scholarly journals The Distinct Role of Medium Spiny Neurons and Cholinergic Interneurons in the D2/A2A Receptor Interaction in the Striatum: Implications for Parkinson's Disease

2011 ◽  
Vol 31 (5) ◽  
pp. 1850-1862 ◽  
Author(s):  
A. Tozzi ◽  
A. de Iure ◽  
M. Di Filippo ◽  
M. Tantucci ◽  
C. Costa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Receptor Interaction ◽  
Medium Spiny Neurons ◽  
Cholinergic Interneurons ◽  
Spiny Neurons ◽  
A2a Receptor ◽  
Distinct Role

Parkinsonism-like disease induced by rotenone in rats: Treatment role of curcumin, dopamine agonist and adenosine A2A receptor antagonist

2021 ◽  
Vol 14 ◽  
Author(s):  
Asmaa Fathy Aboul Naser ◽  
Wessam Magdi Aziz ◽  
Yomna Rashad Ahmed ◽  
Wagdy Khalil Bassaly Khalil ◽  
Manal Abdel Aziz Hamed
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Mediator ◽  
Adenosine A2a Receptor ◽  
Control Group ◽  
A2a Receptor ◽  
Adenosine A2a

Background: Parkinsonism is a neurodegenerative disorder that affects elderly people worldwide. Methods: Curcumin, adenosine A2AR antagonist (ZM241385) and Sinemet® (L-dopa) were evaluated against Parkinson’s disease (PD) induced by rotenone in rats and comparativelyrelatively compared with our previous study on mice model. Results: Rats injected with rotenone showed severe alterations in adenosine A2A receptor gene expression, oxidative stress markers, inflammatory mediator, energetic indices, apoptotic marker and DNA fragmentation levels as compare with the control group. Treatments with curcumin, ZM241385, and Sinemet® restored all the selected parameters. The brain histopathological features of cerebellum regions confirmed our results. By comparing our results with the previous results on mice, we noticed that mice respond to rotenone toxicity and treatments more than rats regarding to behavioral observation, A2AR gene expression, neurotransmitter levels, inflammatory mediator and apoptotic markers, while rats showed higher response to treatments regarding to oxidative stress and energetic indices. Conclusion: Curcumin succeeded to attenuate the severe effects of Parkinson’s disease in rat model and can be consider as a potential dietary supplement. Adenosine A2AR antagonist has almost the same pattern of improvement as Sinemet® and may be considered as a promising therapy against PD. By comparing the role of animal species in response to PD symptoms and treatments, our previous report on mice explore the response of mice to rotenone toxicity than rats, while rats showed higher response to treatments. Therefore, no animal model can perfectly recapitulate all the pathologies of PD.

Ultrastructure of Striatal Dopamine Synapses in Rats with Striatal Dopamine Depletion

2001 ◽  
Vol 7 (S2) ◽  
pp. 660-661
Author(s):  
W. Gray (Jay) Jerome ◽  
Thomas J. Montine ◽  
Ariel Y. Deutch
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Striatal Dopamine ◽  
Medium Spiny Neurons ◽  
Dopamine Depletion ◽  
Proximate Cause ◽  
Spiny Neurons ◽  
Neuronal Reorganization ◽  
Striatal Dopamine Depletion ◽  
6 Hydroxydopamine

Parkinson's disease (PD) is characterized by rigidity, tremor, bradykinesia, and postural instability. The proximate cause of these symptoms is striatal dopamine (DA) insufficiency. The motor symptoms of PD can be alleviated by DA replacement therapy. However, late in the course of the disease patients appear to become less responsive to DA replacement. This therapeutic change suggests the possibility of structural and/or functional defects in striatal medium spiny neurons, which receive convergent DA and cortical (glutamate) inputs.To understand the neuronal reorganization occurring in Parkinson's disease, we used ultrastructural methods to examine the striatum of rats with striatal dopaminergic deafferentation induced by unilateral intranigral injection of 6-hydroxydopamine. After a six month survival, rats were deeply anesthetized with pentobarbital and perfused with 4% paraformaldehyde-1 % glutaraldehdyde solution in 0.1M Sorenson's phosphate buffer (pH 7.4). The brains were removed, post-fixed for 12 hours, embedded in paraffin, and coronal sections cut through the striatum and midbrain.

scholarly journals On the Role of Adenosine A2A Receptor Gene Transcriptional Regulation in Parkinson’s Disease

2019 ◽  
Vol 13 ◽  
Author(s):  
Anastasia Falconi ◽  
Alessandra Bonito-Oliva ◽  
Martina Di Bartolomeo ◽  
Marcella Massimini ◽  
Francesco Fattapposta ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Transcriptional Regulation ◽  
Receptor Gene ◽  
Adenosine A2a Receptor ◽  
Gene Transcriptional Regulation ◽  
A2a Receptor ◽  
Adenosine A2a

scholarly journals Role of 5-HT1A Receptor in Vilazodone-Mediated Suppression of L-DOPA-Induced Dyskinesia and Increased Responsiveness to Cortical Input in Striatal Medium Spiny Neurons in an Animal Model of Parkinson’s Disease

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5790
Author(s):  
Feras Altwal ◽  
Fernando E. Padovan-Neto ◽  
Alexandra Ritger ◽  
Heinz Steiner ◽  
Anthony R. West
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Partial Agonist ◽  
Critical Role ◽  
Medium Spiny Neurons ◽  
Cortical Input ◽  
Spiny Neurons ◽  
Underlying Mechanisms

L-DOPA therapy in Parkinson’s disease (PD) is limited due to emerging L-DOPA-induced dyskinesia. Research has identified abnormal dopamine release from serotonergic (5-HT) terminals contributing to this dyskinesia. Selective serotonin reuptake inhibitors (SSRIs) or 5-HT receptor (5-HTr) agonists can regulate 5-HT activity and attenuate dyskinesia, but they often also produce a loss of the antiparkinsonian efficacy of L-DOPA. We investigated vilazodone, a novel multimodal 5-HT agent with SSRI and 5-HTr1A partial agonist properties, for its potential to reduce dyskinesia without interfering with the prokinetic effects of L-DOPA, and underlying mechanisms. We assessed vilazodone effects on L-DOPA-induced dyskinesia (abnormal involuntary movements, AIMs) and aberrant responsiveness to corticostriatal drive in striatal medium spiny neurons (MSNs) measured with in vivo single-unit extracellular recordings, in the 6-OHDA rat model of PD. Vilazodone (10 mg/kg) suppressed all subtypes (axial, limb, orolingual) of AIMs induced by L-DOPA (5 mg/kg) and the increase in MSN responsiveness to cortical stimulation (shorter spike onset latency). Both the antidyskinetic effects and reversal in MSN excitability by vilazodone were inhibited by the 5-HTr1A antagonist WAY-100635, demonstrating a critical role for 5-HTr1A in these vilazodone actions. Our results indicate that vilazodone may serve as an adjunct therapeutic for reducing dyskinesia in patients with PD.

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