Coherence of neuronal firing of the entopeduncular nucleus with motor cortex oscillatory activity in the 6-OHDA rat model of Parkinson’s disease with levodopa-induced dyskinesias

2016 ◽  
Vol 234 (4) ◽  
pp. 1105-1118 ◽  
Author(s):  
Xingxing Jin ◽  
Kerstin Schwabe ◽  
Joachim K. Krauss ◽  
Mesbah Alam
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Cortex ◽  
Rat Model ◽  
Neuronal Firing ◽  
Oscillatory Activity ◽  
Entopeduncular Nucleus

scholarly journals Neuronal Entropy-Rate Feature of Entopeduncular Nucleus in Rat Model of Parkinson’s Disease

2016 ◽  
Vol 26 (02) ◽  
pp. 1550038 ◽  
Author(s):  
Olivier Darbin ◽  
Xingxing Jin ◽  
Christof Von Wrangel ◽  
Kerstin Schwabe ◽  
Atsushi Nambu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Normal Condition ◽  
Rat Model ◽  
Neuronal Firing ◽  
Entopeduncular Nucleus ◽  
Motor Processing ◽  
Firing Rates ◽  
Sensory Motor

The function of the nigro-striatal pathway on neuronal entropy in the basal ganglia (BG) output nucleus, i.e. the entopeduncular nucleus (EPN) was investigated in the unilaterally 6-hyroxydopamine (6-OHDA)-lesioned rat model of Parkinson’s disease (PD). In both control subjects and subjects with 6-OHDA lesion of dopamine (DA) the nigro-striatal pathway, a histological hallmark for parkinsonism, neuronal entropy in EPN was maximal in neurons with firing rates ranging between 15 and 25[Formula: see text]Hz. In 6-OHDA lesioned rats, neuronal entropy in the EPN was specifically higher in neurons with firing rates above 25[Formula: see text]Hz. Our data establishes that the nigro-striatal pathway controls neuronal entropy in motor circuitry and that the parkinsonian condition is associated with abnormal relationship between firing rate and neuronal entropy in BG output nuclei. The neuronal firing rates and entropy relationship provide putative relevant electrophysiological information to investigate the sensory-motor processing in normal condition and conditions such as movement disorders.

scholarly journals Oscillatory activity in basal ganglia and motor cortex in an awake behaving rodent model of Parkinson's disease

Basal Ganglia ◽  
2014 ◽  
Vol 3 (4) ◽  
pp. 221-227 ◽  
Author(s):  
Claire Delaville ◽  
Ana V. Cruz ◽  
Alex J. McCoy ◽  
Elena Brazhnik ◽  
Irene Avila ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Motor Cortex ◽  
Rodent Model ◽  
Oscillatory Activity

scholarly journals Pallidal Thermolesion Unleashes Gamma Oscillations in the Motor Cortex in Parkinson's Disease

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Doris D Wang ◽  
Coralie de Hemptinne ◽  
Svjetlana Miocinovic ◽  
Witney Chen ◽  
Jill L Ostrem ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Cortex ◽  
Essential Tremor ◽  
Primary Motor Cortex ◽  
Gamma Oscillations ◽  
Gamma Band ◽  
Motor Dysfunction ◽  
Oscillatory Activity ◽  
Motor Network

Abstract INTRODUCTION In Parkinson's disease, the emergence of motor dysfunction is thought to be related to an imbalance between antikinetic and prokinetic patterns of oscillatory activity in the motor network. Invasive recordings from the basal ganglia and cortex in surgical patients have suggested that levodopa and therapeutic deep brain stimulation can suppress antikinetic beta band (13-30 Hz) rhythms while promoting prokinetic gamma band (60-90 Hz) rhythms. Surgical ablation of the globus pallidus internus is one of the oldest effective therapies for Parkinson's disease and gives a remarkable immediate relief from rigidity and bradykinesia, but its effects on oscillatory activity in the motor network have not been studied. We characterize the effects of pallidotomy on cortical oscillatory activity in Parkinson's disease patients. METHODS Using a temporary 6-contact lead placed over the sensorimotor cortex in the subdural space, we recorded acute changes in cortical oscillatory activities in 3 Parkinson's disease patients undergoing pallidotomy and compared the results to that of 3 essential tremor patients undergoing thalamotomy. RESULTS In all 3 Parkinson's disease patients, we observed the emergence of an approximately 70 to 80 Hz narrow-band oscillation with effective thermolesion of the pallidum. This gamma oscillatory activity was spatially localized over the primary motor cortex, was minimally affected by voluntary movements, and was not found in the motor cortex of essential tremor patients undergoing thalamotomy. CONCLUSION Our finding suggests that acute lesioning of the pallidum promotes cortical gamma band oscillations. This may represent an important mechanism for alleviating bradykinesia in Parkinson's disease.

