ABSTRACT
Psychophysiological insomnia is characterized by acquired sleep difficulties and/or a state of hypervigilance when going to bed. This mental and physiological condition prevents sleep onset regardless of the presence of anxious or depressive disorders. Despite the fact that cognitive behavioural therapies have been shown to be effective for this disorder, some people are not responding to this treatment. It is therefore important to explore new ways of increasing the effectiveness of current treatments. Approaches based on mindfulness, which promote a non-judgemental acceptance of the living experience, are increasingly reported in the literature to be effective in the treatment of various physical and psychological health conditions, being particularly efficient in reducing the stress and discomfort associated with these problems. This article focuses on some cognitive factors associated with maintaining insomnia and suggests that approaches based on mindfulness, through certain action mechanisms, may help to improve sleep. A review of recent studies on the application of mindfulness-based approaches to treat insomnia is hereby presented. Avenues for future research to improve insomnia treatment protocols based on mindfulness are suggested.
Subject(s)
Mindfulness , Psychophysiologic Disorders/therapy , Sleep Initiation and Maintenance Disorders/therapy , Attention , Attitude to Health , Cognitive Behavioral Therapy/methods , Conditioning, Classical , Depression/physiopathology , Depression/therapy , Dyssomnias/psychology , Dyssomnias/therapy , Humans , Judgment , Psychological Distance , Psychophysiologic Disorders/psychology , Sleep Initiation and Maintenance Disorders/psychologyABSTRACT
Xenopus retinal ganglion cell growth cones express various voltage-gated potassium (Kv) channels. We showed previously that 4-aminopyridine and tetraethylammonium have different effects on the outward currents of embryonic Xenopus retinal ganglion cells. Therefore, we asked whether these Kv channel inhibitors differentially regulate the response of retinal ganglion cell growth cones to extrinsic cues. First, we tested the role of Kv channels in axon extension mediated by a substrate bound cue and found that 4-aminopyridine blocked, whereas tetraethylammonium enhanced basal extension on laminin. Yet, when the growth cones were stimulated to extend with application of soluble growth factors, both inhibitors resulted in a return to the basal extension rates observed in the presence of laminin alone. Second, we asked if Kv channels modulate the response of retinal ganglion cell growth cones to a guidance cue, the chemorepellent fibroblast growth factor-2. When presented in a gradient to one side of the growth cone, fibroblast growth factor-2 repulsed retinal ganglion cell growth cones in the presence of 4-aminopyridine but not tetraethylammonium. These data argue that tetraethylammonium- and 4-aminopyridine-sensitive Kv channels differ in the manner by which they regulate the response of retinal ganglion cell axons to extension and guidance cues. Non-ratiometric calcium imaging indicated that differences in the ability of tetraethylammonium- and 4-aminopyridine-sensitive Kv channels to regulate calcium activity within the growth cone may underlie their unique modulation of growth cone behaviour.