Long-Lasting Glucocorticoid Suppression of Opioid-Induced Antinociception

Ratka, Anna; Sutanto, W.; Kloet, Ronald De

doi:10.1159/000125046

Cited by 50 publications

(24 citation statements)

References 24 publications

(33 reference statements)

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“…1-7 days before the experiments, the rats were quickly ADX or sham-operated under ether anaesthesia as described elsewhere [38]. The animals were housed in an animal room with alternating light/dark (08: 00-20: 00/20: 00-08 : 00) cycle and received food and water (sham) or saline (after ADX) ad libitum.…”

Section: Methodsmentioning

confidence: 99%

Corticosteroid receptor-dependent modulation of calcium currents in rat hippocampal CA1 neurons

1994

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Link to publication Citation for published version (APA):Karst, H., Wadman, W. J., & Joëls, M. (1994). Corticosteroid receptor-dependent modulation of calcium currents in rat hippocampal CA1 neurons. Brain Research, 649, 234-242. DOI: 10.1016/0006-8993(94)91069-3 General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. AbstractPyramidal CA1 neurons in the rat hippocampus contain mineralocorticoid (MRs) and glucocorticoid receptors (GRs) for corticosterone, which, in activated form, act as transcription factors of the genome. The relative MR and GR occupation changes throughout the day, with predominant MR occupation under rest in the morning and additional GR occupation in the evening and after stress. We examined the effect of MR and GR activation on Ca currents in hippocampal slices from adrenalectomizcd (ADX) rats under whole-cell voltage-clamp conditions. In slices from ADX rats, where MRs and GRs arc unoccupied, Ca currents (particularly in the low-voltage range) were larger than in neurons from the sham-operated controls; these effects became apparent with a delay of > 3 days after ADX. Selective occupation of MRs in tissue from ADX rats greatly (by 70%) and persistently (up to 3 h) reduced transient but also sustained Ca conductances. Voltage dependency and kinetic properties of the currents were not affected. Occupation of GRs as well as MRs by corticosterone (30 nM) resulted in relatively large Ca currents, comparable to those recorded in tissue from mildly stressed sham-operated control animals. Interestingly, exclusive occupation of GRs with 30 nM RU 28362 was not sufficient to induce large Ca currents. The data suggest that the changes in MR and GR occupation throughout the day, related to circadian and stress-induced corticosterone release, are linked to marked alterations in Ca currents, with small Ca currents in the morning and large currents in the evening or after stress. Corticosteroid hormones may, thus, exert a persistent gene-mediated control over Ca conductances in the brain, affecting the excitability of neurons.

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Section: Methodsmentioning

confidence: 99%

Corticosteroid receptor-dependent modulation of calcium currents in rat hippocampal CA1 neurons

1994

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“…Experiments were performed in male Wistar rats (120-170 g), ADX 5-7 days before the experiments as described elsewhere (10,11). The animals were housed in an animal room with alternating light/dark [(0800-2000 hr)/(2000-0800 hr)] cycle and received food and saline (after ADX) ad libitum.…”

Section: Methodsmentioning

confidence: 99%

Mineralocorticoid receptor-mediated changes in membrane properties of rat CA1 pyramidal neurons in vitro.

Joëls

Kloet

1990

Proc. Natl. Acad. Sci. U.S.A.

