Non-genomic effects of glucocorticoids in the neural system

Makara, Gábor B.; Haller, József

doi:10.1016/s0301-0082(01)00012-0

Cited by 181 publications

(94 citation statements)

References 156 publications

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“…As behavioral problems may also occur in children exposed to severe prenatal stress or repeated administration of betamethasone (French et al, 1999(French et al, , 2004Stott, 1973), continuing research is necessary to determine the mechanisms of the behavioral side effects (Avishai-Eliner et al, 2002;Matthews, 2000;Seckl, 2000;Seckl et al, 2000;. As corticosteroids may utilize multiple pathways for their actions (Beato and Sanchez-Pacheco, 1996;De Kloet, 2004;Makara and Haller, 2001;Meijer, 2002), it is reasonable to anticipate that the mechanisms responsible for the beneficial and desired effects of prenatal betamethasone (lung maturation) are distinct from mechanisms responsible for unwanted side effects on behavior. This model may help in defining pathways of prenatal betamethasone actions and selecting those in which a specific therapeutic intervention would prevent unwanted side effects.…”

Section: Technical Considerationsmentioning

confidence: 99%

Prenatal Exposure to Betamethasone Decreases Anxiety in Developing Rats: Hippocampal Neuropeptide Y as a Target Molecule

Velı́šek

2006

Neuropsychopharmacol

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Repeated antenatal administration of betamethasone is frequently used as a life-saving treatment in obstetrics. However, limited information is available about the outcome of this therapy in children. The initial prospective studies indicate that there are behavioral impairments in children exposed to repeated courses of prenatal betamethasone during the third trimester of pregnancy. In this study, pregnant rats received two betamethasone injections on day 15 of gestation. Using immunohistochemistry, the expression of a powerful anxiolytic molecule neuropeptide Y (NPY) was determined on postnatal day (PN) 20 in the hippocampus and basolateral amygdala (structures related to anxiety and fear) of the offspring. Prenatal betamethasone exposure induced significant increases in NPY expression in the hippocampus but not in the amygdala. Indeed, behavioral tests in the offspring, between PN20 and PN22 in the open field, on the horizontal bar, and in the elevated plus maze, indicated decreases in anxiety, without impairments in motor performance or total activity. Decreased body weight in betamethasone-exposed rats confirmed long-lasting effects of prenatal exposure. Thus, prenatal betamethasone treatment consistently increases hippocampal NPY, with decreases in anxiety-related behaviors and hippocampal role in anxiety in rats. Animal models may assist in differentiation between pathways of the desired main effect of the antenatal corticosteroid treatment and pathways of unwanted side effects. This differentiation can lead to specific therapeutic interventions directed against the side effects without eliminating the beneficial main effect of the corticosteroid treatment.

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Section: Technical Considerationsmentioning

confidence: 99%

Prenatal Exposure to Betamethasone Decreases Anxiety in Developing Rats: Hippocampal Neuropeptide Y as a Target Molecule

Velı́šek

2006

Neuropsychopharmacol

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“…Rapid effects of glucocorticoids can occur at the membrane level affecting intracellular calcium or protein kinases that can alter, for example, vasopressin release (Makara & Haller 2001, Chen & Qiu 1999. We studied if the release of TRH was regulated in hypothalamic cells treated for 1-2 h with dex or 8Br-cAMP, alone or combined.…”

Section: Regulation Of Trh Release and Content In Hypothalamic Culturesmentioning

confidence: 99%

Dexamethasone represses cAMP rapid upregulation of TRH gene transcription: identification of a composite glucocorticoid response element and a cAMP response element in TRH promoter

