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Mark J. Amirtharaj
The basal ganglia thalamocortical (BGT) circuit plays a key role in motor movement in humans and rodents. Previous studies upon rodent models of Parkinson's Disease(PD) have linked the loss of dopamine (DA) cells, associated with PD, with distinct emergence of beta frequency (12-40Hz) oscillations in different nuclei of the BGT circuit. Clinical studies have found this phenomenon to occur in PD patients as well. Synchronous beta activity in the DA lesioned hemisphere of PD rodents, during walking epochs, has been shown to occur between the motor cortex(MCx) and ventral medial thalamus (Vm) as well as between the MCx and substantia nigra pars reticulata (SNpr). Such recordings, however, have only been taken two nuclei at a time. In search of confirmation of BGT network resonance, electrode bundles were chronically implanted in the MCx, Vm, and SNpr of unilaterally lesioned rats, enabling simultaneous recording in all three regions of the circuit. Rats were trained to walk in directions, both ipsiversive and contraversive, to the DA lesion and recordings were then taken during epochs of rest and walk from days 7-35. To then further probe the Vm's role in overall circuit modulation, muscimol, a GABA agonist, was injected into the Vm via a cannula and resultant activity in the MCx and SNpr was monitored. Results show simultaneous beta coherence in the MCx, Vm and SNpr. Vm inhibition, by muscimol, diminished high beta (25-40Hz) power after 1 hour in both the SNpr and MCx by factors of 3.8 and 13.8, respectively. Coherence also declined 18 fold. Significant beta activity reemerged 3 hours post injection. The results support the notion of BGT circuit coherence in walking PD rodents and highlight the Vm's contribution towards resonant beta rhythms. Reduction of high beta activity by means of Vm inhibition did not, however, correlate to improved motor function and suggest GABA agonists applied to the Vm will not serve as an effective therapy against PD.
Last Modified December 23, 2013