China
Africa
Explore chapters and articles related to this topic
Acid-Sensing Ion Channels and Synaptic Plasticity: A Revisit
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Ming-Gang Liu, Michael X. Zhu, Tian-Le Xu
Synaptic plasticity is a generic term that applies to short- or long-lasting experience- or activity-dependent changes in the efficacy or connection of synaptic transmission in the brain. It can be classified into both functional and structural aspects of synaptic plasticity. For the former, except for LTP and LTD, it also includes short-term plasticity (like paired-pulse facilitation or depression), depotentiaion86, metaplasticity (plasticity of synaptic plasticity)87, and homeostatic plasticity88 (scaling up or down of the synaptic strength in response to reduction or elevation of synaptic activity). For the latter, dendritic spines may undergo activity-dependent dynamic alterations in shape, size, density, or even composition during various behavioral tasks and/or synaptic stimulations84. To date, most studies have focused on the classical LTP, with much less emphasis placed on other forms of synaptic plasticity, although the possibilities that ASICs are equally important for depotentiaion (or metaplasticity) have not been fully excluded. It would be both necessary and exciting in future studies to test these possibilities.
Neurophysiology of Old Neurons and Synapses
Published in David R. Riddle, Brain Aging, 2007
In contrast to genetic models that manipulate protein expression, aging is associated with Ca2+ dysregulation, which encourages the activation of signaling cascades that mediate LTD. Thus, it might be concluded that aging results in altered Ca2+ regulation leading to an increase in the AHP, and that the reduced cell excitability and increased susceptibility to LTD represent a functional lesion in the memory system. Furthermore, these data point to the importance of mechanisms inherent in the cell (e.g., Ca2+ and K+ channels) in regulating the synaptic plasticity threshold. Related to this is the possibility that aged animals exhibit deficits in metaplasticity. Metaplasticity refers to the process by which previous neural activity modifies subsequent synaptic plasticity [166]. Tangential evidence is provided by studies demonstrating that learning is associated with a reduction in the amplitude of the Ca2+-dependent AHP [26, 55, 167, 168]. In addition, several reports indicate that learning or behavioral conditioning modifies synaptic function [169–171]. Together, the results imply that prior neural activity associated with training can influence the AHP. In turn, a decrease in the AHP would shift synaptic plasticity thresholds, promoting LTP. Thus, memory-impaired animals may be unable to activate metaplasticity processes to influence cell excitability and synaptic function. This idea remains to be tested.
Biofield Devices
Published in Len Wisneski, The Scientific Basis of Integrative Health, 2017
Len Wisneski, Blake Gurfein, Tiffany Barsotti, Gaétan Chevalier, Paul J. Mills, David Muehsam
TMS has been the topic of numerous clinical studies. Early reports of efficacy for depression [149–152] led to much further inquiry, and TMS has been used to investigate many aspects of cognitive neuroscience [153], including cognition, brain–behavior relationships, and the pathophysiology of a variety of neurologic and psychiatric disorders [146,154]. Therapeutic benefits have been reported for a very wide range of indications, including depression, acute mania, bipolar disorders, panic, hallucinations, obsessions/compulsions, schizophrenia, catatonia, posttraumatic stress disorder, drug craving, Parkinson disease, dystonia, tics, stuttering, tinnitus, spasticity, epilepsy, rehabilitation of aphasia or hand function after stroke, neuropathic pain, visceral pain, and migraine [145,146,154,155]. In recent years, repetitive TMS (rTMS), using magnetic pulses repeating at 1–20 Hz to entrain with neuronal activity, has been widely studied as a treatment tool for various neurological and psychiatric disorders including migraine, stroke, Parkinson disease, dystonia, tinnitus, and depression [146]. A meta-analysis of studies on the efficacy of rTMS in psychiatric disorders suggests its use for depression, auditory and verbal hallucinations, and possibly for negative symptoms of schizophrenia, but not for treatment of obsessive–compulsive disorder (OCD) [156]. A review of studies on the use of rTMS for pain concluded that efficacy is limited by the short duration of the induced analgesia, but prolonged pain relief can be obtained through daily treatment for several weeks [155]. Although this broad range of therapeutic benefits has been reported, the mechanisms underlying TMS have yet to be fully elucidated. In particular, although lasting after effects of TMS have been found in healthy subjects, the neurophysiologic substrates remain unclear. Various mechanisms have been proposed, including synaptic changes resembling experimental long-term depression and long-term potentiation, as well as shifts in network excitability, activation of feedback loops, and activity-dependent metaplasticity [157,158].