Cote-Vélez

Pérez-Martı́nez²,

My³

et al. 2005

Journal of Molecular Endocrinology

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Hypothalamic proTRH mRNA levels are rapidly increased (at 1 h) in vivo by cold exposure or suckling, and in vitro by 8Br-cAMP or glucocorticoids. The aim of this work was to study whether these effects occurred at the transcriptional level. Hypothalamic cells transfected with rat TRH promoter (−776/+85) linked to the luciferase reporter showed increased transcription by protein kinase (PK) A and PKC activators, or by dexamethasone (dex), but co-incubation with dex and 8Br-cAMP decreased their stimulatory effect (as observed for proTRH mRNA levels). These effects were also observed in NIH-3T3-transfected cells supporting a characteristic of TRH promoter and not of hypothalamic cells. Transcriptional regulation by 8Br-cAMP was mimicked by noradrenaline which increased proTRH mRNA levels, but not in the presence of dex. PKA inhibition by H89 avoided 8Br-cAMP or noradrenaline stimulation. TRH promoter sequences, cAMP response element (CRE)-like (−101/−94 and −59/−52) and glucocorticoid response element (GRE) half-site (−210/−205), were analyzed by electrophoretic mobility shift assays with nuclear extracts from hypothalamic or neuroblastoma cultures. PKA stimulation increased binding to CRE (−101/−94) but not to CRE (−59/−52); dex or 12-O-tetradecanoylphorbol-13-acetate (TPA) increased binding to GRE, a composite site flanked by a perfect and an imperfect activator protein (AP-1) site in the complementary strand. Interference was observed in the binding of CRE or GRE with nuclear extracts from cells co-incubated for 3 h with 8Br-cAMP and dex; from cells incubated for 1 h, only the binding to GRE showed interference. Rapid cross-talk of glucocorticoids with PKA signaling pathways regulating TRH transcription constitutes another example of neuroendocrine integration.

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“…It was subsequently shown (Roozendaal et al 2002) that noradrenergic activation is essential for the memory-enhancing effects, and that glucocorticoids play a permissive role in noradrenergic actions, thus promoting memory formation. Notably, it was suggested that the interaction between the two hormones should occur within an interval of 30 min, which is rather a short time-interval for genemediated events to occur (Makara and Haller 2001;Roozendaal 2003). …”

mentioning

confidence: 99%

Corticosterone time-dependently modulates β-adrenergic effects on long-term potentiation in the hippocampal dentate gyrus

Pu¹,

Krugers²,

Joëls³

2007

Learn. Mem.

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Previous experiments in the hippocampal CA1 area have shown that corticosterone can facilitate long-term potentiation (LTP) in a rapid non-genomic fashion, while the same hormone suppresses LTP that is induced several hours after hormone application. Here, we elaborated on this finding by examining whether corticosterone exerts opposite effects on LTP depending on the timing of hormone application in the dentate gyrus as well. Moreover, we tested rapid and delayed actions by corticosterone on ␤-adrenergic-dependent changes in LTP. Unlike the CA1 region, our in vitro field potential recordings show that rapid effects of corticosterone do not influence LTP induced by mild tetanization in the hippocampal dentate gyrus, unless GABA A receptors are blocked. In contrast, the ␤-adrenergic agonist isoproterenol does initiate a slow-onset, limited amount of potentiation. When corticosterone was applied concurrently with isoproterenol, a further enhancement of synaptic strength was identified, especially during the early stage of potentiation. Yet, treatment with corticosterone several hours in advance of isoproterenol fully prevented any effect of isoproterenol on LTP. This emphasizes that corticosterone can regulate ␤-adrenergic modulation of synaptic plasticity in opposite directions, depending on the timing of hormone application.

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Non-genomic effects of glucocorticoids in the neural system

Cited by 181 publications

References 156 publications

Prenatal Exposure to Betamethasone Decreases Anxiety in Developing Rats: Hippocampal Neuropeptide Y as a Target Molecule

Prenatal Exposure to Betamethasone Decreases Anxiety in Developing Rats: Hippocampal Neuropeptide Y as a Target Molecule

Dexamethasone represses cAMP rapid upregulation of TRH gene transcription: identification of a composite glucocorticoid response element and a cAMP response element in TRH promoter

Corticosterone time-dependently modulates β-adrenergic effects on long-term potentiation in the hippocampal dentate gyrus

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