Biology subjects

Balsters, J. H.

Publications and source records attributed to Balsters, J. H..

3 recordsLinked to original sources

bioRxiv2023

Dynamic Causal Modelling Highlights the Importance of Decreased Self-Inhibition of the Sensorimotor Cortex in Motor Fatigability

Motor fatigability emerges when challenging motor tasks must be maintained over an extended period of time. It is a frequently observed phenomenon in everyday life which affects patients as well as healthy individuals. Motor fatigability can be measured using simple tasks like finger tapping at maximum speed for 30s. This typically results in a rapid decrease of tapping frequency, a phenomenon called motor slowing. In a previous study (Bachinger et al. 2019), we showed that motor slowing goes hand in hand with a gradual increase of activation in the primary sensorimotor cortex (SM1), supplementary motor area (SMA), and dorsal premotor cortex (PMd). Previous electrophysiological measurements further suggested that the increase in SM1 activity might reflect a breakdown of inhibition and, particularly, a breakdown of surround inhibition which might have led to heightened coactivation of antagonistic muscles. It is unclear what drives the activity increase in SM1 caused by motor slowing and whether motor fatigability affects the dynamic interactions between SM1 and upstream motor areas like SMA and PMd. Here, we performed dynamic causal modelling to answer this question. Our main findings revealed that motor slowing was associated with a significant reduction in SM1 self-inhibition which is in line with previous electrophysiological results. Additionally, the model revealed a significant decrease in the driving input to premotor areas suggesting that structures other than cortical motor areas might cause motor fatigability.

neuroscience↗

bioRxiv2019

Primate homologs of mouse cortico-striatal circuits

With the increasing necessity of animal models in biomedical research, there is a vital need to harmonise findings across species by establishing similarities and differences in rodent and primate neuroanatomy. Using a connectivity fingerprint matching approach, we compared cortico-striatal circuits across humans, non-human primates, and mice using resting state fMRI data in all species. Our results suggest that the connectivity patterns for both the nucleus accumbens and cortico-striatal motor circuits (posterior/lateral putamen) were conserved across species, making them reliable targets for cross-species comparisons. However, a large number of human and macaque striatal voxels were not matched to any mouse cortico-striatal circuit (mouse->human: 85% unassigned; mouse->macaque 69% unassigned; macaque->human; 31% unassigned). These unassigned voxels were largely localised to the caudate nucleus and anterior putamen, overlapping with executive function and social/language regions of the striatum, and connected to prefrontal-projecting cerebellar lobules and anterior prefrontal cortex, forming circuits that seem to be unique for non-human primates and humans. Our results demonstrate the potential of connectivity fingerprint matching to bridge the gap between rodent and primate neuroanatomy.

neuroscience↗

bioRxiv2019

Motor fatigability as evoked by repetitive movements results from a gradual breakdown of surround inhibition

Motor fatigability emerges when demanding tasks are executed over an extended period of time. Here, we used repetitive low-force movements that cause a gradual reduction in movement speed (or \"motor slowing\") to study the central component of fatigability in healthy adults. We show that motor slowing is associated with a gradual increase of net excitability in the motor network and, specifically, in primary motor cortex (M1), which results from overall disinhibition. Importantly, we link performance decrements to a breakdown of surround inhibition in M1, which is associated with high coactivation of antagonistic muscle groups. This is consistent with the model that a loss of inhibitory control might broaden the tuning of population vectors such that movement patterns become more variable, ill-timed and effortful. We propose that the release of inhibition in M1 is an important mechanism underpinning motor fatigability and, potentially, also pathological fatigue as frequently observed in patients with brain disorders.

neuroscience↗