#Force plate actimeter series#

Although the preferred treatment for ET is pharmacology based, medications for ET may decrease in efficacy over time or not be efficacious ( Chopra et al., 2013). ET is characterized by a positional and/or volitional 4- to 12-Hz tremor that can affect all body parts ( Marshall, 1962) and affects nearly 1% of the worldвЂ™s population, increasing to 4% of those over age 40 ( MГјller et al., 2016).

As specific neuronal firing patterns like oscillation or burst are considered important for information processing, our results suggest that VL thalamic DBS may modify pathophysiologic relay information rather than simply inhibit the information transmission.Д®ssential tremor (ET) is a neurological condition that causes shaking or rhythmic motion in body parts. Four activity patterns вЂ“ including oscillatory burst, oscillatory non-burst, irregular burst, and irregular non-burst вЂ“ were identified by harmaline administration and those firing patterns were differentially affected by VL thalamic DBS, which seems to drive pathologic cortical signals to signals in normal status. To examine this, we measured single-unit neuronal activities in the resting state in M1 during VL thalamic DBS in harmaline-induced tremor rats and analyzed neuronal activity patterns in the thalamo-cortical circuit. As the motor thalamus is the most popular DBS target for ET, and it is known that the thalamic nucleus plays a key role in relaying information about the external environment to the cerebral cortex, it is important to investigate mechanisms of thalamic DBS in the context of the cerebello-thalamo-cortical neuronal network.

2Department of Neurologic Surgery, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, United StatesДЄlthough deep brain stimulation (DBS) is a clinically effective surgical treatment for essential tremor (ET), and its neurophysiological mechanisms are not fully understood.

1Laboratory of Brain & Cognitive Sciences for Convergence Medicine, College of Medicine, Hallym University, Anyang, South Korea.

These results show that inhibition of GD3S has neuroprotective properties in the MPTP model and may warrant further investigation as a therapeutic target. Stereological counts of Nissl-positive SNc neurons that did not express TH suggest that neuroprotection was complete but TH expression was suppressed in some cells. In contrast, lesion size was only 22.5% in GD3S-/- mice and striatal dopamine was reduced by 37.2%. In wild-type mice, MPTP destroyed 53% of the tyrosine-hydroxylase (TH)-positive neurons in the substantia nigra pars compacta (SNc) and reduced striatal dopamine 60.7%. More sensitive measuresВ -В such as the force-plate actimeter and treadmill gait parametersВ -В detected subtle effects of MPTP, some of which were absent in mice lacking GD3S. The typical battery of tests used to assess parkinsonism failed to detect deficits in MPTP-treated mice.

#Force plate actimeter series#

MPTP was administered to GD3S-/- mice or controls using a subchronic regimen consisting of three series of low-dose injections (11вЂ‰mg/kg/dayвЂ‰Г—вЂ‰5вЂ‰days each, 3вЂ‰weeks apart), and motor function was assessed after each. In this study, we investigated the effects of GD3S deletion on parkinsonism induced by 1-methyl-4phenyl-1,2,3,6-tetrahydropyridine (MPTP). We have shown that interventions that simultaneously increase the neuroprotective GM1 ganglioside and decrease the pro-apoptotic GD3 gangliosideВ -В such as inhibition of GD3 synthase (GD3S) or administration of sialidaseВ -В are neuroprotective in vitro and in a number of preclinical models. Converging evidence implicates gangliosides in the pathogenesis of several neurodegenerative diseases, suggesting a potential new class of therapeutic targets. Parkinson's disease is a debilitating neurodegenerative condition for which there is no cure.