Abstract
Recent evidence highlighted the importance of white matter tracts in typical and atypical behaviors. White matter dynamically changes in response to learning, stress, and social experiences. Several lines of evidence have reported white matter dysfunction in psychiatric conditions, including depression, stress- and anxiety-related disorders. The mechanistic underpinnings of these associations, however, remain poorly understood. Here, we outline an integrative perspective positing a link between aberrant myelin plasticity and anxiety. Drawing on extant literature and emerging new findings, we suggest that in anxiety, unique changes may occur in response to threat and to safety learning and the ability to discriminate between both types of stimuli. We propose that altered myelin plasticity in the neural circuits underlying these two forms of learning relates to the emergence of anxiety-related disorders, by compromising mechanisms of neural network synchronization. The clinical and translational implications of this model for anxiety-related disorders are discussed.
Highlights
Myelination in vertebrates, represents a successful mechanism of adaptation to the development of complex behaviors, requiring increased speed of axonal conduction
We propose that altered myelin plasticity in the neural circuits underlying these two forms of learning relates to the emergence of anxiety-related disorders, by compromising mechanisms of neural network synchronization
While in some invertebrates fast transmission is achieved by decreasing resistance due to axonal expansion, in craniates and jawed fish the insulation provided by myelin allows axons of similar caliber to increase their speed of communication by several hundred folds (Tomassy et al, 2016)
Summary
Myelination in vertebrates, represents a successful mechanism of adaptation to the development of complex behaviors, requiring increased speed of axonal conduction. The importance of myelin plasticity in response to external conditions and shaping behavioral consequences led to the concept that myelination of white matter tracts regulating learning about threat may be altered in pathologies characterized by behavioral maladaptation and are associated with changes in brain function. Temporal precision is necessary for interregional communication, when BLA gamma oscillations are coupled to PFC theta oscillations during a successfully discriminated non-threat (Stujenske et al, 2014), suggesting that prefrontal input has a direct or indirect role in driving gamma activity in the BLA (Rosenkranz and Grace, 2001; Amano et al, 2010; Bukalo et al, 2015; Strobel et al, 2015; Bloodgood et al, 2018) This faster oscillatory mode of crossregional communication is shaped by excitatory-inhibitory interactions that require millisecond range timing of inhibitory activity (Buzsáki and Wang, 2012; Courtin et al, 2014). We further predict that specific alterations of these mechanisms may be related to the development of anxiety disorders
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