Effect of 6-hydroxydopamine on in vitro hippocampal corticosterone binding capacity in the male rat

Weidenfeld, Joseph; Siegel, Richard A.; Corcos, A; Chen, M.; Feldman, Shaul; Chowers, I.

doi:10.1007/bf00237156

Cited by 17 publications

(9 citation statements)

References 10 publications

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“…Previous studies using more selective de pleting agents indicate that both norepinephrine and serotonin depletions can decrease [3H]-corticosterone binding in the hip pocampus [10,11], However, serotonin depletions have also been reported to increase hippocampal [3H]-corticosterone binding [22]. In contrast, a single injection of the serotonergic neurotoxin, 3,4-methylenedioxymethamphetamine selectively decreased type II corticosteroid receptor levels in the striatum, but not in the hippocampus or frontal cortex [23].…”

Section: Discussionmentioning

confidence: 95%

“…Neurotransmitters such as serotonin and norepi nephrine also have complex regulatory influences on brain cor ticosteroid receptors. This is based on studies using depleting agents such as 6-hydroxydopamine [10] and 5,7-dihydroxytryptamine [11] which have generally demonstrated that de creasing neuronal levels of serotonin and/or catecholamines decreases [3H]-corticosterone binding in the hippocampus. However, since biogenic amines are involved in adrenocortical regulation [ 12], the effects of biogenic amine depleting regi mens on corticosteroid receptor levels could be due to alter ations in circulating corticosterone levels rather than to a direct effect on receptor levels.…”

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confidence: 99%

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Reserpine-Induced Decrease in Type I and II Corticosteroid Receptors in Neuronal and Lymphoid Tissues of Adrenalectomized Rats

Lowy

1990

Neuroendocrinology

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The effect of the biogenic amine depleting drug, reserpine, on the concentration of type II corticosteroid receptors (i.e., glucocorticoid receptors) in neuronal (hippocampus, frontal cortex, hypothalamus), lymphoid (circulating lymphocytes, spleen, thymus) and pituitary tissues as well as hippocampal type I (i.e., mineralocorticoid) receptors was examined in adrenal-intact and adrenalectomized (ADX) rats. Reserpine (2 mg/kg) or vehicle was administered to adrenal-intact rats for 2 consecutive days. Following the second injection rats were ADX and sacrificed 24 h later. Reserpine significantly decreased type I and II hippocampal receptors as well as type II receptors in frontal cortex, hypothalamus, lymphocytes and spleen. Since the reserpine-induced decreases in receptor content could be due to reserpine-induced elevations in circulating corticosterone levels, reserpine (2 mg/kg) or vehicle was administered to 1-day ADX rats which were then sacrificed 2 days later (i.e., 3 days post ADX). A 1-day ADX control group was also included. The 3-day ADX regimen produced significant or nearly significant increases in type II receptors in hippocampus, frontal cortex, hypothalamus, lymphocytes and spleen in vehicle-treated rats. Reserpine attenuated the ADX-induced upregulation of type II receptors in hippocampus, frontal cortex, lymphocytes and spleen, but had no effect on the ADX-induced upregulation of type II receptors in the hypothalamus. The ADX-induced increase in hippocampal type I receptors was not affected by reserpine treatment. In a final experiment, reserpine (2 mg/kg) or vehicle was administered immediately after ADX and rats were sacrificed 24 h later in order to assess the effect of reserpine on basal (i.e., nonupregulated) corticosteroid receptor levels in the absence of circulating corticosterone levels. Reserpine decreased type II receptor levels in hippocampus, frontal cortex, lymphocytes, spleen and pituitary. Hippocampal type I receptors were also decreased by reserpine. A correlational analysis of data pooled from all three studies indicated significant positive correlations between type II receptor content in lymphocytes and type II receptor levels in hippocampus, frontal cortex and spleen. These studies indicate that depletion of biogenic amines by reserpine produces differential decreases in type II receptor levels in a variety of tissues under basal and upregulated conditions. The ability of reserpine to produce decreases in type I and II receptors in ADX rats indicates that these receptors can be regulated by an adrenal-independent mechanism. The differential response of ADX-induced upregulated hippocampal type I and II receptors to reserpine provide further evidence that corticosteroid receptors in this structure have distinct regulatory mechanisms. Finally, these studies also suggest that the regulation of neuronal and lymphoid type II receptors are similar and help validate the utility of lymphocyte type II receptor measurements in human disease states, such as depression.

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Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

Reserpine-Induced Decrease in Type I and II Corticosteroid Receptors in Neuronal and Lymphoid Tissues of Adrenalectomized Rats

Lowy

1990

Neuroendocrinology

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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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“…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.…”

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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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Effect of 6-hydroxydopamine on in vitro hippocampal corticosterone binding capacity in the male rat

Cited by 17 publications

References 10 publications

Reserpine-Induced Decrease in Type I and II Corticosteroid Receptors in Neuronal and Lymphoid Tissues of Adrenalectomized Rats

Reserpine-Induced Decrease in Type I and II Corticosteroid Receptors in Neuronal and Lymphoid Tissues of Adrenalectomized 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

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

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