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Corticosteroid‐mediated modulation of carbachol responsiveness in CA1 pyramidal neurons: A voltage clamp analysis

HESEN, W. & JOELS, M., Aug-1995, In : Synapse. 20, 4, p. 299-304 6 p.

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  • Corticosteroid‐mediated modulation of carbachol responsiveness in CA1 pyramidal neurons: A voltage clamp analysis

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DOI

Pyramidal neurons in the rat hippocampal CA1 area contain mineralocorticoid (MRs) and glucocorticoid (GRs) receptors for corticosterone. Previous current clamp experiments showed that depolarizations evoked by carbachol (1-3 mu M) depend on relative MR/GR occupation: carbachol responses are small with predominant MR-activation and larger when both receptor types are occupied. Multiple K-conductances underlie the carbachol-induced depolarization. In the present study we used the single electrode voltage clamp technique to examine which K-conductances modulated by carbachol are sensitive to corticosteroid treatment in vitro. We observed that 1 mu M carbachol significantly reduced the I-K,I-Leak while the I-M was hardly affected; carbachol effects on the I-K,I-Leak were significantly reduced under conditions of predominant MR activation compared to simultaneous activation of MRs and GRs. With a higher (10 mu M) carbachol dose, steroid modulation of the I-K,I-Leak showed a similar tendency. The amplitude of the I-M was largely reduced by 10 mu M carbachol but appeared to be not affected by steroid treatment. We conclude that the previously described suppression of the carbachol-induced depolarization with predominant activation MRs is caused by an attenuation of the carbachol action on the I-K,I-Leak. (C) 1995 Wiley-Liss, Inc.

Original languageEnglish
Pages (from-to)299-304
Number of pages6
JournalSynapse
Volume20
Issue number4
Publication statusPublished - Aug-1995
Externally publishedYes

    Keywords

  • ADRENALECTOMY, MINERALOCORTICOID RECEPTOR, GLUCOCORTICOID RECEPTOR, MUSCARINIC RECEPTORS, SINGLE ELECTRODE VOLTAGE CLAMP, HIPPOCAMPUS, HIPPOCAMPAL-NEURONS, RAT-BRAIN, HORMONES, MECHANISMS, OCCUPATION, RECEPTORS, SYSTEMS, INVITRO

ID: 66162626