A5037793616- Parkinson's Disease Mechanisms and Treatments
- Neurological disorders and treatments
- Neuroscience and Neuropharmacology Research
- Nerve injury and regeneration
- Neurotransmitter Receptor Influence on Behavior
- Cervical Cancer and HPV Research
- Autism Spectrum Disorder Research
- Receptor Mechanisms and Signaling
- Genetic Neurodegenerative Diseases
- Neuroscience and Neural Engineering
- Neurogenesis and neuroplasticity mechanisms
- Diet and metabolism studies
- Botulinum Toxin and Related Neurological Disorders
- Neural dynamics and brain function
- Neurological diseases and metabolism
- Alzheimer's disease research and treatments
- AI in cancer detection
- Nuclear Receptors and Signaling
- Memory and Neural Mechanisms
- Ion channel regulation and function
- Prenatal Substance Exposure Effects
- Neuroinflammation and Neurodegeneration Mechanisms
- Breast Lesions and Carcinomas
- Adenosine and Purinergic Signaling
- RNA regulation and disease
Lund University
2015-2024
Azienda Ospedaliera San Giovanni Addolorata
2023-2024
Skåne University Hospital
2016
Cleveland Clinic Florida
2016
The Memory Clinic
2015
University College London
2015
Banner Sun Health Research Institute
2015
Mayo Clinic in Arizona
2015
University of Cagliari
2015
Azienda Unita' Sanitaria Locale Di Modena
2014
Abstract In an attempt to define clinically relevant models of akinesia and dyskinesia in 6‐hydroxydopamine (6‐OHDA)‐lesioned rats, we have examined the effects drugs with high ( l ‐DOPA) vs. low (bromocriptine) dyskinesiogenic potential Parkinson's disease on three types motor performance, namely: (i) abnormal involuntary movements (AIMs) (ii) rotational behaviour, (iii) spontaneous forelimb use (cylinder test). Rats unilateral 6‐OHDA lesions received single daily i.p. injections ‐DOPA or...
Rats sustaining unilateral near-complete 6-hydroxydopamine lesions of the mesostriatal dopamine pathway received daily injections 3,4 dihydroxyphenyl-l-alanine (L-DOPA, 8 mg/kg plus 15 benserazide) for 3 weeks. During this period, about 50% rats gradually developed abnormal involuntary movements, lasting 2–3 h following each L-DOPA dose. were killed days after last injection, and sections through striatum processed in situ hybridization histochemistry. Within L-DOPA-treated group, levels...
Abstract Rats sustaining unilateral near‐complete 6‐hydroxydopamine lesions of the mesostriatal dopamine pathway received daily injections 3,4 dihydroxyphenyl‐ l ‐alanine (L‐DOPA, 8 mg/kg plus 15 benserazide) for 3 weeks. During this period, about 50% rats gradually developed abnormal involuntary movements, lasting 2–3 h following each L‐DOPA dose. were killed days after last injection, and sections through striatum processed in situ hybridization histochemistry. Within L‐DOPA‐treated group,...
L-DOPA-induced dyskinesia in Parkinson's disease is associated with large increases brain dopamine (DA) levels following drug dosing, but the precise significance of this phenomenon not understood. Here we compare DA efflux and metabolism striatum substantia nigra dyskinetic non-dyskinetic animals a standard dose L-DOPA. Rats 6-hydroxydopamine lesions were treated chronically L-DOPA, monitored on abnormal involuntary movements scale, then subjected to intracerebral microdialysis under...
This unit provides detailed protocols for establishing rodent models of L-DOPA-induced dyskinesia. The 6-hydroxydopamine (6-OHDA) lesion procedure is described in more detail mice than rats since the lesioning has been extensively previous work and less difficult to perform. Unlike primate models, dyskinesia are relatively simple fast set up, thus being affordable most laboratories. These allow studying dyskinetic complications L-DOPA treatment on large groups animals under strictly...
Abstract Objective: Striatal serotonin projections have been implicated in levodopa‐induced dyskinesia by providing an unregulated source of dopamine release. We set out to determine whether these are affected levodopa treatment a way that would favor the occurrence dyskinesia. Methods: As index terminal innervation density, we measured radioligand binding plasma membrane transporter (SERT) levodopa‐treated dyskinetic and nondyskinetic subjects, using brain tissue from both rat monkey models...
Abstract Metabotropic glutamate receptor type 5 (mGluR5) modulates dopamine and neurotransmission at central synapses. In this study, we addressed the role of mGluR5 in l ‐DOPA‐induced dyskinesia, a movement disorder that is due to abnormal activation both receptors basal ganglia. A selective potent antagonist, 3‐[(2‐methyl‐1,3‐thiazol‐4‐yl)ethynyl] pyridine, was tested for its ability modulate molecular, behavioural neurochemical correlates dyskinesia 6‐hydroxydopamine‐lesioned rats treated...
The sigma-1 receptor, an endoplasmic reticulum-associated molecular chaperone, is attracting great interest as a potential target for neuroprotective treatments. We provide the first evidence that pharmacological modulation of this protein produces functional neurorestoration in experimental parkinsonism. Mice with intrastriatal 6-hydroxydopamine lesions were treated daily selective receptor agonist, PRE-084, 5 weeks. At dose 0.3 mg/kg/day, PRE-084 produced gradual and significant...
l-DOPA-induced dyskinesia (LID) in Parkinson9s disease has been linked to altered dopamine and glutamate transmission within the basal ganglia. In present study, we compared compounds targeting specific subtypes of receptors or calcium channels for their ability attenuate LID associated activation striatal nuclear signaling gene expression rat. Rats with 6-hydroxydopamine lesions were treated acutely chronically l-DOPA combination following selective compounds: antagonists group I...