Short-term and long-term effects of p-chloroamphetamine on hippocampal serotonin and corticosteroid receptor levels

Novotney, Susan; Lowy, Martin T.

doi:10.1016/0006-8993(95)00371-v

Cited by 11 publications

(12 citation statements)

References 37 publications

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“…The PCPA-induced increase in hippocampal MR-binding sites can be related to the previously described decrease of hippocampal MR-binding sites following acute PCA [16]. Indeed, these authors emphasize that the first effect of PCA is to increase 5-HT release before depleting 5-HT levels, so that the observed decrease in hippocampal MR-binding sites could result from the primary increase in 5-HT release.…”

Section: Discussionmentioning

confidence: 54%

“…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%

“…To our knowledge, Novotney and Lowy [16]were the only ones who studied the effect of short-term manipulation of 5-HT neurotransmission on hippocampal GR regulation. This study showed that 3 h after an acute PCA treatment hippocampal GR were decreased.…”

Section: Discussionmentioning

confidence: 99%

“…A decrease in hippocampal MR and GR site levels was found 3 h after an acute p -chloroamphetamine (PCA) treatment in 24-hour adrenalectomized (ADX) rats [16]. By contrast, 16 h after an acute 3-4-methylenedioxymethamphetamine (MDMA) administration in ADX rats complemented with corticosterone, hippocampal GR mRNA expression was not modified, while MR mRNA expression was increased only in the dentate gyrus [17].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Sémont

Fache²,

Ouafik³

et al. 1999

Neuroendocrinology

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“…in order to prevent lesioning of noradrenergic neurons [47]. PCA administration results in hyperthermia that can be fatal [48]. Therefore, for 12 h following PCA administration, animal cages were surrounded by ice to prevent hyperthermia.…”

Section: Serotonergic Lesioningmentioning

confidence: 99%

Specific Serotonin Reuptake Inhibitor-Induced Decreases in Lymphocyte Activity Require Endogenous Serotonin Release

Pellegrino

Bayer

2000

Neuroimmunomodulation

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Objectives: We have previously reported that acute administration of the specific serotonin reuptake inhibitor (SSRI), fluoxetine, resulted in a decrease in mitogen-induced blood lymphocyte proliferation. The present studies further examine the specificity of this response to serotonin reuptake systems and the potential role of endogenous serotonin in mediating these effects. Methods: Male Sprague-Dawley rats were treated intraperitoneally with the SSRIs, fluoxetine (6–10 mg/kg) or sertraline (20 mg/kg), dopamine and norepinephrine reuptake inhibitors, GBR 12909 and desipramine, respectively (6 mg/kg) or the serotonin precursor, 5-hydoxytryptophan (5-HTP, 50 mg/kg) 2 h prior to sacrifice. The serotonin-depleting agents, p-chlorophenylalanine (PCPA, 2 × 200 mg/kg) or the serotonin-lesioning agent, p-chloroamphetamine (PCA, 2 × 10 mg/kg) were administered intraperitoneally 5–7 days prior to fluoxetine (10 mg/kg) administration. Results: Unlike the SSRIs, which significantly suppressed lymphocyte proliferation responses, selective norepinephrine or dopamine reuptake inhibition had no effect on lymphocyte proliferation. Elevation of extracellular serotonin levels with the serotonin precursor, 5-HTP, resulted in a similar decrease in lymphocyte proliferation as that seen with SSRI administration. Conversely, decreases in endogenous serotonin following PCA or PCPA treatment prevented the fluoxetine-induced decreases in lymphocyte proliferation. Conclusions: These results suggest that decreases in mitogen-induced lymphocyte proliferation following acute fluoxetine administration were due to elevations in extracellular serotonin following reuptake inhibition.

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Effects of flesinoxan on corticosteroid receptor expression in the rat hippocampus

Sibug¹,

Compaan

Meijer

et al. 2000

European Journal of Pharmacology

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Short-term and long-term effects of p-chloroamphetamine on hippocampal serotonin and corticosteroid receptor levels

Cited by 11 publications

References 37 publications

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

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

Specific Serotonin Reuptake Inhibitor-Induced Decreases in Lymphocyte Activity Require Endogenous Serotonin Release

Effects of flesinoxan on corticosteroid receptor expression in the rat hippocampus

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