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.
Although complex in nature, the pathophysiology of depression involves reduced or impaired neuroplastic capabilities. Restoring or enhancing neuroplasticity may serve as a treatment target for ...developing therapies for depression. Aerobic exercise (AEx) has antidepressant benefits and may enhance neuroplasticity in depression although the latter has yet to be substantiated. Therefore, we sought to examine the acute effect of AEx on neuroplasticity in depression.
Sixteen individuals with (DEP; 13 female; age = 28.5 ± 7.3; Montgomery-Äsberg Depression Rating Scale MADRS = 21.3 ± 5.2) and without depression (HC; 13 female; age 27.2 ± 7.5; MADRS = 0.8 ± 1.2) completed three experimental visits consisting of 15 min of low intensity AEx (LO) at 35% heart rate reserve (HRR), high intensity AEx (HI) at 70% HRR, or sitting (CON). Following AEx, excitatory paired associative stimulation (PAS25ms) was employed to probe neuroplasticity. Motor evoked potentials (MEP) were assessed via transcranial magnetic stimulation before and after PAS25ms to indicate acute changes in neuroplasticity.
PAS25ms primed with HI AEx led to significant increases in MEP amplitude compared to LO and CON. HI AEx elicited enhanced PAS25ms-induced neuroplasticity for up to 1-h post-PAS. There were no significant between-group differences.
HI AEx enhances PAS measured neuroplasticity in individuals with and without depression. HI AEx may have a potent influence on the brain and serve as an effective primer, or adjunct, to therapies that seek to harness neuroplasticity.
•Fifteen minutes of high intensity aerobic exercise enhanced neuroplasticity.•A window of enhanced neuroplasticity may persist for at least 1-h post-exercise.•Exercise-enhanced neuroplasticity was not inhibited by depression.•Aerobic exercise may be used to prime the brain for other therapeutic strategies.
This study aims to investigate the structural reorganization in the sensorimotor area of the brain in patients with gliomas, distinguishing between those with impaired and unimpaired strength. Using ...voxel‐based morphometry (VBM) and region of interest (ROI) analysis, gray matter volumes (GMV) were compared in the contralesional primary motor gyrus, primary sensory gyrus, premotor area, bilateral supplementary motor area, and medial Brodmann area 8 (BA8). The results revealed that in patients with right hemisphere gliomas, the right medial BA8 volume was significantly larger in the impaired group than in the unimpaired group, with both groups exceeding the volume in 16 healthy controls (HCs). In patients with left hemisphere gliomas, the right supplementary motor area (SMA) was more pronounced in the impaired group compared to the unimpaired group, and both groups were greater than HCs. Additionally, the volumes of the right medial BA8 in both the impaired group were greater than HCs. Contralateral expansions in the gray matter of hand‐ and trunk‐related cortices of the premotor area, precentral gyrus, and postcentral gyrus were observed compared to HCs. Furthermore, a negative correlation was found between hand Medical Research Council (MRC) score and volumes of the contralateral SMA and bilateral medial BA8. Notably, our findings reveal consistent results across both analytical approaches in identifying significant structural reorganizations within the sensorimotor cortex. These consistent findings underscore the adaptive neuroplastic responses to glioma presence, highlighting potential areas of interest for further neurosurgical planning and rehabilitation strategies.
Exploring neuroplasticity in sensorimotor gliomas: This study reveals how gliomas affect brain eloquent areas, highlighting increased cortical volume in specific regions as a compensatory response to maintain motor function. By comparing 59 patients with sensorimotor gliomas, we demonstrate significant cortical changes correlating with motor strength, emphasizing the dynamic brain's adaptability in the face of motor impairment.
Cannabidiol (CBD) is a phytocannabinoid devoid of psychostimulant properties and is currently under investigation as a potential antidepressant drug. However, the mechanisms underlying CBD's ...antidepressant effects are not yet well understood. CBD targets include a variety of receptors, enzymes, and transporters, with different binding-affinities. Neurochemical and pharmacological evidence indicates that both serotonin and BDNF-TrkB signalling in the prefrontal cortex are necessary for the antidepressant effects induced by CBD in animal models. Herein, we reviewed the current literature to dissect if these are independent mechanisms or if CBD-induced modulation of the serotonergic neurotransmission could mediate its neuroplastic effects through subsequent regulation of BDNF-TrkB signalling, thus culminating in rapid neuroplastic changes. It is hypothesized that: a) CBD interaction with serotonin receptors on neurons of the dorsal raphe nuclei and the resulting disinhibition of serotonergic neurons would promote rapid serotonin release in the PFC and hence its neuroplastic and antidepressant effects; b) CBD facilitates BDNF-TRKB signalling, especially in the PFC, which rapidly triggers neurochemical and neuroplastic effects. These hypotheses are discussed with perspectives for new drug development and clinical applications.
