Neuroscience
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Brain-derived neurotrophic factor, BDNF, is one of the most important neurotrophic factors acting in the peripheral and central nervous system. In the auditory system its function was initially defined by using constitutive knockout mouse mutants and shown to be essential for survival of neurons and afferent innervation of hair cells in the peripheral auditory system. Further examination of BDNF null mutants also revealed a more complex requirement during re-innervation processes involving the efferent system of the cochlea. ⋯ Additionally, BDNF is required for maintenance of voltage-gated potassium channels (KV) in cochlear neurons, which may form part of a maturation step within the ascending auditory pathway with onset of hearing and might be essential for cortical acuity of sound-processing and experience-dependent plasticity. A presumptive harmful role of BDNF during acoustic trauma and consequences of a loss of cochlear BDNF during aging are discussed in the context of a partial reversion of this maturation step. We compare the potentially beneficial and harmful roles of BDNF for the mature auditory system with those BDNF functions known in other sensory circuits, such as the vestibular, visual, olfactory, or somatosensory system.
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Nogo-A interaction with its different receptors (Nogo receptor 1 (NgR1), S1P receptor 2 (S1PR2), paired immunoglobulin-like receptor B (PirB)) restricts plasticity and growth-dependent processes leading, via the activation of different signaling pathway to the stabilization of the neuronal networks (either developmentally or during processes of memory consolation in the mature nervous system). Taking away these molecular brakes might allow for the induction of extensive structural and functional rearrangements and might promote compensatory growth processes after an injury of the CNS, in cortical structures as well as in the spinal cord. However, it is important to keep in mind that this could as well be a dangerous endeavor, since it might facilitate unwanted and unnecessary (and probably even maladaptive) neuronal connections.
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Stress is an adaptive response to demands of the environment and thus essential for survival. Exposure to stress triggers hypothalamic-pituitary-adrenocortical (HPA) axis activation and associated neurochemical reactions, following glucocorticoid release from the adrenal glands, accompanied by rapid physiological responses. Stimulation of this pathway results in the activation of specific brain regions, including the hippocampus, amygdala and prefrontal cortex which are enriched with glucocorticoid receptors (GRs). ⋯ Whereas an optimal stress level leads to enhancement of memory performance, the exposure to extreme, traumatic or chronic stressors is a risk factor for psychopathologies which are associated with memory impairment and cognitive deficits such as posttraumatic stress disorder (PTSD). In this review article, we will outline the implications of stress exposure on memory formation involving the role of glucocorticoids and BDNF. Within this context, potential adverse effects of neuroplastic alterations will be discussed using the example of PTSD.
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Brain injuries such as focal stroke initiate a myriad of neural events leading to local and remote alterations in cerebral networks. The neurochemical and neurophysiological mechanisms underlying these postlesion changes raise the question of their beneficial or adverse effects on functional recovery. In this review, we aim to reconcile findings from animal and patients studies using a "from cellular-to network-levels" perspective to gain further insights into the neuroplasticity mechanisms underlying recovery of sensorimotor functions. Ultimately, an integrative view of the multiple facets of poststroke changes should give an impetus to novel neurorehabilitation strategies by providing evidence of how neuroscience findings can be translated and operationalized within the context of restorative stroke.
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One of the most striking demonstrations of experience-dependent plasticity comes from studies of sensory-deprived individuals (e.g., blind or deaf), showing that brain regions deprived of their natural inputs change their sensory tuning to support the processing of inputs coming from the spared senses. These mechanisms of crossmodal plasticity have been traditionally conceptualized as having a double-edged sword effect on behavior. On one side, crossmodal plasticity is conceived as adaptive for the development of enhanced behavioral skills in the remaining senses of early-deaf or blind individuals. ⋯ In the present review we stress that this dichotomic vision is oversimplified and we emphasize that the notions of the unavoidable adaptive/maladaptive effects of crossmodal reorganization for sensory compensation/restoration may actually be misleading. For this purpose we critically review the findings from the blind and deaf literatures, highlighting the complementary nature of these two fields of research. The integrated framework we propose here has the potential to impact on the way rehabilitation programs for sensory recovery are carried out, with the promising prospect of eventually improving their final outcomes.