scholarly journals Polysynaptic regulation of glutamate receptors and mitochondrial enzyme activities in the basal ganglia of rats with unilateral dopamine depletion

1994 ◽  
Vol 14 (11) ◽  
pp. 7192-7199 ◽  
Author(s):  
RH Porter ◽  
JG Greene ◽  
DS Higgins ◽  
JT Greenamyre
Keyword(s):  
Basal Ganglia ◽  
Glutamate Receptors ◽  
Enzyme Activities ◽  
Mitochondrial Enzyme ◽  
Dopamine Depletion

Dynamic Changes in the Cortex-Basal Ganglia Network After Dopamine Depletion in the Rat

2008 ◽  
Vol 100 (1) ◽  
pp. 385-396 ◽  
Author(s):  
Cyril Dejean ◽  
Christian E. Gross ◽  
Bernard Bioulac ◽  
Thomas Boraud
Keyword(s):  
Basal Ganglia ◽  
Local Field ◽  
Signal Transmission ◽  
Local Field Potentials ◽  
Cellular Level ◽  
Cortical Activation ◽  
Field Potentials ◽  
Dopamine Depletion ◽  
Indirect Pathway ◽  
Before And After

It is well established that parkinsonian syndrome is associated with alterations in the temporal pattern of neuronal activity and local field potentials in the basal ganglia (BG). An increase in synchronized oscillations has been observed in different BG nuclei in parkinsonian patients and animal models of this disease. However, the mechanisms underlying this phenomenon remain unclear. This study investigates the functional connectivity in the cortex-BG network of a rodent model of Parkinson's disease. Single neurons and local field potentials were simultaneously recorded in the motor cortex, the striatum, and the substantia nigra pars reticulata (SNr) of freely moving rats, and high-voltage spindles (HVSs) were used to compare signal transmission before and after dopaminergic depletion. It is shown that dopaminergic lesion results in a significant enhancement of oscillatory synchronization in the BG: the coherence between pairs of structures increased significantly and the percentage of oscillatory auto- and cross-correlograms. HVS episodes were also more numerous and longer. These changes were associated with a shortening of the latency of SNr response to cortical activation, from 40.5 ± 4.8 to 10.2 ± 1.07 ms. This result suggests that, in normal conditions, SNr neurons are likely to be driven by late inputs from the indirect pathway; however, after the lesion, their shorter latency also indicates an overactivation of the hyperdirect pathway. This study confirms that neuronal signal transmission is altered in the BG after dopamine depletion but also provides qualitative evidence for these changes at the cellular level.

Stretch-induced growth in chicken wing muscles: a new model of stretch hypertrophy

1980 ◽  
Vol 238 (1) ◽  
pp. C62-C71 ◽  
Author(s):  
R. G. Holly ◽  
J. G. Barnett ◽  
C. R. Ashmore ◽  
R. G. Taylor ◽  
P. A. Mole
Keyword(s):  
Cross Section ◽  
Muscle Activity ◽  
Enzyme Activities ◽  
Latissimus Dorsi ◽  
Capillary Density ◽  
Oxidative Enzyme ◽  
Longitudinal Growth ◽  
Mitochondrial Enzyme ◽  
New Model ◽  
Anterior Latissimus Dorsi

A new model of stretch-induced growth is evaluated in four chicken wing muscles stretched to different extents by a spring-loaded tubular assembly. Muscles grew in length and cross section in proportion to the extent to which they were stretched. Longitudinal growth was essentially completed within 1 wk, while muscles grew in cross section through at least 5 wk of stretch. The muscles were neither denervated nor immobilized, and muscle activity as measured by EMG was not increased. Oxidative enzyme activities increased substantially with stretch in the patagialis (PAT), a twitch muscle, but were relatively unchanged in the slow-tonic anterior latissimus dorsi (ALD). Stretch altered mitochondrial enzyme proportions in the PAT, but had little effect in the ALD. Capillary density was unchanged with stretch in the PAT, but decreased in the ALD. Capillary density was unchanged with stretch in the PAT, but decreased in the ALD. Capillary-to-fiber ratio, however, increased in both muscles. We conclude that muscles grow and adapt enzymatically due to stretch, but that these responses are dissimilar in twitch and tonic muscles.

scholarly journals Changes in excitability properties of ventromedial motor thalamic neurons in 6-OHDA lesioned mice

