mg/day). Both 6-and 12-week fluvoxamine treatments were associated with a significant and robust reduction of the adrenocorticotrophic hormone (ACTH) and cortisol response to the DEX/CRH test. The magnitude of the reduction was dependent on the presence of sustained childhood abuse, but not on the presence of comorbid MDD or PTSD: patients with a history of sustained childhood abuse showed the strongest reduction in ACTH and cortisol. In conclusion, Fluvoxamine treatment reduces the hyperresponsiveness of the HPA axis in BPD patients with a history of sustained childhood abuse. This effect is likely to be obtained in the first 6 weeks of treatment.

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Acute and Long‐Term Treatments with the Selective Serotonin Reuptake Inhibitor Citalopram Modulate the HPA Axis Activity at Different Levels in Male Rats

Cited by 92 publications

References 38 publications

Regulation of Corticotropin-Releasing Factor Neuronal Systems and Hypothalamic-Pituitary-Adrenal Axis Activity by Stress and Chronic Antidepressant Treatment

Regulation of Corticotropin-Releasing Factor Neuronal Systems and Hypothalamic-Pituitary-Adrenal Axis Activity by Stress and Chronic Antidepressant Treatment

Time-course of the effect of dietaryl-tryptophan on plasma cortisol levels in rainbow troutOncorhynchus mykiss

Fluvoxamine Reduces Responsiveness of HPA Axis in Adult Female BPD Patients with a History of Sustained Childhood Abuse

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