Increased Gamma Oscillatory Activity in the Subthalamic Nucleus During Tremor in Parkinson's Disease Patients

2009 ◽  
Vol 101 (2) ◽  
pp. 789-802 ◽  
Author(s):  
M. Weinberger ◽  
W. D. Hutchison ◽  
A. M. Lozano ◽  
M. Hodaie ◽  
J. O. Dostrovsky
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Subthalamic Nucleus ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Neuronal Firing ◽  
Oscillatory Activity ◽  
Frequency Range ◽  
Resting Tremor ◽  
Gamma Frequency

Rest tremor is one of the main symptoms in Parkinson's disease (PD), although in contrast to rigidity and akinesia, the severity of the tremor does not correlate well with the degree of dopamine deficiency or the progression of the disease. Studies suggest that akinesia in PD patients is related to abnormal increased beta (15–30 Hz) and decreased gamma (35–80 Hz) synchronous oscillatory activity in the basal ganglia. Here we investigated the dynamics of oscillatory activity in the subthalamic nucleus (STN) during tremor. We used two adjacent microelectrodes to simultaneously record neuronal firing and local field potential (LFP) activity in nine PD patients who exhibited resting tremor during functional neurosurgery. We found that neurons exhibiting oscillatory activity at tremor frequency are located in the dorsal region of STN, where neurons with beta oscillatory activity are observed, and that their activity is coherent with LFP oscillations in the beta frequency range. Interestingly, in 85% of the 58 sites examined, the LFP exhibited increased oscillatory activity in the low gamma frequency range (35–55 Hz) during periods with stronger tremor. Furthermore, in 17 of 26 cases where two LFPs were recorded simultaneously, their coherence in the gamma range increased with increased tremor. When averaged across subjects, the ratio of the beta to gamma coherence was significantly lower in periods with stronger tremor compared with periods of no or weak tremor. These results suggest that resting tremor in PD is associated with an altered balance between beta and gamma oscillations in the motor circuits of STN.

scholarly journals Motor Cortex Stimulation Reversed Hypernociception, Increased Serotonin in Raphe Neurons, and Caused Inhibition of Spinal Astrocytes in a Parkinson’s Disease Rat Model

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1158
Author(s):  
Ana Carolina P. Campos ◽  
Miriã B. Berzuíno ◽  
Gabriela R. Barbosa ◽  
Helena M. R. C. Freire ◽  
Patricia S. Lopes ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Spinal Cord ◽  
Parkinson's Disease ◽  
Motor Cortex ◽  
Rat Model ◽  
Analgesic Efficacy ◽  
Persistent Pain ◽  
Motor Cortex Stimulation ◽  
Spinal Neurons ◽  
Nociceptive Responses

Persistent pain is a prevalent symptom of Parkinson’s disease (PD), which is related to the loss of monoamines and neuroinflammation. Motor cortex stimulation (MCS) inhibits persistent pain by activating the descending analgesic pathways; however, its effectiveness in the control of PD-induced pain remains unclear. Here, we evaluated the analgesic efficacy of MCS together with serotonergic and spinal glial modulation in an experimental PD (ePD) rat model. Wistar rats with unilateral striatal 6-OHDA and MCS were assessed for behavioral immobility and nociceptive responses. The immunoreactivity of dopamine in the substantia nigra and serotonin in the nucleus raphe magnus (NRM) and the neuronal, astrocytic, and microglial activation in the dorsal horn of the spinal cord were evaluated. MCS, without interfering with dopamine loss, reversed ePD-induced immobility and hypernociception. This response was accompanied by an exacerbated increase in serotonin in the NRM and a decrease in neuronal and astrocytic hyperactivation in the spinal cord, without inhibiting ePD-induced microglial hypertrophy and hyperplasia. Taken together, MCS induces analgesia in the ePD model, while restores the descending serotonergic pathway with consequent inhibition of spinal neurons and astrocytes, showing the role of MCS in PD-induced pain control.

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