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Classically steroid hormones acts through genomic mechanism. In the last period there is more evidence that some steroid hormones exert fast (in order of seconds) effects on membrane receptors. In the presented work we analysed the effects of some steroid hormones on muscle acetylcholine receptor (AChR) channel kinetics. We divided steroid hormone on two groups which exert different effects. The first group including hydrocortisone (HC), corticosterone (COR), dexamethasone decrease the mean open time increasing the number of openings in bursts. The effects do not depend on agonist concentration. Some effects of HC and COR are voltage-dependent. The mechanism of such voltage dependent action caused by steroids hormones that are uncharged molecules, is unknown. Some experiments suggest however that an agonist molecule is involved in the mechanism of steroid action. The second group consists of progesterone, some of its derivatives and deoxycorticosterone. For this group the most evident effect was decrease in the probability of openings without a decrease in the mean open time. The effect depends on agonist concentration, suggesting an involvement of an agonist molecule in the mechanism. For this hormones an involvement of an charged agonist molecule does not however induce a voltage dependency. Most probably two groups of steroids acts on different part of the AChR. The localization of a steroid action site can be crucial for inducing voltage dependency.

Disturbances in the serotonin (5-HT) system and the limbic-hypothalamo-pituitary-adrenal axis (LHPA) have been implicated in the pathophysiology of depression. It is well established that hippocampus is a central component of limbic circuitry that participates in the modulation of cognition, mood and behavior, and is involved in the control of the LHPA axis. Therefore, the hippocampus provides a unique environment to study the interplay between serotonergic system, antidepressants and corticosteroids. Activity of hippocampal cells can be modulated by 5-HT via inhibitory 5-HT1A and excitatory 5-HT4 receptors. Repeated treatment with antidepressants increases the responsiveness of hippocampal pyramidal neurons to the 5-HT1A and attenuates the responsiveness to the 5-HT4 receptor agonists, with a time course which correlates with the delayed onset of the therapeutic effect of antidepressants in humans. Moreover, repeated corticosterone, which may constitute a model of a prolonged nonadaptable stress, has opposite effect on hippocampal responsiveness to the 5-HT1A and 5-HT4 receptor activation. Such an action results in an enhancement of the 5-HT-mediated inhibition by antidepressants and a reduction in the inhibitory effect of 5-HT by corticosterone which may be relevant to antidepressant/antiaxiety and proaxiety effects, respectively, of both treatments.