Objective <p>To investigate how ischemic stroke alters neural activity in the caudal forelimb area (CFA) and identify electrophysiological mechanisms underlying post-stroke motor deficits.</p> Methods <p>Local field potentials were recorded bilaterally from ipsilateral and contralateral CFA in rats under anesthesia and during a single-pellet retrieval task. Analyses included spectral power across canonical frequency bands, aperiodic 1/f slope characterization of excitation–inhibition balance, and cross-frequency coupling assessment of interhemispheric coordination.</p> Results <p>Stroke induced widespread bilateral disruptions in oscillatory dynamics across delta, theta, alpha, beta, and gamma bands. The aperiodic 1/f slope shifted, reflecting altered excitation–inhibition balance. Cross-frequency coupling between hemispheres, particularly low-frequency phase to gamma amplitude, was reorganized, indicating impaired interhemispheric coordination and bilateral motor network imbalance. Notably, the main experimental cohort did not include a sham-operated control group; however, a pilot experiment with three sham and three MCAO animals, conducted using identical procedures, provided supportive evidence for the stability of key measures under sham conditions.</p> Conclusions <p>This study demonstrates that ischemic stroke induces coordinated alterations in spectral organization, excitation–inhibition balance, and cross-frequency interactions within the bilateral caudal forelimb cortex. These findings indicate that post-stroke motor dysfunction arises from disrupted, state-dependent dynamics of distributed motor networks rather than isolated changes within the lesioned hemisphere.</p>

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Bilateral cortical network disruptions in the rat caudal forelimb area after unilateral stroke

  • Cheng’an Cao,
  • Di Chen,
  • Jin Gong,
  • Shuangqi Gao,
  • Jianwei Huang,
  • Chaoran Jia,
  • Hongyu Liu,
  • Yuanqing Li,
  • Ying Guo

摘要

Objective

To investigate how ischemic stroke alters neural activity in the caudal forelimb area (CFA) and identify electrophysiological mechanisms underlying post-stroke motor deficits.

Methods

Local field potentials were recorded bilaterally from ipsilateral and contralateral CFA in rats under anesthesia and during a single-pellet retrieval task. Analyses included spectral power across canonical frequency bands, aperiodic 1/f slope characterization of excitation–inhibition balance, and cross-frequency coupling assessment of interhemispheric coordination.

Results

Stroke induced widespread bilateral disruptions in oscillatory dynamics across delta, theta, alpha, beta, and gamma bands. The aperiodic 1/f slope shifted, reflecting altered excitation–inhibition balance. Cross-frequency coupling between hemispheres, particularly low-frequency phase to gamma amplitude, was reorganized, indicating impaired interhemispheric coordination and bilateral motor network imbalance. Notably, the main experimental cohort did not include a sham-operated control group; however, a pilot experiment with three sham and three MCAO animals, conducted using identical procedures, provided supportive evidence for the stability of key measures under sham conditions.

Conclusions

This study demonstrates that ischemic stroke induces coordinated alterations in spectral organization, excitation–inhibition balance, and cross-frequency interactions within the bilateral caudal forelimb cortex. These findings indicate that post-stroke motor dysfunction arises from disrupted, state-dependent dynamics of distributed motor networks rather than isolated changes within the lesioned hemisphere.