Cortical Inhibition State-Dependent iTBS Induced Neural Plasticity

Abstract

BackgroundIntermittent theta burst stimulation (iTBS) is an effective stimulus for long-term potentiation (LTP)-like plasticity. However, iTBS-induced effects varied greatly between individuals. Ample evidence suggested that an initial decrease in local γ-aminobutyric acid (GABA) or enhancement in N-methyl-D-aspartate (NMDA) facilitation neurotransmission is of vital importance for allowing LTP-like plasticity to occur. Therefore, we aimed to investigate whether the individual level of GABA or NMDA receptor-mediated activity before stimulation is correlated with the after-effect in cortical excitability induced by iTBS.MethodsFifteen healthy volunteers were recruited for the present study. We measured short-interval intracortical inhibitory (SICI), long-interval intracortical inhibitory (LICI), and intracortical facilitation (ICF), which index GABAA receptor-, GABAB receptor-, and glutamate receptor-mediated activity, respectively, in the cortex before conducting iTBS. After iTBS intervention, the changes of motor-evoked potential (MEP) amplitude were taken as a measure for cortical excitability in response to iTBS protocol.ResultsThere was a significant negative correlation between the amount of SICI measured before iTBS and the after-effect of iTBS-induced LTP-like plasticity at the time points of 5, 10, and 15 min after inducing iTBS. A multiple linear regression model indicated that SICI was a good predictor of the after-effect in cortical excitability induced by iTBS at 5, 10, and 15 min following stimulation.ConclusionThe present study found that GABAA receptor-mediated activity measured before stimulation is negatively correlated with the after-effect of cortical excitability induced by iTBS. SICI, as the index of GABAA receptor-mediated activity measured before stimulation, might be a good predictor of iTBS-induced LTP-like plasticity for a period lasting 15 min following stimulation.

Effects of combined use of intermittent theta burst stimulation and cognitive training on post-stroke cognitive impairment : a single-blind randomized controlled trial

“…The left DLPFC, prefrontal polar cortex, and left Broca's area of the patients showed significant activation after iTBS treatment in the analysis of the results shown by near-infrared functional imaging, suggesting that patients with iTBS stimulation of the left DLPFC may have had local activation at the stimulation site, in addition to increased excitability in the cerebral cortex at the stimulation site. Based on the etiology of poststroke cognitive impairment and its mechanism of action, 26,27 we hypothesized that iTBS might support the DLPFC and prefrontal polar cortex. The network connectivity of Broca's area was improved, which could stimulate the distant cerebral cortex.…”

Current evidence, clinical applications, and future directions of transcranial magnetic stimulation as a treatment for ischemic stroke

“…It has also been shown that the proliferation and differentiation of newborn neural stem cells to the ischemic lesion area after stroke is regulated by BDNF, and overexpression of BDNF accelerates the recruitment of newborn neural stem cells and their migration to the ischemic brain tissue area ( Young et al, 2011 ; Jansson et al, 2012 ). In addition to the above possible mechanisms, it has also been shown that iTBS regulates intrasynaptic Ca 2+ concentration by affecting N-methyl-D-aspartate (NMDA) activity, thereby increasing intrasynaptic transmission efficiency and promoting LTP-like effects ( Saudargiene et al, 2015 ; Diao et al, 2022 ). It is thus clear that TMS promotes improved neurological function after stroke and is closely related to multiple pathway-mediated neurogenesis.…”

A comparative transcranial magnetic stimulation study: Assessing cortical excitability and plasticity in Alzheimer's disease, dementia with Lewy bodies and Frontotemporal dementia

“…Although studies with larger sample sizes revealed substantial inter‐ and intra‐individual variability in response to TBS, 6,8,9 MEPs were able to demonstrate the efficacy of TBS in effectively modulating cortical excitability 10 . The underlying mechanism in facilitating MEP amplitudes after iTBS is supposedly the long‐term potentiation‐like (LTP‐like) plasticity 11 …”

“…10 The underlying mechanism in facilitating MEP amplitudes after iTBS is supposedly the long-term potentiation-like (LTP-like) plasticity. 11 Several prior studies found that cortical excitability measured by rMTs was increased in Alzheimer's disease (AD), and LTP-like plasticity induced by iTBS as a measure of synaptic plasticity was decreased, compared to healthy controls. [12][13][14][15][16][17] Prior studies in patients with dementia with Lewy bodies (DLB) are limited and consist mainly of cortical motor paradigms such as short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), and short-latency afferent inhibition.…”