Hippocampal cell nuclear binding of corticosterone following 5,7-dihydroxytryptamine

Siegel, Richard A.; Weidenfeld, Joseph; Chen, Meir; Feldman, Shaul; Melamed, Eldad; Chowers, I.

doi:10.1016/0303-7207(83)90152-1

Cited by 22 publications

(13 citation statements)

References 12 publications

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“…GR and MR biosynthesis appears to be under control of central monoaminergic systems (Maccari et al, 1990(Maccari et al, , 1992Mitchell et al, 1990;Weidenfeld and Feldmann, 1991). In vivo studies with monoamine-depleting agents (eg reserpine) and neurotoxic substances that specifically destroy serotonergic, noradrenergic, and/or dopaminergic nerve terminals have provided evidence for a modulatory role of monoamines in brain corticosteroid receptor regulation (Lowy, 1990;Seckl et al, 1990;Siegel et al, 1983;Weidenfeld et al, 1983). After chronic fluoxetine treatment, in vivo microdialysis studies have shown that extracellular levels of serotonin are markedly elevated (Rutter et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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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“…Indeed, most studies which examined the effects of long-term alteration of the serotoninergic transmission on hippocampal MR-binding sites and/or MR mRNA report no change [16]or a decrease in corticosterone-binding sites [12]and in MR mRNA expression [32]. Nevertheless, it is important to notice that all these studies were performed in adrenal intact rats.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, it was of interest to study whether 5-HT can modulate the number of hippocampal MR and GR. Lesions of serotoninergic neurons by 5-7-dihydroxytryptamine (5-7-DHT) induced selective decreases in hippocampal MR and GR messenger ribonucleic acid (mRNA) expression [11], and decreased nuclear corticosterone-binding sites in hippocampal extracts [12]. Facilitation of the serotoninergic neurotransmission induced by the treatment with the antidepressant drugs citalopram and amitriptyline, enhanced the expression of either hippocampal MR mRNA or hippocampal MR and GR mRNA, respectively [13].…”

Section: Introductionmentioning

confidence: 99%

Effect of Serotonin Inhibition on Glucocorticoid and Mineralocorticoid Expression in Various Brain Structures

Sémont

Fache²,

Ouafik³

et al. 1999

Neuroendocrinology

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Many studies have shown the existence of functional interactions between central neurotransmitter systems and the hypothalamo-pituitary adrenal axis. Mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) are regulated by multiple factors including glucocorticoids themselves. Neurotransmitters such as serotonin (5-hydroxytryptamine: 5-HT) can regulate brain corticosteroid receptors in a complex way. The present study examined the short-term (48 h) effects of parachlorophenylalanine (PCPA), a drug which specifically inhibits 5-HT synthesis, on corticosteroid receptor levels and on the expression of their respective messenger ribonucleic acids (mRNA) in the rat hippocampus, hypothalamus and brain stem. The study was performed in bilaterally adrenalectomized animals, in order to avoid potential drug-induced changes in plasma corticosterone levels, which could secondarily regulate MR and GR. Short-term inhibition of 5-HT synthesis by PCPA significantly increased the number of hippocampal MR-binding sites. PCPA treatment did not alter the number of GR-binding sites in the hippocampus, hypothalamus and brain stem. We observed no change in the affinities of GR and MR sites in all the structures studied. In PCPA-treated rats, restoration of control 5-HT levels by injection of its immediate precursor, 5-hydroxytryptophan (5-HTP) brings the number of hippocampal MR-binding sites back to control levels. It can therefore be concluded that the increase in number of MR-binding sites induced by acute PCPA treatment is dependent on the decrease in 5-HT levels. The increase in hippocampal MR binding sites was correlated with an induction of their messengers, suggesting that 5-HT modulates the synthesis of MR protein. Although PCPA did not modify the number of hippocampal GR-binding sites, a decrease in hippocampal GR mRNA expression was observed. This study shows that 5-HT inhibits hippocampal mineralocorticoid receptor synthesis and that this effect is not mediated by changes in corticosterone hormone secretion, and illustrates the existence of complex mechanisms for corticosteroid receptor regulation in the hippocampus.

