<p>Parkinsonian symptoms such as tremors, rigidity, bradykinesia, and postural instability typically arise from basal ganglia dysfunction, but growing evidence suggests cerebellar circuits also play a key role. Here, we investigated multiunit activity (MUA) in the inferior olive (IO), dentate nucleus (DN), and Crus II of the cerebellum in a rat model of tract lesion-induced parkinsonism triggered by ventrolateral striatum (VLS) injury. Thirty-six male Wistar rats were divided into a Lesion group and an Intact group. Monopolar electrodes were implanted to record MUA in IO, DN, or Crus II for four consecutive weeks. Basal and tremor-associated signals were analyzed using generalized linear models and post hoc comparisons. In rats with VLS lesions, IO activity initially increased and then declined over time, whereas DN activity remained consistently elevated, suggesting compensatory upregulation. Crus II showed no significant shifts in baseline activity. During tremor episodes, all three structures exhibited distinct temporal fluctuations in MUA. These findings reveal cerebellar structure-specific responses to striatal injury and highlight the cerebellum’s role in both the acute and chronic phases of Parkinsonian motor dysfunction. Careful consideration of possible inflammatory responses to electrode implantation remains essential for future studies.</p>

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Compensatory and Dynamic Cerebellar Responses to Striatal Lesions in Experimental Parkinsonism

  • Luis I. García,
  • Gerardo Marín,
  • Cristofer Zárate-Calderón,
  • Iraís Viveros-Martínez,
  • Mario E. Valerio-Nolasco,
  • Luis Beltrán-Parrazal,
  • Donaji Chi-Castañeda

摘要

Parkinsonian symptoms such as tremors, rigidity, bradykinesia, and postural instability typically arise from basal ganglia dysfunction, but growing evidence suggests cerebellar circuits also play a key role. Here, we investigated multiunit activity (MUA) in the inferior olive (IO), dentate nucleus (DN), and Crus II of the cerebellum in a rat model of tract lesion-induced parkinsonism triggered by ventrolateral striatum (VLS) injury. Thirty-six male Wistar rats were divided into a Lesion group and an Intact group. Monopolar electrodes were implanted to record MUA in IO, DN, or Crus II for four consecutive weeks. Basal and tremor-associated signals were analyzed using generalized linear models and post hoc comparisons. In rats with VLS lesions, IO activity initially increased and then declined over time, whereas DN activity remained consistently elevated, suggesting compensatory upregulation. Crus II showed no significant shifts in baseline activity. During tremor episodes, all three structures exhibited distinct temporal fluctuations in MUA. These findings reveal cerebellar structure-specific responses to striatal injury and highlight the cerebellum’s role in both the acute and chronic phases of Parkinsonian motor dysfunction. Careful consideration of possible inflammatory responses to electrode implantation remains essential for future studies.