Neuroplasticity
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Primary organization of the neuronal circuits is based on the genetic program. In addition, individual elements of these circuits are able to adjust their function and structure to the changes in external and internal conditions. In a given moment, formation and rearrangement of the neuronal circuits are based on the mutual cooperation between mechanisms assuring plasticity and rigidity. Plasticity is related not only to the development of the organism or to changes in the internal or external conditions, it may also reflect the progress of some pathological states or the recovery of an injured nervous structure. Intensification of the natural neuroplastic mechanisms or the introduction of an active (or activated) neuronal tissue into the impaired circuits might improve the process of recovery in the central nervous system.
Plasticity is a specific feature of the nervous system, characterized by two basic phenomena: The first type of "functional plasticity" develops comparatively quickly, brings about mainly functional changes and is usually reversible. The second type has the features of an adaptation and affects the expression of genotype into phenotype. Neuroplastic mechanisms are triggered by various natural or artificial stimuli which may differ quantitatively (they arise in the internal or external environment) or qualitatively. Neuroplastic mechanisms are based on modulation of the signal transmission over synapses (e.g., the transmitter release, activity of postsynaptic receptors, efficiency changes in the transmission in the postsynaptic segment). They can be related to the interneuronal relations changes (e.g., number of certain types of synapses, significance of the wiring of different elements of the neuronal circuits). Resulting changes may occur in the communication between neurons (synaptic level), in the activity of the local neuronal circuits (level of local circuits) or in the relations between individual functional brain systems (multimodular level). Neuroplasticity might be based on structural changes which can be revealed by morphological methods. Such forms of plasticity are more frequent during the development, or as a reaction to injury (proliferation and decease of neurons, formation of their processes and spines, remodelling, or formation of synapses). More specific methods have determined that these changes are located on the molecular level (enzyme activity, production and release of transmitters or modulators, receptor activation, modulation of ion channels). Both levels of neuroplastic mechanisms bring about changes of functional parameters of the synaptic transmission (changes in the duration or amplitude of the membrane potentials and resulting facilitation, posttetanic potentiation or changes of opposite character). Effects of plasticity can reside either in positive or negative changes during the development (evolutional plasticity), after a short-term exposition (reactive plasticity), after long-term or permanent stimuli (adaptational plasticity), and during functional or structural recovery of the damaged neuronal circuits (reparation plasticity). Manifestations of plasticity have probably the same basis, irrespectively of the cause which has triggered them, or the brain region where they have been accomplished. (Tab. 7, Ref. 45.)
The authors propose an integrative theory of the organization of neuroplastic processes. Neuroplasticity is assumed to be one of the essential characteristics of the nervous tissue which may be manifested comparatively rapidly and result in reversible changes (functional plasticity). It may also modulate the expression of genotype into phenotype (adaptation) and thus bring about long-lasting effects. Neuroplastic mechanisms are triggered by various natural or artificial stimuli, which may arise in the internal or external environment, and they may differ quantitatively or qualitatively. The effects of plasticity can lead to either positive or negative changes during development (evolutionary plasticity), after short-term exposition (reactive plasticity), after long-term or continuous stimuli (adaptational plasticity), and during functional or structural recovery of damaged neuronal circuits (reparation plasticity). Manifestations of plasticity have probably the same basis, irrespective of the cause which triggered them or the brain region where they were accomplished. Neuroplastic mechanisms are based on the modulation of signal transmission across synapses. They can be related to interneuronal relations. The resulting changes may occur in the communication between neurons (synaptic level), in the activity of local neuronal circuits (at the level of local circuits) or in the relations between individual functional brain systems (multimodular level).
Transient receptor potential channels sensitive to vanilloids (TRPVs) are group of ion channels which are sensitive to various tissue damaging signals and their activation is generally perceived as pain. Therefore, they are generally named as nociceptors. Understanding their activation and function as well as their interaction with intracellular pathways is crucial for the development of pharmacological interference in order to reduce pain perception. The current review summarizes basic facts in regard to TRPV and discusses their relevance in the sensing of (pain-) signals and their intracellular processing, focussing on their modulation of the intracellular calcium ([Ca(2+)]i) signal. Furthermore we discuss the basic mechanisms how the modification of [Ca(2+)]i through TRPV might induce long-term-potentiation (LTP) or long-term- depression (LTD) and from "memories" of pain. Understanding of these mechanisms is needed to localize the best point of interference for pharmacological treatment. Therefore, high attention is given to highlight physiological and pathological processes and their interaction with significant modulators and their roles in neuroplasticity and pain modulation.