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“…Furthermore, though chronic antidepressant administration may atte nuate corticosterone release to stress [31] (not tested in this study), some [28,29], though not all [23], reports sug gest that even major changes in glucocortioid levels have little effect per se on hippocampal corticosteroid receptor mRNA expression [28,29], Whether the action of antide pressants is mediated directly on hippocampal neurons [11,13,16], or indirectly, as shown by imipramine-induced alterations of GR immunoreactivity in mono amine-containing brain stem nuclei [32], is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…In dissociated cultures of fetal hippocampal cells increased 5-HT concentrations lead to elevated glu cocorticoid but not mineralocorticoid binding sites [12], However, results in adult animals in vivo have been less clear-cut. Thus, neurotoxic lesions of the hippocampal serotoninergic innervation reduce corticosterone binding sites in nuclear extracts [13], but others have shown simi lar lesions increase cytosolic binding sites for corticoste rone [14], The hippocampal noradrenergic [15] (and/or dopaminergic) innervations may also play a role as cen tral 6-hydroxydopamine lesions reduce hippocampal nu clear corticosterone binding sites [16]. Reserpine, which depletes all monoamines, reduces both MR and GR in hippocampal cytosol [17], Antidepressant drugs, which inhibit 5-HT and/or noradrenaline reuptake and there fore potentiate monoamine actions, decrease cytosolic binding sites for corticosterone, but so do 5-HT receptor antagonists [14], Thus hippocampal monoaminergic in nervations may modulate corticosteroid receptor levels, although the receptor types involved (corticosterone binds to both GR and MR) and nature of the control are unclear.…”

mentioning

confidence: 99%

Antidepressants Increase Glucocorticoid and Mineralocorticoid Receptor mRNA Expression in Rat Hippocampus in vivo

1992

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Adrenal corticosteroids bind to hippocampal glucocorticoid (GR) and mineralocorticoid receptors (MR), thereby affecting neurochemical transmission leading to altered mood, behaviour and neuroendocrine control. Serotoninergic (5-HT) and noradrenergic projections innervate the hippocampus, interacting with corticosteroid-sensitive cells. We have previously demonstrated that lesions of 5-HT neurons reduce hippocampal GR and MR mRNA levels and now examine whether acute or chronic treatment with antidepressant drugs, which potentiate endogenous monoamines by inhibiting their reuptake, affect hippocampal GR and MR mRNA expression in vivo. Rats were treated with amitriptyline (20 mg/kg · day^–1), desipramine (10 mg/kg · day^–1) or citalopram (20 mg/kg · day^–1). After 2 or 14 days animals were killed, RNA extracted and GR and MR mRNA expression quantified by slot blot hybridization. Amitriptyline for 2 days led to a significant increase in MR (by 23 ± 6%, compared with saline-treated controls), but not GR, mRNA expression. After 14 days amitriptyline, expression of both MR (87 ± 27% rise) and GR mRNA (56 ± 18% rise) had increased significantly in hippocampus, but not in parietal cortex. Desipramine for 14 days also increased MR (60 ± 9%) and GR (42 ± 9%) mRNA expression, though 14 days of citalopram altered only MR mRNA expression (17 ± 5%). Thus, antidepressant drug administration elevates MR and GR mRNA expression in hippocampus, but not parietal cortex, in a time-dependent manner.

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Hippocampal cell nuclear binding of corticosterone following 5,7-dihydroxytryptamine

Cited by 22 publications

References 12 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

Effect of Serotonin Inhibition on Glucocorticoid and Mineralocorticoid Expression in Various Brain Structures

Antidepressants Increase Glucocorticoid and Mineralocorticoid Receptor mRNA Expression in Rat Hippocampus in vivo

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