Local field potential dynamics in the primate cortex in relation to parkinsonism reveled by machine learning: A comparison between the primary motor cortex and the supplementary area

2020 ◽  
Vol 156 ◽  
pp. 66-79 ◽  
Author(s):  
Olivier Darbin ◽  
Nobuhiko Hatanaka ◽  
Sayuki Takara ◽  
Masaya Kaneko ◽  
Satomi Chiken ◽  
...  
2019 ◽  
Author(s):  
David T. Bundy ◽  
David J Guggenmos ◽  
Maxwell D Murphy ◽  
Randolph J. Nudo

AbstractFollowing injury to motor cortex, reorganization occurs throughout spared brain regions and is thought to underlie motor recovery. Unfortunately, the standard neurophysiological and neuroanatomical measures of post-lesion plasticity are only indirectly related to observed changes in motor execution. While substantial task-related neural activity has been observed during motor tasks in rodent primary motor cortex and premotor cortex, the long-term stability of these responses in healthy rats is uncertain, limiting the interpretability of longitudinal changes in the specific patterns of neural activity during motor recovery following injury. This study examined the stability of task-related neural activity associated with execution of reaching movements in healthy rodents. Rats were trained to perform a novel reaching task combining a ‘gross’ lever press and a ‘fine’ pellet retrieval. In each animal, two chronic microelectrode arrays were implanted in motor cortex spanning the caudal forelimb area (rodent primary motor cortex) and the rostral forelimb area (rodent premotor cortex). We recorded multiunit spiking and local field potential activity from 10 days to 7-10 weeks post-implantation to characterize the patterns of neural activity observed during each task component and analyzed the consistency of channel-specific task-related neural activity. Task-related changes in neural activity were observed on the majority of channels. While the task-related changes in multi-unit spiking and local field potential spectral power were consistent over several weeks, spectral power changes were more stable, despite the trade-off of decreased spatial and temporal resolution. These results show that rodent primary and premotor cortex are both involved in reaching movements with stable patterns of task-related activity across time, establishing the relevance of the rodent for future studies designed to examine changes in task-related neural activity during recovery from focal cortical lesions.


2019 ◽  
Vol 122 (6) ◽  
pp. 2621-2629
Author(s):  
Ana María Estrada-Sánchez ◽  
Courtney L. Blake ◽  
Scott J. Barton ◽  
Andrew G. Howe ◽  
George V. Rebec

Abnormal communication between cerebral cortex and striatum plays a major role in the motor symptoms of Huntington’s disease (HD), a neurodegenerative disorder caused by a mutation of the huntingtin gene ( mHTT). Because cortex is the main driver of striatal processing, we recorded local field potential (LFP) activity simultaneously in primary motor cortex (M1) and dorsal striatum (DS) in BACHD mice, a full-length HD gene model, and in a conditional BACHD/Emx-1 Cre (BE) model in which mHTT is suppressed in cortical efferents, while mice freely explored a plus-shaped maze beginning at 20 wk of age. Relative to wild-type (WT) controls, BACHD mice were just as active across >40 wk of testing but became progressively less likely to turn into a perpendicular arm as they approached the choice point of the maze, a sign of HD motor inflexibility. BE mice, in contrast, turned as freely as WT throughout testing. Although BE mice did not exactly match WT in LFP activity, the reduction in alpha (8–13 Hz), beta (13–30 Hz), and low-gamma (30–50 Hz) power that occurred in M1 of turning-impaired BACHD mice was reversed. No reversal occurred in DS. In fact, BE mice showed further reductions in DS theta (4–8 Hz), beta, and low-gamma power relative to the BACHD model. Coherence analysis indicated a dysregulation of corticostriatal information flow in both BACHD and BE mice. Collectively, our results suggest that mHTT in cortical outputs drives the dysregulation of select cortical frequencies that accompany the loss of behavioral flexibility in HD. NEW & NOTEWORTHY BACHD mice, a full-length genetic model of Huntington’s disease (HD), express aberrant local field potential (LFP) activity in primary motor cortex (M1) along with decreased probability of turning into a perpendicular arm of a plus-shaped maze, a motor inflexibility phenotype. Suppression of the mutant huntingtin gene in cortical output neurons prevents decline in turning and improves alpha, beta, and low-gamma activity in M1. Our results implicate cortical networks in the search for therapeutic strategies to alleviate HD motor signs.


2018 ◽  
Vol 12 ◽  
Author(s):  
Gonzalo Martín-Vázquez ◽  
Toshitake Asabuki ◽  
Yoshikazu Isomura ◽  
Tomoki Fukai

1998 ◽  
Vol 79 (1) ◽  
pp. 159-173 ◽  
Author(s):  
John P. Donoghue ◽  
Jerome N. Sanes ◽  
Nicholas G. Hatsopoulos ◽  
Gyöngyi Gaál

Donoghue, John P., Jerome N. Sanes, Nicholas G. Hatsopoulos, and Gyöngyi Gaál. Neural discharge and local field potential oscillations in primate motor cortex during voluntary movements. J. Neurophysiol. 79: 159–173, 1998. The role of “fast,” or gamma band (20–80 Hz), local field potential (LFP) oscillations in representing neuronal activity and in encoding motor behavior was examined in motor cortex of two alert monkeys. Using chronically implanted microwires, we simultaneously recorded LFPs and single or multiple unit (MU) discharge at a group of sites in the precentral gyrus during trained finger force or reaching movements, during natural reaching and grasping, and during quiet sitting. We evaluated the coupling of oscillations with task-related firing at the same site, the timing of oscillations with respect to the execution of trained and untrained movement, and the temporal synchrony of oscillations across motor cortical sites. LFPs and neural discharge were examined from a total of 16 arm sites (7 sites in 1 monkey and 9 in the other), each showing movement-related discharge modulation and arm microstimulation effects. In the trained tasks, fast LFP and MU oscillations occurred most often during a premovement delay period, ceasing around movement onset. The decrease in oscillation roughly coincided with the appearance of firing rate modulation coupled to the motor action. During this delay, LFP oscillations exhibited either “overlapping” or “mixed” relationships with the simultaneously recorded neural discharge at that site. Overlap was characterized by coincident epochs of increased neural discharge and LFP oscillations. For the mixed pattern, episodes of LFP oscillation typically coincided with periods of diminished firing but overlap also sometimes appeared. Both patterns occurred concurrently across motor cortex during preparation; LFP suppression with motor action was ubiquitous. Fast oscillations reappeared quickly upon transition from quiet sitting to resumption of task performance, indicating an association with task engagement, rather than the general motor inaction of the delay period. In contrast to trained movements, fast oscillations often appeared along with movement during untrained reaching, but oscillations occurred erratically and were not reliably correlated with elevated neural discharge. Synchronous oscillations occurred at sites as much as 5 mm apart, suggesting widespread coupling of neurons and LFP signals in motor cortex. Widespread coupling of oscillatory signals is consistent with the concept that temporal coding processes operate in motor cortex. However, because the relationship between neuronal discharge and the appearance of fast oscillations may be altered by behavioral condition, they must reflect a global process active in conjunction with motor planning or preparatory functions, but not details of motor action encoded in neuronal firing rate.


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