Abstract
We aimed to verify whether indirect-wave (I-wave) recruitment and cortical inhibition can regulate or predict the plastic response to paired associative stimulation with an inter-stimulus interval of 25 ms (PAS25), and also whether water immersion (WI) can facilitate the subsequent PAS25-induced plasticity. To address the first question, we applied transcranial magnetic stimulation (TMS) to the M1 hand area, while alternating the direction of the induced current between posterior-to-anterior and anterior-to-posterior to activate two independent synaptic inputs to the corticospinal neurons. Moreover, we used a paired stimulation paradigm to evaluate the short-latency afferent inhibition (SAI) and short-interval intracortical inhibition (SICI). To address the second question, we examined the motor evoked potential (MEP) amplitudes before and after PAS25, with and without WI, and used the SAI, SICI, and MEP recruitment curves to determine the mechanism underlying priming by WI on PAS25. We demonstrated that SAI, with an inter-stimulus interval of 25 ms, might serve as a predictor of the response to PAS25, whereas I-wave recruitment evaluated by the MEP latency difference was not predictive of the PAS25 response, and found that 15 min WI prior to PAS25 facilitated long-term potentiation (LTP)-like plasticity due to a homeostatic increase in cholinergic activity.
Highlights
The use-dependent changes in synaptic strength are essential for learning and memory [1].Among the multiple types of synaptic plasticity described far [2,3], Hebbian long-term potentiation (LTP) and depression (LTD) are the most thoroughly studied as potential neuroplastic mechanisms for learning
The interclass correlation coefficients (ICC) calculated to test consistency between latency values measured in the same individual on different days were 0.921 for PA latency, 0.926 for AP latency, 0.905 for LM latency, 0.852 for the PA–LM latency difference, and 0.874 for the AP–LM latency difference, indicating that the data spread was almost entirely due to inter-individual differences in the transcranial magnetic stimulation (TMS) response
This priming effect was observed in 17 participants, irrespective of whether they were responders or non-responders to PAS25 alone, as there was little inter-individual variability in the homeostatic short-latency afferent inhibition (SAI) increase after water immersion (WI)
Summary
The use-dependent changes in synaptic strength (plasticity) are essential for learning and memory [1]. Among the multiple types of synaptic plasticity described far [2,3], Hebbian long-term potentiation (LTP) and depression (LTD) are the most thoroughly studied as potential neuroplastic mechanisms for learning. LTP and LTD are mutually dependent as induction thresholds, and are influenced by the prior history of neuronal activity and functional state of the synapse, termed as metaplasticity [4]. Metaplasticity represents a neuroprotective mechanism that stabilizes synaptic weights in neuronal networks while maintaining the capacity for synaptic plasticity by varying the induction thresholds according to the integrated postsynaptic activity [5]. Res. Public Health 2020, 17, 215; doi:10.3390/ijerph17010215 www.mdpi.com/journal/ijerph
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