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Hydrocortisone and 11-desoxycortisone modify acetylcholine receptor channel gating
1Instituto de Investigaciones Bioquímicas, CONICET, Bahía Blanca, Argentina.
Neuroreport
|February 1, 1993
Summary
Hydrocortisone (HC) affects the nicotinic acetylcholine receptor (AchR) by altering channel gating kinetics, reducing open time and burst duration. These findings suggest corticoids interact with the AchR or surrounding lipid environment.
Area of Science:
- Neuroscience
- Pharmacology
- Biophysics
Background:
- Nicotinic acetylcholine receptors (AchR) are crucial ion channels involved in neurotransmission.
- Corticosteroids, like hydrocortisone (HC), are known to modulate various cellular functions.
Purpose of the Study:
- To investigate the acute effects of hydrocortisone (HC) on the functional properties of the nicotinic acetylcholine receptor (AchR).
- To explore the mechanism of corticoid action on AchR channel gating.
Main Methods:
- Electrophysiological recordings of single-channel currents from AchRs.
- Application of hydrocortisone (HC) and 11-desoxycortisone to membrane patches.
- Dose-response analysis and assessment of concentration dependence from different membrane faces.
Main Results:
- Hydrocortisone (HC) induced a dose-dependent decrease in AchR channel open time and burst duration.
- HC increased the channel closed time without affecting channel amplitude.
- Similar effects were observed with 11-desoxycortisone, and HC's action showed membrane sidedness.
Conclusions:
- Corticoids like hydrocortisone (HC) acutely modulate AchR channel gating kinetics.
- The mechanism involves interaction with the AchR or its associated lipid environment, potentially at the lipid-protein interface.
- The oxygen at position 11 is not essential for this channel modification.