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

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.

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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

Experimental Brain Research ◽

10.1007/s00221-015-4532-1 ◽

2016 ◽

Vol 234 (4) ◽

pp. 1105-1118 ◽

Cited By ~ 9

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

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Internal Pallidal Neuronal Activity During Mild Drug-Related Dyskinesias in Parkinson's Disease: Decreased Firing Rates and Altered Firing Patterns

Journal of Neurophysiology ◽

10.1152/jn.00443.2006 ◽

2007 ◽

Vol 97 (4) ◽

pp. 2627-2641 ◽

Cited By ~ 29

Author(s):

J. I. Lee ◽

L. Verhagen Metman ◽

S. Ohara ◽

P. M. Dougherty ◽

J. H. Kim ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Firing Rate ◽

Spike Trains ◽

Neuronal Firing ◽

Low Doses ◽

Significant Group ◽

Firing Patterns ◽

Firing Rates ◽

Before And After

The neuronal basis of hyperkinetic movement disorders has long been unclear. We now test the hypothesis that changes in the firing pattern of neurons in the globus pallidus internus (GPi) are related to dyskinesias induced by low doses of apomorphine in patients with advanced Parkinson's disease (PD). During pallidotomy for advanced PD, the activity of single neurons was studied both before and after administration of apomorphine at doses just adequate to induce dyskinesias (21 neurons, 17 patients). After the apomorphine injection, these spike trains demonstrated an initial fall in firing from baseline. In nine neurons, the onset of on was simultaneous with that of dyskinesias. In these spike trains, the initial fall in firing rate preceded and was larger than the fall at the onset of on with dyskinesias. Among the three neurons in which the onset of on occurred before that of dyskinesias, the firing rate did not change at the time of onset of dyskinesias. After injection of apomorphine, dyskinesias during on with dyskinesias often fluctuated between transient periods with dyskinesias and those without. Average firing rates were not different between these two types of transient periods. Transient periods with dyskinesias were characterized by interspike interval (ISI) independence, stationary spike trains, and higher variability of ISIs. A small but significant group of neurons demonstrated recurring ISI patterns during transient periods of on with dyskinesias. These results suggest that mild dyskinesias resulting from low doses of apomorphine are related to both low GPi neuronal firing rates and altered firing patterns.

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