- Klíčová slova
- Currents, Neuroplasticity, Nociception, TRPV receptors, Therapy,
- MeSH
- kationtové kanály TRPV metabolismus fyziologie MeSH
- lidé MeSH
- mozek metabolismus fyziologie MeSH
- neurony metabolismus fyziologie MeSH
- neuroplasticita * MeSH
- nocicepce fyziologie MeSH
- signální transdukce MeSH
- vápníková signalizace MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- kationtové kanály TRPV MeSH
Perineuronal nets (PNNs) are chondroitin sulphate proteoglycan-containing structures on the neuronal surface that have been implicated in the control of neuroplasticity and memory. Age-related reduction of chondroitin 6-sulphates (C6S) leads to PNNs becoming more inhibitory. Here, we investigated whether manipulation of the chondroitin sulphate (CS) composition of the PNNs could restore neuroplasticity and alleviate memory deficits in aged mice. We first confirmed that aged mice (20-months) showed memory and plasticity deficits. They were able to retain or regain their cognitive ability when CSs were digested or PNNs were attenuated. We then explored the role of C6S in memory and neuroplasticity. Transgenic deletion of chondroitin 6-sulfotransferase (chst3) led to a reduction of permissive C6S, simulating aged brains. These animals showed very early memory loss at 11 weeks old. Importantly, restoring C6S levels in aged animals rescued the memory deficits and restored cortical long-term potentiation, suggesting a strategy to improve age-related memory impairment.
- MeSH
- chondroitinsulfáty * MeSH
- extracelulární matrix MeSH
- mozek MeSH
- myši MeSH
- neuroplasticita * MeSH
- stárnutí MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- chondroitinsulfáty * MeSH
BACKGROUND: There is numerous literature on mechanisms underlying variability of practice advantages. Literature includes both behavioral and neuroimaging studies. Unfortunately, no studies are focusing on practice in constant conditions to the best of our knowledge. Hence it is essential to assess possible differences in mechanisms of neuroplasticity between constant vs. variable practice conditions. The primary objectives of the study described in this protocol will be: (1) to determine the brain's structural and functional changes following constant and variable practice conditions in motor learning (structural and functional magnetic resonance imaging, MRI); (2) to determine the EEG activation and connectivity between cognitive, sensory, and motor cerebral cortex areas (central, temporal, parietal, occipital) in constant and variable practice conditions and as a function of practice time. METHODS: The study will follow the interventional (experimental) design with two arms (parallel groups). Fifty participants will be randomly assigned to two groups practicing in constant (CG) and variable conditions (VG). CG will be practicing only one pattern of step isometric contractions during unimanual index finger abduction, i.e., 90 trials in all training sessions, whereas VG will practice three different patterns. Each will be practiced 30 times per session in variable conditions. Resting-state fMRI, EEG (cortical networking), and motor task proficiency will be examined before (pre-) and after practice (post- and retentions tests). DISCUSSION: Findings will enhance our understanding of structural and functional neural changes following practice in constant and variable conditions. Therefore, the study can be considered pure (basic) research (clinical research in healthy individuals). CLINICAL TRIAL REGISTRATION: Study registered at clinicaltrials.gov (ID# NCT04921072) on 9 June 2021. Last version update: 21 December 2021.The protocol has been prepared according to the complete SPIRIT checklist (http://www.spirit-statement.org/), although the item order has been modified in order to comply with the manuscript structure.
- Klíčová slova
- motor learning, neuroplasticity, practice conditions, sensorimotor cortex activity, specificity of practice, variability of practice,
- Publikační typ
- časopisecké články MeSH
OBJECTIVE: To determine the effects of low- vs. high-intensity aerobic and resistance training on motor and cognitive function, brain activation, brain structure, and neurochemical markers of neuroplasticity and the association thereof in healthy young and older adults and in patients with multiple sclerosis, Parkinson's disease, and stroke. DESIGN: Systematic review and robust variance estimation meta-analysis with meta-regression. DATA SOURCES: Systematic search of MEDLINE, Web of Science, and CINAHL databases. RESULTS: Fifty studies with 60 intervention arms and 2283 in-analyses participants were included. Due to the low number of studies, the three patient groups were combined and analyzed as a single group. Overall, low- (g=0.19, p = 0.024) and high-intensity exercise (g=0.40, p = 0.001) improved neuroplasticity. Exercise intensity scaled with neuroplasticity only in healthy young adults but not in healthy older adults or patient groups. Exercise-induced improvements in neuroplasticity were associated with changes in motor but not cognitive outcomes. CONCLUSION: Exercise intensity is an important variable to dose and individualize the exercise stimulus for healthy young individuals but not necessarily for healthy older adults and neurological patients. This conclusion warrants caution because studies are needed that directly compare the effects of low- vs. high-intensity exercise on neuroplasticity to determine if such changes are mechanistically and incrementally linked to improved cognition and motor function.
