Basal Ganglia Network Synchronization in Animal Models of Parkinson’s Disease

Beta frequency synchronization in basal ganglia output during rest and walk in a hemiparkinsonian rat

“…Marked increases are observed in the incidence of oscillatory activity in the ~1 Hz range in basal ganglia spike trains recorded throughout the lesioned hemisphere of systemically anesthetized rats with unilateral dopamine cell lesions. This activity is coherent with the ~1 Hz oscillatory firing patterns dominant in the cortex of the anesthetized rat, and phase relationship data show that loss of dopamine dramatically affects the extent to which the 1 Hz cortical oscillations entrain activity throughout the basal ganglia and modify basal ganglia output (Belluscio et al, 2003; Kasanetz et al, 2002; Magill et al, 2001; Mallet et al, 2006; Murer et al, 2002; Parr-Brownlie et al, 2007, 2009; Tseng et al, 2001b; Walters and Bergstrom, 2009; Walters et al, 2007; Zold et al, 2007). Increased beta frequency activity has also been observed in the STN and the external segment of the globus pallidus (GPe) of the anesthetized hemiparkinsonian rats during periods of desynchronized cortical activity (Mallet et al, 2008a, 2008b).…”

“…The increase in high beta power in the SNpr in the lesioned hemisphere during treadmill walking is significantly attenuated after L-DOPA administration, consistent with observations from PD patients showing that beta activity in STN and GPi LFPs in the 8–35 Hz range is reduced following L-DOPA treatment. These findings add to the accumulating evidence that loss of dopamine selectively enhances expression of synchronized and oscillatory activity in the basal ganglia in the dopamine-depleted hemisphere (Alegre et al, 2005; Alonso-Frech et al, 2006; Bergman et al, 1994, 1998; Brown, 2003, 2007; Brown et al, 2001; Cassidy et al, 2002; Chen et al, 2007; Costa et al, 2006; Doyle et al, 2005; Filion, 1979; Foffani et al, 2005; Gatev and Wichmann, 2009; Goldberg et al, 2004; Heimer et al, 2002; Kuhn et al, 2004; Leblois et al, 2006, 2007; Levy et al, 2000, 2001, 2002; Magill et al, 2001; Mallet et al, 2008a, 2008b; Murer et al, 2002; Nini et al, 1995; Parr- Brownlie et al, 2007, 2009; Priori et al, 2002, 2004; Raz et al, 2000, 2001; Sharott et al, 2005; Tseng et al, 2001b; Walters et al, 2007, 2009; Weinberger et al, 2006; Wichmann et al, 1994; Williams et al, 2002, 2003). Moreover, the novel observation that neuronal activity in the high beta range is prominent in the SNpr of the dopamine-depleted hemisphere during episodes of treadmill walking adds support to the view that increased beta synchronization in basal ganglia output may play a role in the motor impairment associated with loss of dopamine.…”

Direct Evaluation of L-DOPA Actions on Neuronal Activity of Parkinsonian TissueIn Vitro

“…Therefore, the use of this preparation may also be used to shed light on the development of L-DOPA induced receptor hypersensitivity and later dyskinesia in animal models [19, 21]. Moreover, the combination of selective dopamine receptor ligands with transgenic mice would allow the testing of the different models of Parkinsonism [12, 14, 18, 19]. …”

Altered neuronal activity in the primary motor cortex and globus pallidus after dopamine depletion in rats

“…Alterations of neuronal activity in the basal ganglia and cortices have been reported in patients with Parkinson's disease (PD) as well as in animal models of PD [4][5][6][7][8][9][10][11]. These changes in neuronal activity are believed to mediate many of the dysfunctional effects seen in PD because they impact the circuits connecting the basal ganglia and the cortex [10,[12][13][14]. However, the specific pathological changes that occur with DA loss in oscillation activity and functional connectivity from the cortex to the basal ganglia remain poorly understood.…”