Prelimbic Cortex Deep Brain Stimulation Reduces Binge Size in a Chronic Binge Eating Rat Model

2018 ◽  
Vol 96 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Can Sarica ◽  
Mazhar Ozkan ◽  
Husniye Hacioglu Bay ◽  
Umit Sehirli ◽  
Filiz Onat ◽  
...  
2018 ◽  
Vol 9 ◽  
Author(s):  
Wilder T. Doucette ◽  
Lucas Dwiel ◽  
Jared E. Boyce ◽  
Amanda A. Simon ◽  
Jibran Y. Khokhar ◽  
...  

2015 ◽  
Vol 5 (12) ◽  
pp. e695-e695 ◽  
Author(s):  
W T Doucette ◽  
J Y Khokhar ◽  
A I Green

2018 ◽  
Author(s):  
Wilder T. Doucette ◽  
Lucas Dwiel ◽  
Jared E. Boyce ◽  
Amanda A. Simon ◽  
Jibran Y. Khokhar ◽  
...  

AbstractNeuromodulation-based interventions continue to be evaluated across an array of appetitive disorders but broader implementation of these approaches remains limited due to variable treatment outcomes. We hypothesize that individual variation in treatment outcomes may be linked to differences in the networks underlying these disorders. Here, Sprague-Dawley rats received deep brain stimulation separately within each nucleus accumbens (NAc) sub-region (core and shell) using a within-animal crossover design in a rat model of binge eating. Significant reductions in binge size were observed with stimulation of either target but with significant variation in effectiveness across individuals. When features of local field potentials (LFPs) recorded from the NAc were used as predictors of the pre-defined stimulation outcomes (response or non-response) from each rat using a machine-learning approach (lasso), stimulation outcomes could be predicted with greater accuracy than expected by chance (effect sizes: core = 1.13, shell = 1.05). Further, these LFP features could be used to identify the best stimulation target for each animal (core vs. shell) with an effect size = 0.96. These data suggest that individual differences in underlying network activity may contribute to the variable outcomes of circuit based interventions and that measures of network activity have the potential to individually guide the selection of an optimal stimulation target and improve overall treatment response rates.


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 ◽  
...  

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