- Klíčová slova
- Aging, Cognition motor function, Exercise, Intensity Dose-response relationship,
- MeSH
- biologické markery MeSH
- cvičení fyziologie MeSH
- kognice fyziologie MeSH
- lidé MeSH
- neuroplasticita MeSH
- odporový trénink * MeSH
- roztroušená skleróza * MeSH
- senioři MeSH
- Check Tag
- lidé MeSH
- senioři MeSH
- Publikační typ
- časopisecké články MeSH
- metaanalýza MeSH
- práce podpořená grantem MeSH
- systematický přehled MeSH
- Názvy látek
- biologické markery MeSH
In the CA3 area of the hippocampus the pyramidal neurons were destroyed by intraventricular application of kainic acid. After transplantation of a suspension of embryonic hippocampal cells agglomerations of cells at the site of injection were observed. Some of them were in the layer of the destroyed neuronal population. These neurons formed dendritic branches and dendritic spines. As compared with control areas with a normal neuronal population, the neurons at the site of transplantation had less regular branching of dendrites and some of the branches were quite chaotic.
- MeSH
- hipokampus cytologie fyziologie MeSH
- inbrední kmeny potkanů MeSH
- krysa rodu Rattus MeSH
- neurony transplantace MeSH
- neuroplasticita * MeSH
- regenerace nervu * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- anglický abstrakt MeSH
- časopisecké články MeSH
Binge alcohol consumption among adolescents affects the developing neural networks underpinning reward and stress processing in the nucleus accumbens (NAc). This study explores in rats the long-lasting effects of early intermittent exposure to intoxicating alcohol levels at adolescence, on: (1) the response to natural positive stimuli and inescapable stress; (2) stress-axis functionality; and (3) dopaminergic and glutamatergic neuroadaptation in the NAc. We also assess the potential effects of the non-intoxicating phytocannabinoid cannabidiol, to counteract (or reverse) the development of detrimental consequences of binge-like alcohol exposure. Our results show that adolescent binge-like alcohol exposure alters the sensitivity to positive stimuli, exerts social and novelty-triggered anxiety-like behaviour, and passive stress-coping during early and prolonged withdrawal. In addition, serum corticosterone and hypothalamic and NAc corticotropin-releasing hormone levels progressively increase during withdrawal. Besides, NAc tyrosine hydroxylase levels increase at late withdrawal, while the expression of dopamine transporter, D1 and D2 receptors is dynamically altered during binge and withdrawal. Furthermore, the expression of markers of excitatory postsynaptic signaling-PSD95; Homer-1 and -2 and the activity-regulated spine-morphing proteins Arc, LIM Kinase 1 and FOXP1-increase at late withdrawal. Notably, subchronic cannabidiol, during withdrawal, attenuates social- and novelty-induced aversion and passive stress-coping and rectifies the hyper-responsive stress axis and NAc dopamine and glutamate-related neuroplasticity. Overall, the exposure to binge-like alcohol levels in adolescent rats makes the NAc, during withdrawal, a locus minoris resistentiae as a result of perturbations in neuroplasticity and in stress-axis homeostasis. Cannabidiol holds a promising potential for increasing behavioural, neuroendocrine and molecular resilience against binge-like alcohol harmful effects.
- Klíčová slova
- adolescence, binge alcohol drinking, cannabidiol, nucleus accumbens,
- Publikační typ
- časopisecké články MeSH
Previous evidence suggests that prenatal exposure to THC (pTHC) derails the neurodevelopmental trajectories towards a vulnerable phenotype for impaired emotional regulation and limbic memory. Here we aimed to investigate pTHC effect on hippocampus-related cognitive functions and markers of neuroplasticity in adolescent male offspring. Wistar rats were exposed to THC (2 mg/kg) from gestational day 5 to 20 and tested for spatial memory, object recognition memory and reversal learning in the reinforce-motivated Can test and in the aversion-driven Barnes maze test; locomotor activity and exploration, anxiety-like behaviour, and response to natural reward were assessed in the open field, elevated plus maze, and sucrose preference tests, respectively. The gene expression levels of NMDA NR1-2A subunits, mGluR5, and their respective scaffold proteins PSD95 and Homer1, as well as CB1R and the neuromodulatory protein HINT1, were measured in the hippocampus. pTHC offspring exhibited deficits in spatial and object recognition memory and reversal learning, increased locomotor activity, increased NR1-, decreased NR2A- and PSD95-, increased mGluR5- and Homer1-, and augmented CB1R- and HINT1-hippocampal mRNA levels. Our data shows that pTHC is associated with specific impairment in spatial cognitive processing and effectors of hippocampal neuroplasticity and suggests novel targets for future pharmacological challenges.
- Klíčová slova
- CB1R expression, adolescent rat offspring, hippocampal excitatory plasticity, prenatal THC exposure, spatial learning and memory,
- Publikační typ
- časopisecké články MeSH
