“Serotonin modulates neuroplasticity, especially during early life, and dysfunctions in both systems likewise contribute to pathophysiology of depression. recent findings demonstrate that serotonin reuptake inhibitors trigger reactivation of juvenile-like neuroplasticity. how these findings translate to clinical antidepressant treatment in major depressive disorder remains unclear. with this review, we link preclinical with clinical work on serotonin and neuroplasticity to bring two pathophysiologic models in clinical depression closer together. dysfunctional developmental plasticity impacts on later-life cognitive and emotional functions, changes of synaptic serotonin levels and receptor levels are coupled with altered synaptic plasticity and neurogenesis. structural magnetic resonance imaging in patients reveals disease-state-specific reductions of gray matter, a marker of neuroplasticity, and reversibility upon selective serotonin reuptake inhibitor treatment. translational evidence from magnetic resonance imaging in animals support that reduced densities and sizes of neurons and reduced hippocampal volumes in depressive patients could be attributable to changes of serotonergic neuroplasticity. since ketamine, physical exercise or learning enhance neuroplasticity, combinatory paradigms with selective serotonin reuptake inhibitors could enhance clinical treatment of depression.”

“Many studies have revealed the structural or functional brain changes induced by occupational factors. however, it remains largely unknown how occupation-related connectivity shapes the brain. in this paper, we denote occupational neuroplasticity as the neuroplasticity that takes place to satisfy the occupational requirements by extensively professional training and to accommodate the long-term, professional work of daily life, and a critical review of occupational neuroplasticity related to the changes in brain structure and functional networks has been primarily presented. furthermore, meta-analysis revealed a neurophysiological mechanism of occupational neuroplasticity caused by professional experience. this meta-analysis of functional neuroimaging studies showed that experts displayed stronger activation in the left precentral gyrus [brodmann area (ba)6], left middle frontal gyrus (ba6), and right inferior frontal gyrus (ba9) than novices, while meta-analysis of structural studies suggested that experts had a greater gray matter volume in the bilateral superior temporal gyrus (ba22) and right putamen than novices. together, these findings not only expand the current understanding of the common neurophysiological basis of occupational neuroplasticity across different occupations and highlight some possible targets for neural modulation of occupational neuroplasticity but also provide a new perspective for occupational science research.”

“Clinical studies suggest the therapeutic potential of psychedelics, including ayahuasca, dmt, psilocybin, and lsd, in stress-related disorders. these substances induce cognitive, antidepressant, anxiolytic, and antiaddictive effects suggested to arise from biological changes similar to conventional antidepressants or the rapid-acting substance ketamine. the proposed route is by inducing brain neuroplasticity. this review attempts to summarize the evidence that psychedelics induce neuroplasticity by focusing on psychedelics’ cellular and molecular neuroplasticity effects after single and repeated administration. when behavioral parameters are encountered in the selected studies, the biological pathways will be linked to the behavioral effects. additionally, knowledge gaps in the underlying biology of clinical outcomes of psychedelics are highlighted. the literature searched yielded 344 results. title and abstract screening reduced the sample to 35; eight were included from other sources, and full-text screening resulted in the final selection of 16 preclinical and four clinical studies. studies ( n = 20) show that a single administration of a psychedelic produces rapid changes in plasticity mechanisms on a molecular, neuronal, synaptic, and dendritic level. the expression of plasticity-related genes and proteins, including brain-derived neurotrophic factor (bdnf), is changed after a single administration of psychedelics, resulting in changed neuroplasticity. the latter included more dendritic complexity, which outlasted the acute effects of the psychedelic. repeated administration of a psychedelic directly stimulated neurogenesis and increased bdnf mrna levels up to a month after treatment. findings from the current review demonstrate that psychedelics induce molecular and cellular adaptations related to neuroplasticity and suggest those run parallel to the clinical effects of psychedelics, potentially underlying them. future (pre)clinical research might focus on deciphering the specific cellular mechanism activated by different psychedelics and related to long-term clinical and biological effects to increase our understanding of the therapeutic potential of these compounds.”

“Neuroplasticity can be defined as the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections. major advances in the understanding of neuroplasticity have to date yielded few established interventions. to advance the translation of neuroplasticity research towards clinical applications, the national institutes of health blueprint for neuroscience research sponsored a workshop in 2009. basic and clinical researchers in disciplines from central nervous system injury/stroke, mental/addictive disorders, paediatric/developmental disorders and neurodegeneration/ageing identified cardinal examples of neuroplasticity, underlying mechanisms, therapeutic implications and common denominators. promising therapies that may enhance training-induced cognitive and motor learning, such as brain stimulation and neuropharmacological interventions, were identified, along with questions of how best to use this body of information to reduce human disability. improved understanding of adaptive mechanisms at every level, from molecules to synapses, to networks, to behaviour, can be gained from iterative collaborations between basic and clinical researchers. lessons can be gleaned from studying fields related to plasticity, such as development, critical periods, learning and response to disease. improved means of assessing neuroplasticity in humans, including biomarkers for predicting and monitoring treatment response, are needed. neuroplasticity occurs with many variations, in many forms, and in many contexts. however, common themes in plasticity that emerge across diverse central nervous system conditions include experience dependence, time sensitivity and the importance of motivation and attention. integration of information across disciplines should enhance opportunities for the translation of neuroplasticity and circuit retraining research into effective clinical therapies. © 2011 the author.”