Current perspectives on the benefits, risks, and limitations of noninvasive brain stimulation (NIBS) for post-stroke dysphagia
Published in Expert Review of Neurotherapeutics, 2021
One of the key areas for improvement in NIBS research is the robustness of treatment outcomes. A possible strategy is to adopt an individualized approach when designing treatment protocols. For example, severe unihemispheric stroke patients may benefit from NIBS protocols that promote the recruitment of compensatory neural networks from the unaffected hemisphere. With data from various high-quality RCTs published in the literature, clinicians can afford to be more flexible in deciding which protocol to use instead of employing the ‘one-size-fits-all’ approach. Another potential solution is to manipulate the brain regulation on plasticity changes (metaplasticity). This can be achieved by preconditioning the cortex into a desirable state before NIBS treatments. Although preliminary data show that this approach can enhance stimulation outcomes in healthy young adults, further work is required to explore whether similar effects can be observed in patients and the preconditioning effects of different modalities. Finally, advances in the field and the translation into clinical practice rely largely on data from large-scale clinical trials. This will depend on the financial support from corporate sponsors, charitable organizations, and the government.
Effect of tDCS on Fine Motor Control of Patients in Subacute and Chronic Post-Stroke Stages
Published in Journal of Motor Behavior, 2020
E. L. Pavlova, R. V. Semenov, A. B. Guekht
Among other factors, timing of tDCS application is an important factor for the size and direction of stimulation effect (Ziemann & Siebner, 2008). In our study, the subacute stage of recovery after stroke is associated with significantly greater effects after tDCS compared to concurrent stimulation. Training during the stimulation has also been shown to lead to improvement in performance (Reis et al., 2009; Reis & Fritsch, 2011; Stagg et al., 2011). On the other hand, deterioration of performance is observed when both anodal and cathodal tDCS are applied prior or after motor task (Stagg et al., 2011). The former is explained by gating mechanisms when shift in membrane polarization causes strengthening of synapsis and latter – by homeostatic metaplasticity which stabilizes the system after previous too high activity.
Noradrenergic gating of long-lasting synaptic potentiation in the hippocampus: from neurobiology to translational biomedicine
Published in Journal of Neurogenetics, 2018
Peter V. Nguyen, Jennifer N. Gelinas
Activation of β-ARs can alter the state of a synapse so that its responses to future stimulation may be modified, by a process known as ‘metaplasticity’ (reviewed by Abraham, 2008). It is noteworthy that LTP enhancement by β-AR activation can persist long after the brief exposure to β-AR agonists had ended (Hu et al., 2007; Seol et al., 2007; Tenorio et al., 2010). Increased excitability and boosted AMPAR phosphorylation may persist for an hour or more (Dunwiddie, Taylor, Heginbotham, & Proctor, 1992; Tenorio et al., 2010; Vanhoose & Winder, 2003). However, β-AR regulation of translation may also play key roles in this form of metaplasticity. Weaker stimulation elicits long-lasting LTP when delivered 1 h after transient activation of β-ARs (Tenorio et al., 2010), and this was blocked by application of inhibitors of translation during β-AR activation, but not when the inhibitors were applied during electrical stimulation delivered 1 h after β-ARs were activated. Thus, increased translation triggered by β-AR activation may ‘prime’ synapses for future long-lasting plasticity. There is evidence that translation of mRNAs encoding GluR1/GluR2 subunits is boosted by NE during this form of metaplastic enhancement of LTP (Maity, Rah, Sonenberg, Gkogkas, & Nguyen, 2015). Thus, increased synthesis of GluR1 subunits for maintaining persistent potentiation likely occurs, under some conditions, in addition to phosphorylation-triggered trafficking and insertion of AMPARs following β-AR activation by either isoproterenol or by the naturally-occurring transmitter, NE.