2020 ◽  
Author(s):  
Edyta K Bichler ◽  
Francesco Cavarretta ◽  
Dieter Jaeger
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Potassium Current ◽  
Cellular Level ◽  
Inhibitory Input ◽  
Dopamine Depletion ◽  
Thalamic Nuclei ◽  
Adult Mice ◽  
Motor Thalamus

AbstractThe activity of basal ganglia input receiving motor thalamus (BGMT) makes a critical impact on motor cortical processing, but modification in BGMT processing with Parkinsonian conditions have not be investigated at the cellular level. Such changes may well be expected due to homeostatic regulation of neural excitability in the presence of altered synaptic drive with dopamine depletion. We addressed this question by comparing BGMT properties in brain slice recordings between control and unilaterally 6-OHDA treated adult mice. At a minimum of 1 month post 6-OHDA treatment, BGMT neurons showed a highly significant increase in intrinsic excitability, which was primarily due to a decrease in M-type potassium current. BGMT neurons after 6-OHDA treatment also showed an increase in T-type calcium rebound spikes following hyperpolarizing current steps. Biophysical computer modeling of a thalamic neuron demonstrated that an increase in rebound spiking can also be accounted for by a decrease in the M-type potassium current. Modeling also showed that an increase in sag with hyperpolarizing steps found after 6-OHDA treatment could in part but not fully be accounted for by the decrease in M-type current. These findings support the hypothesis that homeostatic changes in BGMT neural properties following 6-OHDA treatment likely influence the signal processing taking place in basal ganglia thalamocortical processing in Parkinson’s disease.Significance StatementOur investigation of the excitability properties of neurons in the basal ganglia input receiving motor thalamus (BGMT) is significant because they are likely to be different from properties in other thalamic nuclei due to the additional inhibitory input stream these neurons receive. Further, they are important to understand the role of BGMT in the dynamic dysfunction of cortico – basal ganglia circuits in Parkinson’s disease. We provide clear evidence that after 6-OHDA treatment of mice important homeostatic changes occur in the intrinsic properties of BGMT neurons. Specifically we identify the M-type potassium current as an important thalamic excitability regulator in the parkinsonian state.

scholarly journals Effects of Dopamine Depletion on Network Entropy in the External Globus Pallidus

2009 ◽  
Vol 102 (2) ◽  
pp. 1092-1102 ◽  
Author(s):  
Ana V. Cruz ◽  
Nicolas Mallet ◽  
Peter J. Magill ◽  
Peter Brown ◽  
Bruno B. Averbeck
Keyword(s):  
Basal Ganglia ◽  
Globus Pallidus ◽  
Dopamine Depletion ◽  
Information Coding ◽  
Logistic Regression Models ◽  
Firing Rates ◽  
Before And After ◽  
Network Entropy ◽  
Coding Capacity

Dopamine depletion in cortical-basal ganglia circuits in Parkinson's disease (PD) grossly disturbs movement and cognition. Classic models relate Parkinsonian dysfunction to changes in firing rates of basal ganglia neurons. However, disturbances in other dynamics of neural activity are also common. Taking both inappropriate firing rates and other dynamics into account and determining how changes in the properties of these neural circuits that occur during PD impact on information coding are thus imperative. Here, we examined in vivo network dynamics in the external globus pallidus (GPe) of rats before and after chronic dopamine depletion. Dopamine depletion led to decreases in the firing rates of GPe neurons and increases in synchronized network oscillations in the β frequency (13–30 Hz) band. Using logistic regression models, we determined the combined and separate impacts of these factors on network entropy, a measure of the upper bound of information coding capacity. Importantly, changes in these features in dopamine-depleted rats led to a significant decrease in GPe network entropy. Changes in firing rates had the largest impact on entropy, with changes in synchrony also decreasing entropy at the network level. Changes in autocorrelations tended to offset these effects because autocorrelations decreased entropy more in the control animals. Thus it is possible that reduced information coding capacity within basal ganglia networks may contribute to the behavioral deficits accompanying PD.

