Müri, R. M. | bioRxiv Science

bioRxiv2021

Saccades, attentional orienting and disengagement: the effects of anodal tDCS over right posterior parietal cortex (PPC) and frontal eye field (FEF)

In the present work, we applied anodal transcranial direct current stimulation (tDCS) over the posterior parietal cortex (PPC) and frontal eye field (FEF) of the right hemisphere in healthy subjects to modulate attentional orienting and disengagement in a gap-overlap task. Both stimulations led to bilateral improvements in saccadic reaction times (SRTs), with larger effects for gap trials. However, analyses showed that the gap effect was not affected by tDCS. Importantly, we observed significant effects of baseline performance that may mediate side- and task-specific effects of brain stimulation.

neuroscience↗

bioRxiv2020

Repetitive Transcranial Magnetic Stimulation Activates Glial Cells and Inhibits Neurogenesis after Pneumococcal Meningitis

Pneumococcal meningitis (PM) causes damage to the hippocampus, a brain structure critically involved in learning and memory. Hippocampal injury - which compromises neurofunctional outcome - occurs as apoptosis of progenitor cells and immature neurons of the hippocampal dentate granule cell layer thereby impairing the regenerative capacity of the hippocampal stem cell niche. Repetitive transcranial magnetic stimulation (rTMS) harbours the potential to modulate the proliferative activity of this neuronal stem cell niche. In this study, specific rTMS protocols - namely continuous and intermittent theta burst stimulation (cTBS and iTBS) - were applied on infant rats microbiologically cured from PM by five days of antibiotic treatment. Following two days of exposure to TBS, differential gene expression was analysed by whole transcriptome analysis using RNAseq. cTBS provoked a prominent effect in inducing differential gene expression in the cortex and the hippocampus, whereas iTBS only affect gene expression in the cortex. TBS induced polarisation of microglia and astrocytes towards an inflammatory phenotype, while reducing neurogenesis, neuroplasticity and regeneration. cTBS was further found to induce the release of pro-inflammatory cytokines in vitro. We conclude that cTBS intensified neuroinflammation after PM, which translated into increased release of pro-inflammatory mediators thereby inhibiting neuroregeneration.

neuroscience↗