Cooperative synthesis of dopamine by non-dopaminergic neurons as a compensatory mechanism in the striatum of mice with MPTP-induced Parkinsonism

Козина, Е. А.; Kim, A. R.; Kurina, A.; Ugrumov, M. V.

doi:10.1016/j.nbd.2016.12.005

Cited by 41 publications

(40 citation statements)

References 79 publications

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“…On the control side, single 2.5 ms blue light stimuli elicited large (~1 μM) release of dopamine, but on the lesioned side, there was no measurable release of dopamine despite the fact that the optical stimulus caused spiking in simultaneously recorded THINs and GABAergic IPSPs and suppression of induced firing in SPNs. These data demonstrate conclusively that THINs are non-dopaminergic, GABAergic striatal interneurons that do not release dopamine, and further, that activation of THINs in vivo in experimental models of Parkinson’s disease does not activate “cooperative” synthesis and release of dopamine with other striatal interneurons, at least in brain slices, and likely in vivo as well, despite claims by others (Ugrumov, 2009 ; Kozina et al, 2017 ).…”

Section: Updates On Previously Identified Striatal Gabaergic Interneumentioning

confidence: 56%

Heterogeneity and Diversity of Striatal GABAergic Interneurons: Update 2018

et al. 2018

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Our original review, “Heterogeneity and Diversity of Striatal GABAergic Interneurons,” to which this is an invited update, was published in December, 2010 in Frontiers is Neuroanatomy. In that article, we reviewed several decades’ worth of anatomical and electrophysiological data on striatal parvalbumin (PV)-, neuropeptide Y (NPY)- and calretinin(CR)-expressing GABAergic interneurons from many laboratories including our own. In addition, we reported on a recently discovered novel tyrosine hydroxylase (TH) expressing GABAergic interneuron class first revealed in transgenic TH EGFP reporter mouse line. In this review, we report on further advances in the understanding of the functional properties of previously reported striatal GABAergic interneurons and their synaptic connections. With the application of new transgenic fluorescent reporter and Cre-driver/reporter lines, plus optogenetic, chemogenetic and viral transduction methods, several additional subtypes of novel striatal GABAergic interneurons have been discovered, as well as the synaptic networks in which they are embedded. These findings make it clear that previous hypotheses in which striatal GABAergic interneurons modulate and/or control the firing of spiny neurons principally by simple feedforward and/or feedback inhibition are at best incomplete. A more accurate picture is one in which there are highly selective and specific afferent inputs, synaptic connections between different interneuron subtypes and spiny neurons and among different GABAergic interneurons that result in the formation of functional networks and ensembles of spiny neurons.

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Section: Updates On Previously Identified Striatal Gabaergic Interneumentioning

confidence: 56%

Heterogeneity and Diversity of Striatal GABAergic Interneurons: Update 2018

et al. 2018

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“… 29 In the striatum of PD model mice, compensatory synthesis of dopamine by nondopaminergic neurons was observed. 30 These compensatory mechanisms have a possibility to have contributed to the effect of dopaminergic medication in the de novo patients who required smaller LED to improve motor function as follows. Such patients are speculated to have larger endogenous dopamine and/or grater compensatory mechanisms, and their baseline dopaminergic titers are speculated to be relatively strong.…”

Section: Discussionmentioning

confidence: 99%

Effects of dopaminergic drug adjustment on executive function in different clinical stages of Parkinson’s disease

Murakami

Nohara

Shozawa

et al. 2017

NDT

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BackgroundEffects of dopaminergic medication on executive function in patients with Parkinson’s disease (PD) are inconsistent.ObjectiveWe examined the effect of dopaminergic medication on executive function in 24 drug-naïve PD patients (de novo group) and in 21 PD patients on chronic dopaminergic medication (chronic medication group).MethodsPD patients without dementia were included in this study. For the de novo group patients, dopaminergic medication was initiated, and the dose was increased to improve motor symptoms. For the chronic medication group patients, dopaminergic medication was adjusted to relieve clinical problems. All participants were tested prior to and at 4–7 months after the drug initiation/adjustment. Executive function was assessed by using the Behavioral Assessment of the Dysexecutive Syndrome (BADS). Motor function was assessed by using the Unified Parkinson’s Disease Rating Scale (UPDRS; part III). Improvement in executive function was compared with a simultaneous change in levodopa equivalent doses (LED) of dopaminergic medication and with improvement in motor functions.ResultsThe mean standardized BADS scores showed no significant improvement in both the groups. In the de novo group, percent improvement in the standardized BADS scores showed a significant positive correlation with the LED, but not with percent improvement in UPDRS part III. In the chronic medication group, percent improvement in the standardized BADS scores was negatively correlated with change in the LED, but not with percent improvement in UPDRS part III. Multiple regression analysis using improvement in the standardized BADS score as a dependent variable and patient’s background factors (ie, age, education, disease duration, and motor and executive assessments at baseline) as independent variable showed that improvement in the executive assessment is significantly correlated with the LED only in the de novo group.ConclusionEffects of dopaminergic drug adjustment on executive function differ according to the patient’s clinical stage and depend on LED in de novo stage.

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“…The underlying mechanisms of the benefit are only beginning to be revealed. For example, mice with MPTP (1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine)–induced PD show the potential of some neurons to replace the deficient dopaminergic input to the striatum 37 . In addition, in PD rats, it was shown that treadmill running is beneficial by inhibiting apoptosis in the cerebellum 38 .…”

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Parkinson's Kinesia Paradoxa Is Not a Paradox

Duysens

Nonnekes

2021

Movement Disorders

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Kinesia paradoxa is defined as "the sudden transient ability of a patient with Parkinson's disease (PD) to perform a task he or she was previously unable to perform." 1 Classic accounts report how persons with PD were seen running when triggered by a life-threatening event (fire, earthquake). Even some wheelchair-bound patients with advanced disease could run. 2 Apparently, these patients could use locomotor abilities no one suspected to be present. 3 Similarly, it is frequently seen that patients have difficulty walking slowly, yet are able to run swiftly when chasing a ball, for example, in tennis or hockey.

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Cooperative synthesis of dopamine by non-dopaminergic neurons as a compensatory mechanism in the striatum of mice with MPTP-induced Parkinsonism

Cited by 41 publications

References 79 publications

Heterogeneity and Diversity of Striatal GABAergic Interneurons: Update 2018

Heterogeneity and Diversity of Striatal GABAergic Interneurons: Update 2018

Effects of dopaminergic drug adjustment on executive function in different clinical stages of Parkinson’s disease

Parkinson's Kinesia Paradoxa Is Not a Paradox

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Cooperative synthesis of dopamine by non-dopaminergic neurons as a compensatory mechanism in the striatum of mice with MPTP-induced Parkinsonism

Cited by 41 publications

References 79 publications

Heterogeneity and Diversity of Striatal GABAergic Interneurons: Update 2018

Heterogeneity and Diversity of Striatal GABAergic Interneurons: Update 2018

Effects of dopaminergic drug adjustment on executive function in different clinical stages of Parkinson&rsquo;s disease

Parkinson's Kinesia Paradoxa Is Not a Paradox

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Effects of dopaminergic drug adjustment on executive function in different clinical stages of Parkinson’s disease