Pathophysiology of L-dopa-induced motor and non-motor complications in Parkinson's disease

MF Bastide, WG Meissner, B Picconi, S Fasano… - Progress in …, 2015 - Elsevier
Involuntary movements, or dyskinesia, represent a debilitating complication of levodopa (L-
dopa) therapy for Parkinson's disease (PD). L-dopa-induced dyskinesia (LID) are ultimately …

Basal Ganglia disorders associated with imbalances in the striatal striosome and matrix compartments

JR Crittenden, AM Graybiel - Frontiers in neuroanatomy, 2011 - frontiersin.org
The striatum is composed principally of GABAergic, medium spiny striatal projection neurons
(MSNs) that can be categorized based on their gene expression, electrophysiological …

The pharmacology of L-DOPA-induced dyskinesia in Parkinson's disease

P Huot, TH Johnston, JB Koprich, SH Fox… - Pharmacological …, 2013 - Elsevier
Abstract l-3, 4-Dihydroxyphenylalanine (l-DOPA) remains the most effective symptomatic
treatment of Parkinson's disease (PD). However, long-term administration of l-DOPA is …

The 6-hydroxydopamine model of Parkinson's disease

N Simola, M Morelli, AR Carta - Neurotoxicity research, 2007 - Springer
Abstract The neurotoxin 6-hydroxydopamine (6-OHDA) continues to constitute a valuable
topical tool used chiefly in modeling Parkinson's disease in the rat. The classical method of …

Chromatin remodeling is a key mechanism underlying cocaine-induced plasticity in striatum

A Kumar, KH Choi, W Renthal, NM Tsankova… - Neuron, 2005 - cell.com
Given that cocaine induces neuroadaptations through regulation of gene expression, we
investigated whether chromatin remodeling at specific gene promoters may be a key …

Regulation of gene expression and cocaine reward by CREB and ΔFosB

CA McClung, EJ Nestler - Nature neuroscience, 2003 - nature.com
ΔFosB (a truncated form of FosB) and CREB (cAMP response element binding protein) are
transcription factors induced in the brain's reward pathways after chronic exposure to drugs …

[HTML][HTML] Brain-region-specific changes in neurons and glia and dysregulation of dopamine signaling in Grin2a mutant mice

Z Farsi, A Nicolella, SK Simmons, S Aryal, N Shepard… - Neuron, 2023 - cell.com
A genetically valid animal model could transform our understanding of schizophrenia (SCZ)
disease mechanisms. Rare heterozygous loss-of-function (LoF) mutations in GRIN2A …

[HTML][HTML] Pathways to neurodegeneration: mechanistic insights from GWAS in Alzheimer's disease, Parkinson's disease, and related disorders

VK Ramanan, AJ Saykin - American journal of neurodegenerative …, 2013 - ncbi.nlm.nih.gov
The discovery of causative genetic mutations in affected family members has historically
dominated our understanding of neurodegenerative diseases such as Alzheimer's disease …

Animal models of neurological deficits: how relevant is the rat?

MA Cenci, IQ Whishaw, T Schallert - Nature Reviews Neuroscience, 2002 - nature.com
Animal models of neurological deficits are essential for the assessment of new therapeutic
options. It has been suggested that rats are not as appropriate as primates for the …

L-DOPA-induced dyskinesia in the intrastriatal 6-hydroxydopamine model of parkinson's disease: relation to motor and cellular parameters of nigrostriatal function

C Winkler, D Kirik, A Björklund, MA Cenci - Neurobiology of disease, 2002 - Elsevier
In order to assess the role of striatal dopamine (DA) afferents in l-DOPA-induced dyskinesia,
we have studied a large series of rats sustaining 2, 3, or 4 unilateral injections of 6 …