Acute Cortical Stroke Alters Neural Activity in Subthalamic Nucleus, Which Correlates With Motor Disability in Rats.

Abstract

Background: The subthalamic nucleus (STN) plays a role in motor control, yet it is unclear whether acute cortical stroke (ACS) causes abnormal STN activity and neural oscillations. Moreover, the correlation between these subthalamic neurophysiological changes and motor disability remains unknown. To address this, we studied the impact of ACS on neural activity in the STN. We then examined the correlation between changes in STN activity and motor disability.

Methods: Fifty-six Sprague-Dawley rats were used. Although rats were anesthetized, we inserted electrodes in the STN and induced an ACS by creating a photothrombotic lesion in the ipsilateral motor cortex. Local field potentials were recorded before and after ACS. The motor behavior was assessed before and after ACS using a single-pellet reaching task.

Results: Rats experienced significant motor disability after ACS. STN firing rate significantly decreased after ACS. Additionally, delta (0.5-4 Hz) and gamma (80-130 Hz) power significantly decreased after ACS. Furthermore, the decrease in delta mean power correlated with decreases in success rate (r=0.77; P=0.009) and first try success rate (r=0.69; P=0.028). The decreases in gamma mean power (r=0.68; P=0.029) and gamma peak power (r=0.74; P=0.015) correlated with the decrease in success rate. The decrease in gamma power significantly correlated with the decreased STN firing rate. However, decreased delta power exhibited no correlation with decreased gamma power.

Conclusions: Our study provides the first evidence that ACS causes significant subthalamic inhibition and abnormal oscillatory activity in rats, with these effects significantly correlated with motor disability. Notably, these abnormal STN oscillations serve as a predictive biomarker for motor disability during the acute phase of cortical stroke. Furthermore, our findings highlight the potential of neuromodulation strategies to mitigate poststroke motor disability by targeting and reducing abnormal STN activity.