Tongue force and tongue motility are differently affected by unilateral vs bilateral nigrostriatal dopamine depletion in rats

In addition to its cardinal symptoms of bradykinesia, muscle rigidity, resting tremor and postural disturbances, Parkinson's disease (PD) also affects orolingual motor function. Orolingual motor deficits can contribute to dysphagia, which increases morbidity and mortality in this population. Previous preclinical studies describing orolingual motor deficits in animal models of PD have focused on unilateral nigrostriatal dopamine (DA) depletion. In this study we compared the effects of unilateral vs bilateral 6-hydroxydopamine (6-OHDA)-induced DA depletion in rats trained to lick water from an isometric force-sensing disc. Rats received either unilateral or bilateral 6-OHDA into the medial forebrain bundle and were tested for four weeks post-lesion. Dependent variables included task engagement (the number of licks per session), tongue force (mean and maximum), and tongue motility (the number of licks per second). While both lesion groups exhibited decreased tongue force output, tongue motility deficits were present in only the group that received unilateral nigrostriatal DA depletion. Task engagement was not significantly diminished by 6-OHDA. Analysis of striatal DA tissue content revealed that DA depletion was ∼97% in the unilateral group and ∼90% in the bilateral group. These results suggest that while nigrostriatal DA depletion affects tongue force output, deficits in tongue motility may instead result from a functional imbalance in neural pathways affecting this midline structure.

► Unilateral and bilateral nigrostriatal dopamine depletion affect orolingual motor function in rats.
► Both unilateral and bilateral nigrostriatal dopamine depletion decrease tongue force during licking.
► Tongue motility is decreased following unilateral but not bilateral nigrostriatal dopamine depletion.
► These results reveal a dissociation between these two movement modalities in the 6-hydroxydopamine rat model of Parkinson's disease.