The cerebral cortex, basal ganglia and thalamus together form looping circuits that are critical for movement. Some cardinal movement difficulties of Parkinson's disease are associated with the emergence of abnormal neuronal oscillations, particularly at beta frequencies (13-30 Hz), in the cortex and basal ganglia. Defining the activity of neurons of the motor thalamus is imperative for understanding the neural basis of normal and impaired movement because they are key mediators of basal ganglia influences on cortical information processing. The motor thalamus is parcellated into two major zones according to their distinct subcortical inputs; the 'basal ganglia-recipient zone' (BZ) is bombarded by inhibitory GABAergic inputs from basal ganglia whereas the 'cerebellar-recipient zone' (CZ) is bombarded by excitatory glutamatergic inputs from cerebellar nuclei. To address the key issue of how their activities might be disturbed in Parkinsonism, we recorded the spontaneous firing of identified BZ and CZ neurons under anesthesia in dopamine-intact rats as well as rats rendered Parkinsonian by unilateral 6-hydroxydopamine (6-OHDA) lesions. In the 6-OHDA-lesioned rats, we found no evidence of pathologically-reduced firing rates in either zone of motor thalamus, contrary to classic schemes of Parkinsonian circuit dysfunction. However, after dopamine depletion, the tight coupling of firing of BZ neurons to cortical slow oscillations was phase-shifted. Moreover, during cortical activation, many BZ neurons, but not CZ neurons, exhibited pronounced beta oscillations, which were not seen in dopamine-intact rats. We conclude that, within motor thalamus, the effects of dopamine loss in Parkinsonism are confined to the BZ, and that the thalamocortical substrates of Parkinsonian movement difficulties are more closely related to abnormal firing patterns, as exemplified by excessive beta oscillations, than altered firing rates.