Abstract WP153: Post-Stroke Physical Exercise Improves Cognition in Middle-Aged Female Rats

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Sharnikha Saravanan ◽  
Weizhao Zhao ◽  
Kunjan R Dave ◽  
Miguel A Perez-Pinzon ◽  
Ami P Raval
Keyword(s):  
Enzyme Activity ◽  
Physical Exercise ◽  
Cognitive Decline ◽  
Fear Conditioning ◽  
Enzyme Activities ◽  
Female Rats ◽  
Male Rats ◽  
Mitochondrial Enzyme ◽  
Post Stroke ◽  
Activity Measurements

Background: A woman’s risk of a stroke increases exponentially following the onset of menopause, andpost-stroke cognitive decline is a significant consequence of stroke survivors. Our earlier study demonstrated that physical exercise (PE) reduced post-stroke brain injury and improved cognitive functions in male rats. The focus of our study is on the improvement of post-stroke cognitive function in female rats. Methods: Reproductively senescent Sprague-Dawley female rats were exposed to transient middle cerebral artery occlusion (tMCAO; 90 min) and randomly assigned to either PE or sham-PE groups. After 3-5 days, rats underwent sham-PE (0m/min speed) or PE (15m/min speed) for 30 mins either every day (continuous) or alternate day for five times on treadmill. The rats that underwent the alternate day paradigm were treated with ER-β agonist (DPN; 1mg/kg) or vehicle-DMSO immediately following PE/sham-PE sessions to determine the synergistic effect. Twenty-one days after the last PE/sham-PE, rats were tested for hippocampal-dependent contextual fear conditioning and freeze time was measured. Rat brains were processed for histology and infarct area was measured with MCID software. From a separate cohort of rat subjected to PE or sham-PE, brain tissue was harvested for various biochemical assays and mitochondrial enzyme activity measurements. Results: Post-tMCAO continuous PE did not reduce ischemic damage. However, alternate PE regimen with or without ER-β agonist reduced infract volume by 20% (p < 0.05) and 23% (p < 0.05), respectively as compared to no-PE. Similarly, alternate PE showed increased freezing on the second day of fear conditioning by 15% (p < 0.05), indicating improved spatial memory. Individual mitochondrial complex I, II, III and IV enzyme activity measurements demonstrated significant improvement in complex III-IV enzyme activities in the alternate PE treated group as compared to sham-PE. Conclusion: An alternate day PE paradigm and ER-β activation improves post-stroke mitochondrial enzyme activities and cognition in reproductively senescent female rats. Future studies delineating underlying mechanism could help identify therapies to prevent/reduce cognitive decline in menopausal female stroke patients.

scholarly journals Chronic Low-Dose Methylmercury Administration Decreases Mitochondrial Enzyme Activities and Induces Myopathic Changes in Rats.

2001 ◽  
Vol 47 (2) ◽  
pp. 162-167 ◽  
Author(s):  
Fusako Usuki ◽  
Akira Yasutake ◽  
Miyuki Matsumoto ◽  
Itsuro Higuchi
Keyword(s):  
Enzyme Activities ◽  
Low Dose ◽  
Mitochondrial Enzyme ◽  
Myopathic Changes

Limb skeletal muscle adaptation in athletes after training at altitude

1990 ◽  
Vol 68 (2) ◽  
pp. 496-502 ◽  
Author(s):  
M. Mizuno ◽  
C. Juel ◽  
T. Bro-Rasmussen ◽  
E. Mygind ◽  
B. Schibye ◽  
...  
Keyword(s):  
Sea Level ◽  
Enzyme Activities ◽  
Buffer Capacity ◽  
Altitude Training ◽  
Mitochondrial Enzyme ◽  
Muscle Adaptation ◽  
Short Term ◽  
Vo2 Max ◽  
Capillary Supply ◽  
O2 Deficit

Morphological and biochemical characteristics of biopsies obtained from gastrocnemius (GAS) and triceps brachii muscle (TRI), as well as maximal O2 uptake (VO2 max) and O2 deficit, were determined in 10 well-trained cross-country skiers before and after a 2-wk stay (2,100 m above sea level) and training (2,700 m above sea level) at altitude. On return to sea level, VO2 max was the same as the prealtitude value, whereas an increase in O2 deficit (29%) and in short-term running performance (17%) was observed (P less than 0.05). GAS showed maintained capillary supply but a 10% decrease in mitochondrial enzyme activities (P less than 0.05), whereas an increase in capillary supply (P less than 0.05) but unchanged mitochondrial enzyme activities were observed in TRI. Buffer capacity was increased by 6% in both GAS and TRI (P less than 0.05). A positive correlation was found between the relative increase in buffer capacity of GAS and short-term running time (P less than 0.05). Thus the present study indicates no effect of 2 wk of altitude training on VO2 max but provides evidence to suggest an improvement in short-term exercise performance, which may be the result of an increase in muscle buffer capacity.

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