Abnormal involuntary movement (AIM) expression following D2 dopamine agonist challenge is determined by the nature of prior dopamine receptor stimulation (priming) in 6-hydroxydopamine lesioned rats

Drake, Jonathan; Kibuuka, Laura N.; Dimitrov, Kroum D.; Pollack, Alexia E.

doi:10.1016/j.pbb.2013.01.014

Cited by 4 publications

(4 citation statements)

References 52 publications

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“…1A). Similar to previous research (Drake et al, 2013; Dupre et al, 2007; Lindenbach et al, 2013), systemic administration of the D1 receptor agonist SKF81297 and the D2 receptor agonist quinpirole independently induced ALO AIMs (Fig. 5D and F) that were similar to L-dopa-induced AIMs (Fig.…”

Section: Resultssupporting

confidence: 89%

“…Unfortunately, prolonged L-dopa treatment often leads to the development of abnormal involuntary movements, otherwise known as L-dopa-induced dyskinesia (Jankovic, 2005). Though DA agonists are less likely to induce this side effect (Chondrogiorgi et al, 2014; Stathis et al, 2015), they can also elicit dyskinesia in PD patients (Rascol et al, 2000, 2001) and hemiparkinsonian rats (Drake et al, 2013; Dupre et al, 2007; Lindenbach et al, 2013). While the causes of dyskinesia are not fully understood, several mechanisms appear to be involved in its expression, including increased corticostriatal extracellular glutamate levels, glutamate transporter expression, and glutamate receptor phosphorylation (Calon et al, 2003; Dupre et al, 2011; Robelet et al, 2004; Sgambato-Faure and Cenci, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease

Dupre

Cruz

McCoy

et al. 2016

Neurobiology of Disease

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Prolonged L-dopa treatment in Parkinson’s disease (PD) often leads to the expression of abnormal involuntary movements known as L-dopa-induced dyskinesia. Recently, dramatic 80 Hz oscillatory local field potential (LFP) activity within the primary motor cortex has been linked to dyskinetic symptoms in a rodent model of PD and attributed to stimulation of cortical dopamine D1 receptors. To characterize the relationship between high gamma (70–110 Hz) cortical activity and the development of L-dopa-induced dyskinesia, cortical LFP and spike signals were recorded in hemiparkinsonian rats treated with L-dopa for 7 days, and dyskinesia was quantified using the abnormal involuntary movements (AIMs) scale. The relationship between high gamma and dyskinesia was further probed by assessment of the effects of pharmacological agents known to induce or modulate dyskinesia expression. Findings demonstrate that AIMs and high gamma LFP power increase between days 1 and 7 of L-dopa priming. Notably, high beta (25–35 Hz) power associated with parkinsonian bradykinesia decreased as AIMs and high gamma LFP power increased during priming. After priming, rats were treated with the D1 agonist SKF81297 and the D2 agonist quinpirole. Both dopamine agonists independently induced AIMs and high gamma cortical activity that were similar to that induced by L-dopa, showing that this LFP activity is neither D1 nor D2 receptor specific. The serotonin 1A receptor agonist 8-OH-DPAT reduced L-dopa- and DA agonist-induced AIMs and high gamma power to varying degrees, while the serotonin 1A antagonist WAY100635 reversed these effects. Unexpectedly, as cortical high gamma power increased, phase locking of cortical pyramidal spiking to high gamma oscillations decreased, raising questions regarding the neural substrate(s) responsible for high gamma generation and the functional correlation between high gamma and dyskinesia.

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Section: Resultssupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease

Dupre

Cruz

McCoy

et al. 2016

Neurobiology of Disease

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“…Moreover, the effects of this lesion on grooming asymmetries were not investigated. One study in 6-OHDA-lesioned rats reported intense grooming directed toward the contralateral side to the lesion following treatments with various dopamine agonists but did not describe grooming deficits in untreated animals [ 25 ]. Our study tested whether grooming could be an informative behavioural analysis, about the effects of unilateral 6-OHDA lesion in mice.…”

Section: Discussionmentioning

confidence: 99%

Unilateral Lesion of Dopamine Neurons Induces Grooming Asymmetry in the Mouse

2015

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Grooming behaviour is the most common innate behaviour in animals. In rodents, it consists of sequences of movements organized in four phases, executed symmetrically on both sides of the animal and creating a syntactic chain of behavioural events. The grooming syntax can be altered by stress and novelty, as well as by several mutations and brain lesions. Grooming behaviour is known to be affected by alterations of the dopamine system, including dopamine receptor modulation, dopamine alteration in genetically modified animals, and after brain lesion. While a lot is known about the initiation and syntactic modifications of this refined sequence of movements, effects of unilateral lesion of dopamine neurons are unclear particularly regarding the symmetry of syntactic chains. In the present work we studied grooming in mice unilaterally lesioned in the medial forebrain bundle by 6-hydroxydopamine. We found a reduction in completion of grooming bouts, associated with reduction in number of transitions between grooming phases. The data also revealed the development of asymmetry in grooming behaviour, with reduced tendency to groom the contralateral side to the lesion. Symmetry was recovered following treatment with L-DOPA. Thus, the present work shows that unilateral lesion of dopamine neurons reduces self-grooming behaviour by affecting duration and numbers of events. It produces premature discontinuation of grooming chains but the sequence syntax remains correct. This deficient grooming could be considered as an intrinsic symptom of Parkinson’s disease in animal models and could present some similarities with abnormalities of motor movement sequencing seen in patients. Our study also suggests grooming analysis as an additional method to screen parkinsonism in animal models.

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“…This approach differs from that of others that have previously analyzed the involvement of iMSNs in LID ( Alcacer et al., 2017 ; Girasole et al., 2018 ) in which D2R expressing iMSNs were manipulated as a whole. Similarly, using pharmacological approaches a clear participation of D2R/D3R signaling was assessed ( Drake et al., 2013 ; Rascol et al, 2006 ; Sebastianutto et al., 2016 ) but the cell types involved in it were not clarified. Using constitutive knockout of D2Rs in mice it was shown that the total loss of D2R signaling had no effects in L-DOPA-treated dyskinetic mice ( Darmopil et al., 2009 ).…”

Section: Discussionmentioning

confidence: 99%