The external globus pallidus in patients with Parkinson's disease and progressive supranuclear palsy

Do gap junctions regulate synchrony in the Parkinsonian basal ganglia?

“…Indeed, Fernandez-Suarez et al [2012] reported prominent cell death of PV-positive GABAergic GPe neurons, commonly projecting to STN and GPi, in 6-OHDA treated rats and in MPTP treated monkeys. In contrast, an earlier study by Hardman and Halliday [1999] did not describe abnormalities in the total number of PV-positive GPe neurons in PD patients. However, when considering cell density rather than absolute cell counts, death of GPe neurons is also possible here as seen in a trend towards a decrease of PVpositive neuron density [Fernandez-Suarez et al, 2012].…”

Do gap junctions regulate synchrony in the Parkinsonian basal ganglia?

“…Indeed, Fernandez-Suarez et al [2012] reported prominent cell death of PV-positive GABAergic GPe neurons, commonly projecting to STN and GPi, in 6-OHDA treated rats and in MPTP treated monkeys. In contrast, an earlier study by Hardman and Halliday [1999] did not describe abnormalities in the total number of PV-positive GPe neurons in PD patients. However, when considering cell density rather than absolute cell counts, death of GPe neurons is also possible here as seen in a trend towards a decrease of PVpositive neuron density [Fernandez-Suarez et al, 2012].…”

Regional brain atrophy in progressive supranuclear palsy and Lewy body disease

“…In particular, pallidal atrophy has been previously reported, 23 and neurofibrillary tangles, neuropil threads, and neurodegeneration are consistently observed in the pallidosubthalamic complex and substantia nigra. 7,12,15,[25][26][27] Our results suggest that there is a reduction in the density of neurofibrillary tangles with ongoing atrophy subcortically. 28 This contrasts with increasing cortical tangle pathology that occurs with atrophic progression in PSP.…”

Cell-specific pallidal intervention induces long-lasting motor recovery in dopamine-depleted mice

“…These results reconcile a number of conflicting reports in the literature: that successful DBS can either increase or decrease firing rates of GPe neurons 37 – 40 , that DBS directly in the GPe can reduce bradykinesia 27 , 41 but restoring autonomous firing after DD has no effect 42 . Finally, because the proportion of PV-GPe neurons in humans is similar to that in mice 43 , our results suggest that interventions that preferentially increase their activity relative to other GPe neurons might provide more persistent prokinetic benefits than current treatments.…”

Do gap junctions regulate synchrony in the Parkinsonian basal ganglia?

“…Indeed, Fernandez-Suarez et al [2012] reported prominent cell death of PV-positive GABAergic GPe neurons, commonly projecting to STN and GPi, in 6-OHDA treated rats and in MPTP treated monkeys. In contrast, an earlier study by Hardman and Halliday [1999] did not describe abnormalities in the total number of PV-positive GPe neurons in PD patients. However, when considering cell density rather than absolute cell counts, death of GPe neurons is also possible here as seen in a trend towards a decrease of PVpositive neuron density [Fernandez-Suarez et al, 2012].…”

Regional brain atrophy in progressive supranuclear palsy and Lewy body disease

“…In particular, pallidal atrophy has been previously reported, 23 and neurofibrillary tangles, neuropil threads, and neurodegeneration are consistently observed in the pallidosubthalamic complex and substantia nigra. 7,12,15,[25][26][27] Our results suggest that there is a reduction in the density of neurofibrillary tangles with ongoing atrophy subcortically. 28 This contrasts with increasing cortical tangle pathology that occurs with atrophic progression in PSP.…”

Cell-specific pallidal intervention induces long-lasting motor recovery in dopamine-depleted mice

“…These results reconcile a number of conflicting reports in the literature: that successful DBS can either increase or decrease firing rates of GPe neurons 37 – 40 , that DBS directly in the GPe can reduce bradykinesia 27 , 41 but restoring autonomous firing after DD has no effect 42 . Finally, because the proportion of PV-GPe neurons in humans is similar to that in mice 43 , our results suggest that interventions that preferentially increase their activity relative to other GPe neurons might provide more persistent prokinetic benefits than current treatments.…”

Do gap junctions regulate synchrony in the Parkinsonian basal ganglia?

“…Indeed, Fernandez-Suarez et al [2012] reported prominent cell death of PV-positive GABAergic GPe neurons, commonly projecting to STN and GPi, in 6-OHDA treated rats and in MPTP treated monkeys. In contrast, an earlier study by Hardman and Halliday [1999] did not describe abnormalities in the total number of PV-positive GPe neurons in PD patients. However, when considering cell density rather than absolute cell counts, death of GPe neurons is also possible here as seen in a trend towards a decrease of PVpositive neuron density [Fernandez-Suarez et al, 2012].…”

Regional brain atrophy in progressive supranuclear palsy and Lewy body disease

“…In particular, pallidal atrophy has been previously reported, 23 and neurofibrillary tangles, neuropil threads, and neurodegeneration are consistently observed in the pallidosubthalamic complex and substantia nigra. 7,12,15,[25][26][27] Our results suggest that there is a reduction in the density of neurofibrillary tangles with ongoing atrophy subcortically. 28 This contrasts with increasing cortical tangle pathology that occurs with atrophic progression in PSP.…”

Cell-specific pallidal intervention induces long-lasting motor recovery in dopamine-depleted mice

“…These results reconcile a number of conflicting reports in the literature: that successful DBS can either increase or decrease firing rates of GPe neurons 37 – 40 , that DBS directly in the GPe can reduce bradykinesia 27 , 41 but restoring autonomous firing after DD has no effect 42 . Finally, because the proportion of PV-GPe neurons in humans is similar to that in mice 43 , our results suggest that interventions that preferentially increase their activity relative to other GPe neurons might provide more persistent prokinetic benefits than current treatments.…”