scholarly journals Effects of repetitive transcranial magnetic and deep brain stimulation on long‐range synchrony of oscillatory activity in a rat model of developmental schizophrenia

Author(s):  
Benjamin Lippmann ◽  
Gleb Barmashenko ◽  
Klaus Funke
Epilepsia ◽  
2021 ◽  
Author(s):  
Barbora Deutschová ◽  
Petr Klimeš ◽  
Zsofia Jordan ◽  
Pavel Jurák ◽  
Lorand Erőss ◽  
...  

2019 ◽  
pp. 1222-18 ◽  
Author(s):  
Elise Gondard ◽  
Lucy Teves ◽  
Lihua Wang ◽  
Chris McKinnon ◽  
Clement Hamani ◽  
...  

2014 ◽  
Vol 111 (10) ◽  
pp. 1949-1959 ◽  
Author(s):  
Alan D. Dorval ◽  
Warren M. Grill

Pathophysiological activity of basal ganglia neurons accompanies the motor symptoms of Parkinson's disease. High-frequency (>90 Hz) deep brain stimulation (DBS) reduces parkinsonian symptoms, but the mechanisms remain unclear. We hypothesize that parkinsonism-associated electrophysiological changes constitute an increase in neuronal firing pattern disorder and a concomitant decrease in information transmission through the ventral basal ganglia, and that effective DBS alleviates symptoms by decreasing neuronal disorder while simultaneously increasing information transfer through the same regions. We tested these hypotheses in the freely behaving, 6-hydroxydopamine-lesioned rat model of hemiparkinsonism. Following the onset of parkinsonism, mean neuronal firing rates were unchanged, despite a significant increase in firing pattern disorder (i.e., neuronal entropy), in both the globus pallidus and substantia nigra pars reticulata. This increase in neuronal entropy was reversed by symptom-alleviating DBS. Whereas increases in signal entropy are most commonly indicative of similar increases in information transmission, directed information through both regions was substantially reduced (>70%) following the onset of parkinsonism. Again, this decrease in information transmission was partially reversed by DBS. Together, these results suggest that the parkinsonian basal ganglia are rife with entropic activity and incapable of functional information transmission. Furthermore, they indicate that symptom-alleviating DBS works by lowering the entropic noise floor, enabling more information-rich signal propagation. In this view, the symptoms of parkinsonism may be more a default mode, normally overridden by healthy basal ganglia information. When that information is abolished by parkinsonian pathophysiology, hypokinetic symptoms emerge.


2013 ◽  
Vol 6 (6) ◽  
pp. 837-844 ◽  
Author(s):  
David A. Stidd ◽  
Kimberly Vogelsang ◽  
Scott E. Krahl ◽  
Jean-Philippe Langevin ◽  
Jean-Marc Fellous

2019 ◽  
Vol 92 ◽  
pp. 269-275
Author(s):  
Milaine Roet ◽  
Sylvana Pol ◽  
Frédéric L.W.V.J. Schaper ◽  
Govert Hoogland ◽  
Ali Jahanshahi ◽  
...  

2016 ◽  
Vol 115 (1) ◽  
pp. 19-38 ◽  
Author(s):  
Todd M. Herrington ◽  
Jennifer J. Cheng ◽  
Emad N. Eskandar

Deep brain stimulation (DBS) is widely used for the treatment of movement disorders including Parkinson's disease, essential tremor, and dystonia and, to a lesser extent, certain treatment-resistant neuropsychiatric disorders including obsessive-compulsive disorder. Rather than a single unifying mechanism, DBS likely acts via several, nonexclusive mechanisms including local and network-wide electrical and neurochemical effects of stimulation, modulation of oscillatory activity, synaptic plasticity, and, potentially, neuroprotection and neurogenesis. These different mechanisms vary in importance depending on the condition being treated and the target being stimulated. Here we review each of these in turn and illustrate how an understanding of these mechanisms is inspiring next-generation approaches to DBS.


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