153

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Pyramidal neurons in the rat hippocampus contain mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) to which the adrenal steroid corticosterone binds with differential affinity. We have used intracellular recording techniques to examine MR-mediated effects on membrane properties of CA1 pyramidal neurons in hippocampal slices from adrenalectomized rats. Low doses of corticosterone (1 nM) applied by perfusion for 20 min decreased the spike accommodation observed during a depolarizing current pulse (0.5 nA for 500 ms) and the amplitude of the subsequent afterhyperpolarization without affecting other membrane properties tested. The decrease became apparent ca. 15 min after steroid perfusion was started and reached its peak value 10-20 min after the steroid perfusion was terminated. The steroid effect was blocked by the MR antagonist spironolactone and mimicked by the natural MR ligand aldosterone (1 nM). Neurons recorded 30-90 min after termination of aldosterone application still displayed a decreased spike accommodation. However, 30-90 min after corticosterone application, the decrease in spike accommodation/afterhyperpolarization appeared to be reversed. Higher doses ofcorticosterone (.30 nM) induced a significant increase in accommodation and amplitude of the afterhyperpolarization, as was previously observed for selective GR ligands. The data indicate that MR and GR activations induce opposite actions on the spike accommodation/afterhyperpolarization of CA1 pyramidal neurons, an important intrinsic mechanism of these neurons to regulate their response to excitatory input. We suggest that occupation of both MR and GR by the endogenous ligand corticosterone will result in an initial MR-mediated enhanced cellular excitability, which is gradually reversed and overridden by a GR-mediated suppression of cellular activity.The endogenous adrenal corticosteroid of the rat, corticosterone, can cross the blood-brain barrier, bind to intracellular receptors in the brain, and, as a steroid-receptor complex, affect the expression of the genome (1, 2). Two types of corticosteroid receptors have been distinguished on the basis of molecular structure (3), binding properties, neuroanatomical topography, and physiological function (4-6): (i) the mineralocorticoid receptor (MR), which is thought to be involved in the control of basal activity throughout the circadian cycle, and (ii) the glucocorticoid receptor (GR), which participates in the feedback control of the stress response. Corticosterone binds to both receptors, displaying a 10-fold higher affinity for the MR than the GR (4).The CAl pyramidal neurons in rat hippocampus contain intracellular . In a recent electrophysiological study on slices from adrenalectomized (ADX) rats, we showed that activation of the GR in CAl neurons increases the amplitude and half-decay time of the afterhyperpolarization (AHP) that follows a brief depolarization (10).Other membrane properties that were tested remained unaffected by the glucocorticoids. The slow onset ...

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“…Uni versity of Nijmegen. The Netherlands) as described previously [23]. The detection limit of the assay is 0.1 pg/dl.…”

Section: Determination O F Corticosteronementioning

confidence: 99%

Corticosterone Modulates Interleukin-Evoked Fever in the Rat

Schöbitz¹,

Holsboer²,

Sutano³

et al. 1994

Neuroendocrinology

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The role of endogenous corticoids in fever responses caused by recombinant murine interleukin (IL)-1β and IL-6 was studied in adult male Wistar rats. Adrenalectomy diminished the development of fever after intracerebroven-tricular (icv) injection of these ILs and lowered body temperature. Intraperitoneal administration of the same doses of ILs did not produce fever in intact animals or hypothermia in adrenalectomized rats, thus suggesting a central site of action of IL-1β and IL-6 in these experiments. Chronic replacement with moderate doses of corticosterone restored the fever response in adrenalectomized animals in response to icv administration of IL-1β but only partially reversed the fever caused by IL-6. Adrenalectomized animals acutely treated with corticosterone and thereafter with either IL-1β or IL-6 developed fever more rapidly than did chronically corticosterone-treated animals. In intact animals corticosterone blocked the fever response to icv injected IL-1β. We propose that in the rat corticosterone acts in a bimodal manner on body temperature; it exerts a permissive central effect on the fever response and limits the production of inflammatory mediators in the brain. Conversely, higher corticosterone doses probably reduce the magnitude of the fever response.

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Long-Lasting Glucocorticoid Suppression of Opioid-Induced Antinociception

Cited by 50 publications

References 24 publications

Corticosteroid receptor-dependent modulation of calcium currents in rat hippocampal CA1 neurons

Corticosteroid receptor-dependent modulation of calcium currents in rat hippocampal CA1 neurons

Mineralocorticoid receptor-mediated changes in membrane properties of rat CA1 pyramidal neurons in vitro.

Corticosterone Modulates Interleukin-Evoked Fever in the Rat

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