Striatal norepinephrine efflux in l-DOPA-induced dyskinesia

Ostock, Corinne Y.; Bhide, Nirmal; Goldenberg, Adam A.; George, Jessica A.; Bishop, Christopher

doi:10.1016/j.neuint.2018.01.010

Cited by 12 publications

(14 citation statements)

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“…In another recent publication, DSP-4 developed motor and nonmotor symptoms in control mice and exacerbated motor disability in mice rendered parkinsonian by the injection of lipopolysaccharide (Song et al, 2019). Some studies performed in 6-OHDA lesioned rodents also suggest that noradrenergic lesions in parkinsonian rats augment dopaminergic neuron vulnerability (Ostock et al, 2014) leading to lower DA levels (Srinivasan and Schmidt, 2003) and worsening motor performance (Srinivasan and Schmidt, 2003;Srinivasan and Schmidt, 2004;Wang et al, 2010;Shin et al, 2014;Ostock et al, 2018). Other studies using the same 6-OHDA model failed, however, to reproduce the latter findings (Delaville et al, 2012a;Guimarães et al, 2013;Ostock et al, 2014;Shin et al, 2014).…”

Section: Noradrenaline Neuroinflammation and Neuroprotectionmentioning

confidence: 99%

“…The contribution of the noradrenergic system to LID has been investigated in animal models using NA/DA neurotoxic lesions. Although some studies report no implication of the noradrenergic system (Pérez et al, 2009;Ostock et al, 2014;Ostock et al, 2018), others have demonstrated that additional noradrenergic lesion worsens dyskinetic movements in parkinsonian rodents chronically treated with L-DOPA (Fulceri et al, 2007;Miguelez et al, 2011b;Shin et al, 2014). Interestingly, in one study, the authors induced the noradrenergic lesion to already dyskinetic animals, showing an increase in the duration of the dyskinetic effect of L-DOPA probably due to impaired striatal DA clearance (Miguelez et al, 2011b).…”

Section: L-dopa and The Noradrenergic Systemmentioning

confidence: 99%

“…Anatomical studies using the unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rat model show that the number of LC neurons is not affected by the DA loss (Miguelez et al, 2011b;Ostock et al, 2018) but NA levels in different projection areas are variably decreased. In the prefrontal cortex of the lesioned hemisphere, some authors found unchanged (Delaville et al, 2012a;Delaville et al, 2012b) or reduced NA concentrations (Shin et al, 2014;Ostock et al, 2018). Similarly, other areas with sparse noradrenergic innervation, as the striatum, show unchanged or lower NA levels (Shin et al, 2014;Ostock et al, 2018).…”

Section: Preclinical Evidencementioning

confidence: 99%

“…In the prefrontal cortex of the lesioned hemisphere, some authors found unchanged (Delaville et al, 2012a;Delaville et al, 2012b) or reduced NA concentrations (Shin et al, 2014;Ostock et al, 2018). Similarly, other areas with sparse noradrenergic innervation, as the striatum, show unchanged or lower NA levels (Shin et al, 2014;Ostock et al, 2018). Bilateral models of 6-OHDA show, however, more robust NA deficits in the cortex and striatum (Vieira et al, 2019).…”

Section: Preclinical Evidencementioning

confidence: 99%

“…For instance, participation of noradrenergic neurons in the ability of L-DOPA to enhance DA extracellular levels is likely an indirect effect that requires the dorsal raphe nucleus (Tanaka et al, 1999;Navailles et al, 2010;Navailles and De Deurwaerdère, 2012;De Deurwaerdère et al, 2017;Miguelez et al, 2017). In dyskinetic rats, lesion of noradrenergic terminals or neurons did not reduce L-DOPA-stimulated extracellular levels of DA in the striatum (Navailles et al, 2014;Ostock et al, 2018). However, the noradrenergic lesion enhanced the effect of L-DOPA in extrastriatal regions in part due to the loss of clearance of extracellular DA by noradrenergic fibers bearing NET (Navailles et al, 2014).…”

Section: L-dopa and The Noradrenergic Systemmentioning

confidence: 99%

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The Noradrenergic System in Parkinson’s Disease

et al. 2020

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Nowadays it is well accepted that in Parkinson's disease (PD), the neurodegenerative process occurs in stages and that damage to other areas precedes the neuronal loss in the substantia nigra pars compacta, which is considered a pathophysiological hallmark of PD. This heterogeneous and progressive neurodegeneration may explain the diverse symptomatology of the disease, including motor and non-motor alterations. In PD, one of the first areas undergoing degeneration is the locus coeruleus (LC). This noradrenergic nucleus provides extensive innervation throughout the brain and plays a fundamental neuromodulator role, participating in stress responses, emotional memory, and control of motor, sensory, and autonomic functions. Early in the disease, LC neurons suffer modifications that can condition the effectiveness of pharmacological treatments, and importantly, can lead to the appearance of common non-motor symptomatology. The noradrenergic system also exerts anti-inflammatory and neuroprotective effect on the dopaminergic degeneration and noradrenergic damage can consequently condition the progress of the disease. From the pharmacological point of view, it is also important to understand how the noradrenergic system performs in PD, since noradrenergic medication is often used in these patients, and drug interactions can take place when combining them with the gold standard drug therapy in PD, L-3,4-dihydroxyphenylalanine (L-DOPA). This review provides an overview about the functional status of the noradrenergic system in PD and its contribution to the efficacy of pharmacologicalbased treatments. Based on preclinical and clinical publications, a special attention will be dedicated to the most prevalent non-motor symptoms of the disease.

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