Differential effects of gaseous versus injectable anesthetics on changes in regional cerebral blood flow and metabolism induced by l -DOPA in a rat model of Parkinson's disease

Bimpisidis, Zisis; Öberg, Carl; Maslava, Natallia; Cenci, M. Angela; Lundblad, Cornelia

doi:10.1016/j.expneurol.2017.03.006

Cited by 6 publications

(6 citation statements)

References 49 publications

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“…[75][76][77] ; see also Table 2). Recently, striking similarities between rodent models of LID and the human disorder have emerged from brain imaging studies addressing the metabolic-hemodynamic effects of L-dopa [78][79][80][81] and from recordings of cortical field potentials 82,83 (Table 2).…”

Section: Construct Validity and Predictive Validity Of Rodent Models mentioning

confidence: 99%

“…Rodent models of LID are highly predictive of pharmacological effects seen in NHP models, which are generally regarded as the gold standard for translational research on the subject because of their remarkable physical similarities to humans. With few PD patients 131 Increased microvessel density in motor striatum/putamen Rat 132 PD patients 132,133 Flow-metabolism dissociation "on" L-dopa in striatum and GP Rat 79,81 PD patients 80 Peaks of striatal DA release shortly after dosing L-dopa Rat 134 PD patients 135 Enhanced theta-band LFP oscillations in STN and/or SNr Rat 136,137 PD patients 138 Narrowband-gamma LFP oscillations in motor cortex Rat 82 PD patients 83 Data from PD patients were obtained through either postmortem biochemical/histochemical analyses or brain imaging studies in vivo. Human data on LFP oscillations were obtained with electrophysiological recordings in patients requiring DBS surgery.…”

Section: Construct Validity and Predictive Validity Of Rodent Models mentioning

confidence: 99%

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Animal models of l‐dopa‐induced dyskinesia in Parkinson's disease

Cenci

Crossman

2018

Movement Disorders

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Understanding the biological mechanisms of l-dopa-induced motor complications is dependent on our ability to investigate these phenomena in animal models of Parkinson's disease. The most common motor complications consist in wearing-off fluctuations and abnormal involuntary movements appearing when plasma levels of l-dopa are high, commonly referred to as peak-dose l-dopa-induced dyskinesia. Parkinsonian models exhibiting these features have been well-characterized in both rodent and nonhuman primate species. The first animal models of peak-dose l-dopa-induced dyskinesia were produced in monkeys lesioned with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and treated chronically with l-dopa to elicit choreic movements and dystonic postures. Seminal studies were performed in these models using both metabolic mapping and electrophysiological techniques, providing fundamental pathophysiological insights that have stood the test of time. A decade later, it was shown possible to reproduce peak-dose l-dopa-induced dyskinesia in rats and mice rendered parkinsonian with nigrostriatal 6-hydroxydopamine lesions. When treated with l-dopa, these animals exhibit abnormal involuntary movements having both hyperkinetic and dystonic components. These models have enabled molecular- and cellular-level investigations into the mechanisms of l-dopa-induced dyskinesia. A flourishing literature using genetically engineered mice is now unraveling the role of specific genes and neural circuits in the development of l-dopa-induced motor complications. Both non-human primate and rodent models of peak-dose l-dopa-induced dyskinesia have excellent construct validity and provide valuable tools for discovering therapeutic targets and evaluating potential treatments. © 2018 International Parkinson and Movement Disorder Society.

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Section: Construct Validity and Predictive Validity Of Rodent Models mentioning

confidence: 99%

Section: Construct Validity and Predictive Validity Of Rodent Models mentioning

confidence: 99%

Animal models of l‐dopa‐induced dyskinesia in Parkinson's disease

Cenci

Crossman

2018

Movement Disorders

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“…This study reported that hyperkinetic movements were associated with a significant overactivation of both supplementary motor area and primary motor cortices, attributing this phenomenon to an altered input from basal ganglia-thalamocortical networks (Rascol et al 1998). The use of rCBF as a surrogate marker of neuronal activity in PD is complicated by the fact that l -DOPA has direct hemodynamic effects in different brain regions, including the motor cortex (Bimpisidis et al 2017; Jourdain et al 2016; Ohlin et al 2012). Nevertheless, the notion that motor cortical areas are hyperactive or dysregulated in LID has now been substantiated by several independent studies based on magnetic resonance imaging (MRI) methodologies (Cerasa et al 2015; Herz et al 2015, 2016; Rajan et al 2017).…”

Section: Cortical Dynamicsmentioning

confidence: 99%

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

2018

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With the advent of rodent models of l-DOPA-induced dyskinesia (LID), a growing literature has linked molecular changes in the striatum to the development and expression of abnormal involuntary movements. Changes in information processing at the striatal level are assumed to impact on the activity of downstream basal ganglia nuclei, which in turn influence brain-wide networks, but very little is actually known about systems-level mechanisms of dyskinesia. As an aid to approach this topic, we here review the anatomical and physiological organisation of cortico-basal ganglia-thalamocortical circuits, and the changes affecting these circuits in animal models of parkinsonism and LID. We then review recent findings indicating that an abnormal cerebellar compensation plays a causal role in LID, and that structures outside of the classical motor circuits are implicated too. In summarizing the available data, we also propose hypotheses and identify important knowledge gaps worthy of further investigation. In addition to informing novel therapeutic approaches, the study of LID can provide new clues about the interplay between different brain circuits in the control of movement.

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“…Performing MRI of animals typically requires anesthesia to obtain adequate immobilization and to reduce stress or pain in relation to diseases and/or invasive procedures . A multitude of different anesthetics and anesthesia procedures are used throughout the literature, potentially affecting the acquired bio‐chemical information and thus imposing constraints on the comparability of studies performed under different circumstances. This is particularly true with the advancement of the metabolic imaging methods, such as hyperpolarized MRI and spectroscopy, which enable in vivo metabolic examinations in real time, and as such, are inherently sensitive to metabolic disturbances imposed by the anesthesia .…”

Section: Introductionmentioning

confidence: 99%

Effects of anesthesia on renal function and metabolism in rats assessed by hyperpolarized MRI

Mariager

Lindhardt

et al. 2018

Magnetic Resonance in Med

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This study demonstrates different renal metabolic and hemodynamic changes under 3 different anesthetics, using hyperpolarized MR in rats. Inactin and sevoflurane were found to affect the renal hemodynamic and metabolic status to a lesser degree than FFM. Sevoflurane anesthesia is particularly easy to induce and maintain during the whole anesthesia procedure, and as such, represents a good alternative to inaction, although it alters the blood glucose level.

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Differential effects of gaseous versus injectable anesthetics on changes in regional cerebral blood flow and metabolism induced by l -DOPA in a rat model of Parkinson's disease

Cited by 6 publications

References 49 publications

Animal models of l‐dopa‐induced dyskinesia in Parkinson's disease

Animal models of l‐dopa‐induced dyskinesia in Parkinson's disease

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

Effects of anesthesia on renal function and metabolism in rats assessed by hyperpolarized MRI

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