Abstract
Non-invasive low-intensity transcranial electrical stimulation (tES) of the brain is an evolving field that has brought remarkable attention in the past few decades for its ability to directly modulate specific brain functions. Neurobiological after-effects of tES seems to be related to changes in neuronal and synaptic excitability and plasticity, however mechanisms are still far from being elucidated. We aim to review recent results from in vitro and in vivo studies that highlight molecular and cellular mechanisms of transcranial direct (tDCS) and alternating (tACS) current stimulation. Changes in membrane potential and neural synchronization explain the ongoing and short-lasting effects of tES, while changes induced in existing proteins and new protein synthesis is required for long-lasting plastic changes (LTP/LTD). Glial cells, for decades supporting elements, are now considered constitutive part of the synapse and might contribute to the mechanisms of synaptic plasticity. This review brings into focus the neurobiological mechanisms and after-effects of tDCS and tACS from in vitro and in vivo studies, in both animals and humans, highlighting possible pathways for the development of targeted therapeutic applications.
Highlights
In the last two decades, therapeutic efficacy of non-invasive transcranial brain stimulation techniques through low-intensity electrical fields has been demonstrated by a number of works and clinical trials providing promising results for many neurological disorders, including stroke [1] and epilepsy [2, 3], movement disorders/Parkinson’s (PD) [4] and Alzheimer’s (AD) [5, 6]
Experimental evidence has demonstrated that weak low-intensity ES induces polarity-specific changes in spontaneous and evoked neuronal activity [9, 10]: anodal polarization increases neuronal activity, whereas cathodal polarization decreases it [11,12,13,14]
While the immediate effects of transcranial electrical stimulation (tES) can be explained by changes in transmembrane potential influencing neuronal firing, it is plausible that the long-term after-effects are likely due to modifications of intracellular calcium dynamics and mechanisms of synaptic plasticity, based on long-term potentiation (LTP)/long-term depression (LTD) processes [18, 22, 23] and/or induction of metaplasticity, the activity-dependent physiological changes that modulate neural plasticity [24]
Summary
In the last two decades, therapeutic efficacy of non-invasive transcranial brain stimulation techniques through low-intensity electrical fields has been demonstrated by a number of works and clinical trials providing promising results for many neurological disorders, including stroke [1] and epilepsy [2, 3], movement disorders/Parkinson’s (PD) [4] and Alzheimer’s (AD) [5, 6]. The effects of tACS could be translated into whole larger brain-network activity through five different neuronal mechanisms [43, 44]: [1] stochastic resonance, consisting in the stochastic response of tACS-affected neurons to be either polarized or hyperpolarized; [2] rhythm resonance, synchronizing tACS frequency with the endogenous oscillations; [3] temporal biasing of spikes, a synergistically excitation of the same groups of neurons during each cycle of stimulation; [4] network entrainment of an endogenous irregular neuronal activity that necessitates an external current with sufficiently stronger amplitude; [5] imposed pattern, tACS overcomes endogenous regular oscillations and introduce a new oscillation. While TMS requires passing of current through coils to generate a magnetic field that in turn generates an electric field and a current density, in tES the electric field and the current density are proportional to injected current [54]
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