Stimulation of the Subthalamic Nucleus Changes the Firing Pattern of Pallidal Neurons

By T. Hashimoto, Christopher M. Elder, M. Okun, S. K. Patrick, J. Vitek. Journal of Neuroscience, 2003

919 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/baf35a37423240e58ad5d3eda9d745dd66f60a49

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Citations in the corpus

The subthalamic nucleus in the context of movement disorders. (2004, background): “In non-human MPTP primates, high frequency stimulation of the STN at therapeutic levels drove GPi (from an average of 63.2 to 81.7 Hz) and GPe (from an average of 50.4 to 65.4 Hz) activity (Hashimoto et al., 2003).”
High Frequency Stimulation of the Subthalamic Nucleus Eliminates Pathological Thalamic Rhythmicity in a Computational Model (2004, methodology): “We model GPi neurons very similarly to GPe neurons, using a voltage equation of the form (4) but with Ge replaced with Gi; however, we renormalize certain parameters to reflect the fact that GPi neurons fire faster than GPe (DeLong, 1971; Filion and Tremblay, 1991; Raz et al., 2000; Hashimoto et al.”
Probing and regulating dysfunctional circuits using deep brain stimulation. (2013, neutral): “STN stimulation (Hashimoto et al., 2003); increased neurotransmitter”
Computational analysis of subthalamic nucleus and lenticular fasciculus activation during therapeutic deep brain stimulation. (2006, methodology): “The three STN neuron geometries, along with the GPi and CST axon trajectories, were placed within the 3D atlas in their respective anatomically realistic positions and orientations (Fig.”
Uncovering the mechanism(s) of action of deep brain stimulation: activation, inhibition, or both. (2004, methodology): “Neural recording experiments have been conducted during and after HFS to address changes in neuronal activity (Dostrovsky and Lozano, 2002; Anderson et al., 2003; Hashimoto et al., 2003).”
High-Frequency Stimulation of the Subthalamic Nucleus Suppresses Oscillatory β Activity in Patients with Parkinson's Disease in Parallel with Improvement in Motor Performance (2008, neutral): “…in the STN means that this activity is no longer propagated, or stimulation-induced high-frequency activity of STN neurons (Garcia et al., 2005) is transmitted to the output structures of the basal ganglia (Hashimoto et al., 2003; Maurice et al., 2003), where it further suppresses activity.”
Patient-specific analysis of the volume of tissue activated during deep brain stimulation (2007, background): “, 2006b) and experimental (Hashimoto et al., 2003) results suggest that therapeutic STN DBS generates an excitatory effect on axons surrounding the electrode.”
Deep brain stimulation. (2006, positive): “Using a scaled-down version of the DBS electrode used clinically, Hashimoto et al. (2003) studied the effect of low- and high-frequency STN stimulation on pallidal neuron firing in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated parkinsonian monkeys (Hashimoto et al. 2003).”
Pathological synchronization in Parkinson's disease: networks, models and treatments. (2007, background): “In other words, is DBS different from or equivalent to a lesion? In vivo studies in conditioned MPTP monkeys [ 60 ], control [61] or neuroleptic-treated rats [62] suggest that the high-frequency stimulation-driven activity of STN neurons is transmitted to GPi, GPe and SNr.”