Modulation of carbachol responsiveness in rat CA1 pyramidal neurons by corticosteroid hormones

Hesen, W.S.; Joëls, Marian

doi:10.1016/0006-8993(93)90760-k

Cited by 46 publications

(40 citation statements)

References 42 publications

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“…The latter response too displayed a similar U-shaped steroid dose-dependency as found earlier with respect to the Ca 2+ currents and the 5-HT 1A receptor mediated responses (54). Thus, small depolarizing responses to carbachol, a muscarinic agonist, were observed with predominant activation of MRs. Additional activation of GRs in vitro led to much larger responses.…”

Section: Corticosteroid Effects On G-protein Coupled Receptorssupporting

confidence: 78%

Corticosteroid Actions in the Hippocampus

Joëls

2001

J Neuroendocrinology

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Corticosteroid hormones can enter the brain and bind to two intracellular receptor types that regulate transcription of responsive genes: (i) the high af®nity mineralocorticoid receptors and (ii) the glucocorticoid receptors with approximately 10-fold lower af®nity. Although most cells in the brain predominantly express glucocorticoid receptors, principal cells in limbic structures such as the hippocampus often contain glucocorticoid as well as mineralocorticoid receptors. Recent electrophysiological studies have examined the consequences of transcriptional regulation via the two receptor types for information transfer in the hippocampus. It was found that, under resting conditions, corticosteroids do not markedly alter electrical activity. However, if neurones are shifted towards more depolarized or hyperpolarized potentials due to the action of neurotransmitters, slow and adaptive effects of the corticosteroid hormones become apparent. In general, mineralocorticoid receptor occupation maintains steady electrical activity in hippocampal neurones. Brief activation of glucocorticoid receptors leads to increased in¯ux of calcium, which normally helps to slowly reverse temporarily raised electrical activity. These slow and persistent corticosteroid actions will alter network function within the hippocampus, thus contributing to behavioural adaptation in response to stress. Modulation of hippocampal activity by corticosteroids also affects hippocampal output (e.g. to inhibitory interneurones which control hypothalamic-pituitary-adrenal axis activity). The enhanced calcium in¯ux after glucocorticoid receptor activation can become a risk factor when cells are simultaneously exposed to strong depolarizing inputs, such as those occuring during ischaemia. Similarly, chronically elevated corticosteroid levels (or lack of corticosteroids) could endanger hippocampal cell function. The latter may contribute to the precipitation of clinical symptoms in diseases associated with chronically aberrant corticosteroid levels.

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Section: Corticosteroid Effects On G-protein Coupled Receptorssupporting

confidence: 78%

Corticosteroid Actions in the Hippocampus

Joëls

2001

J Neuroendocrinology

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181

111

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“…Thus glucocorticoid receptors (GRs) have a much higher a¦nity for dexamethasone than corticosterone (in rats), while for mineralocorticoid receptors (MRs) these relative a¦nities are reversed (Caamano et al 1994). There is considerable evidence that 5-HT 1A function may be regulated di¤erentially by these receptors (Meijer and de Kloet 1995;Hesen and Joels 1996).…”

Section: Discussionmentioning

confidence: 98%

5-Hydroxytryptamine receptor function in humans is reduced by acute administration of hydrocortisone

et al. 1998

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5-Hydroxytryptamine1A (5-HT1A) receptors have been shown to be suppressed by corticosteroid hormones in a variety of animal experimental paradigms. It has been suggested that this effect may be central to the pathophysiology of severe clinical depressive illness, a condition in which 5-HT1A receptor function is reduced and corticosteroid hormones are elevated. We report the effects of acute administration of hydrocortisone in normal volunteers on a neuroendocrine model of 5-HT1A receptor function. Fifteen healthy male volunteers took part in a random order, double blind, placebo controlled study, in which 100 mg hydrocortisone or placebo was administered 11 h before infusion of L-tryptophan (L-TRP). Pre-treatment with hydrocortisone significantly reduced the growth hormone (GH), but not the prolactin (PRL) response to the infusion. These data are consistent with the view that acute administration of corticosteroid hormones significantly impairs 5-HT1A receptor mediated function in healthy human volunteers and are in line with animal studies of the effects of corticosteroid hormones on 5-HT1A receptors. We propose that this finding is relevant to the pathophysiological processes which cause severe depressive illness.

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“…Activation of the 5-HT 1A receptor induces a membrane hyperpolarization or increase in outward current (Andrade and Nicoll 1987;Colino and Halliwell 1987;Beck et al 1992). In the CA1 subfield administration of concentrations of corticosterone to selectively activate only MR or administration of the MR selective steroid aldosterone for several hours (short term) results in a decrease in the magnitude of the hyperpolarization (Beck et al 1996;Hesen and Joels 1996;Joels et al 1991). Chronic treatment (weeks) with basal levels of corticosterone to selectively activate MR does not significantly alter the CA1 hippocampal pyramidal cell 5-HT 1A receptor-mediated hyperpolarization .…”

mentioning

confidence: 99%

Corticosteroids Alter the 5-HT1A Receptor-Mediated Response in CA1 Hippocampal Pyramidal Cells

Mueller

2000

Neuropsychopharmacology

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Modulation of carbachol responsiveness in rat CA1 pyramidal neurons by corticosteroid hormones

Cited by 46 publications

References 42 publications

Corticosteroid Actions in the Hippocampus

Corticosteroid Actions in the Hippocampus

5-Hydroxytryptamine receptor function in humans is reduced by acute administration of hydrocortisone

Corticosteroids Alter the 5-HT1A Receptor-Mediated Response in CA1 Hippocampal Pyramidal Cells

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