Depression is a neuropsychiatric disorder characterized by persistent pleasure loss and behavioral despair. However, the potential mechanisms and therapeutic targets for depression treatment remain ...unclear. Therefore, identifying the underlying pathogenesis of depression would promote the development of novel treatment and provide effective targets for antidepressant drugs. In this study, proteomics analysis showed that the expression level of phosphatase and actin regulator 4 (Phactr4) was significantly increased in the CA1 hippocampus of depressed rats. The upregulated Phactr4 might induce dysfunction of the synaptic structure via suppressing the p-LIMK/p-Cofilin signaling pathway, and promote neuroinflammation via activating the NF-κB/NLRP3 pathway, which ultimately contributes to the pathogenesis of depression. In contrast, the downregulation of Phactr4 in hippocampal CA1 of depressed rats alleviated depression-like behaviors, along with reducing neuroinflammation and improving synaptic plasticity. In conclusion, these findings provide evidence that Phactr4 plays an important role in regulating neuroinflammatory response and impairment of synaptic plasticity, effects seem to involve in the pathogenesis of depression, and Phactr4 may serve as a potential target for antidepressant treatment.
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•CUMS exposure induced depression-like behaviors accompanied with the dysregulation of synaptic plasticity in hippocampal CA1.•CUMS exposure caused neuroinflammation in hippocampal CA1pyramidal neurons.•CUMS exposure caused increased level of Phactr4 in hippocampal CA1 region.•Knockdown Phactr4 alleviated depressive behaviors, reduced neuroinflammation and improved the synaptic injury.
Tinnitus is a symptom with a significant incidence in the general population, usually of unclear etiology, that can cause serious difficulties in people's daily functioning, significantly impair the ...quality of life, and have a negative impact on mental health. The paper aims to present a brief overview of current knowledge about this frequent and unpleasant phenomenon, including epidemiology, etiology, clinical presentation, diagnosis, and treatment. The paper highlights contemporary theories of tinnitus that link damage to the peripheral organ of hearing and the consequent neuronal changes involved in the subjective experience, which are the target sites for treating psychological disorders associated with tinnitus. The psychiatric approach to tinnitus is aimed not so much at reducing the sound intensity as at reducing the negative experience of this phenomenon and preventing the development or worsening of existing psychological disorders. The results of previous researches indicate numerous therapeutic options for treating tinnitus, including drugs, cognitive-behavioral therapy, and neuromodulation techniques with promising results.
Tinitus je simptom sa značajnom pojavnošću u općoj populaciji, najčešće nejasne etiologije, koji može izazvati ozbiljne poteškoće u svakodnevnom funkcioniranju, značajno narušiti kvalitetu života i dovesti do negativnog utjecaja na psihičko zdravlje. Cilj rada je prikazati kratki pregled dosadašnjih spoznaja o ovome, često neugodnom fenomenu, uključujući epidemiologiju, etiologiju, kliničku sliku, dijagnostiku i liječenje. U radu su istaknute suvremene teorije tinitusa koje povezuju oštećenje perifernog organa sluha i posljedične neuronske promjene uključene u subjektivni doživljaj, koje su ciljno mjesto liječenja psihičkih smetnji udruženih s tinitusom. Psihijatrijski pristup tinitusu usmjeren je, ne toliko na smanjenje zvučnog intenziteta, koliko na smanjenje negativnog doživljaja ovoga fenomena i sprječavanje razvoja ili pogoršanja postojećih psihičkih poremećaja. Rezultati dosadašnjih istraživanja ukazuju na brojne terapijske mogućnosti liječenja tinitusa, uključujući lijekove, kognitivno-bihevioralnu terapiju, te neuromodulacijske tehnike s obećavajućim rezultatima.
Neuroplasticity is defined as the property of the brain to adapt to environmental pressures, experiences, and challenges including brain damage. It is a lifelong capacity of the brain to change and ...rewire itself in response to the stimulation of learning and experience. Based upon this input, several conclusions were recently appearing on the surface. First, there appears to be tremendous latent plasticity even in the adult brain. Second, the brain should be thought of, not as a hierarchy of organized autonomous modules, each of which delivers its output to the next level, but as a set of complex interacting networks that are in a state of dynamic equilibrium with the brain’s environment. Both principles can be potentially exploited in a clinical context to facilitate recovery of function. Promoting neuroplasticity in an enriched environment will eventually result in dendritic branching, synapses, glial processes, brain weight, and cortical thickness. Currently, it is believed that activity drives reorganization of cerebral networks, which is paralleled by functional improvements in cases of acquired brain injuries that are usually in need of intense rehabilitation programs. Numeral studies have demonstrated reorganization of brain activity pattern in response to intense training of motor and cognitive tasks and imagination of movements. For instance, promising results were shown using feedback techniques, like mirror visual feedback (MVF) improving chronic regional pain syndrome and hemiparesis following stroke. Evidence based therapeutic interventions using neuroplasticity as its base include aerobic exercise, bilateral arm training, constraint induced movement therapy,body weight supported treadmill training, mirror therapy, action observation, motor imagery/mental practice, functional electrical stimulation and music therapy.Promising therapies that may enhance training-induced cognitive and motor learning, such as brain stimulation and neuropharmacological interventions, were also identified, along with arousing questions involving more updated ways to use neuroplasticity in improving quality of life in cases of human disability.
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