Nigrostriatal dopaminergic depletion produces orofacial static mechanical allodynia

Dieb, Wisam; Ouachikh, Omar; Durif, Franck; Hafidi, Aziz

doi:10.1002/ejp.707

Cited by 20 publications

(15 citation statements)

References 40 publications

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“…The dopamine depletion increased the SMA caused by CCI-IoN. This is in agreement with our previous studies demonstrating the induction of dynamic and static [ 16 , 18 ] mechanical allodynia in the trigeminal system upon midbrain dopamine depletion. Bromocriptine attenuated CCI-IoN-related SMA in a dose dependent manner.…”

Section: Discussionsupporting

confidence: 93%

“…Cell count revealed a significant ( p < 0.001, ***) decrease in TH positive cells (70 % neuronal loss) in SNc of CCI-IoN + 6-OHDA rats (Additional file 1 : Figure S1C). The impact of unilateral or bilateral depletion mesencephalic midbrain depletion on SMA has been studied previously [ 18 ].…”

Section: Resultsmentioning

confidence: 99%

“…Stimulation of striatal D2R suppressed nociceptive neuropathic pain through RVM modulation and activation of D2R and 5-HT receptors at the dorsal spinal horn [ 14 ]. The meso-limbic and meso-cortical dopamine projections can also participate to the increase of pain caused by CCI-IoN since 6-OHDA injection has been demonstrated to induce dopaminergic cell degeneration in the VTA [ 16 , 18 , 33 ]. Alternatively the segmental action of bromocriptine (intracisternal injection) may act via dopaminergic descending pathway which arise from the hypothalamus region A11 [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…Similar results showed that striatal inhibition of nociceptive responses evoked in the trigeminal system [ 15 – 17 ] and chronic oro-facial pain conditions in humans were associated with the alteration of the nigrostriatal dopaminergic system [ 9 , 10 ]. Recent reports showed that bilateral or unilateral nigrostriatal dopaminergic lesions induce dynamic and static mechanical allodynia in the oro-facial region [ 16 , 18 ]. Since the effects of dopamine depletion on the development of PTTN have not been explored, the present study aimed at investigating the effects of nigrostriatal lesions in animals with a peripheral nerve injury: chronic constriction injury of the Infra Orbitary Nerve (chronic constriction of the infraorbitary nerve: CCI-IoN) model [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

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Nigrostriatal dopaminergic depletion increases static orofacial allodynia

et al. 2016

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BackgroundThis study investigated mesencephalic dopamine depletion effects on static mechanical allodynia (SMA) elicited by chronic constriction of the infraorbitary nerve (CCI-IoN).MethodsDopamine depletion (6-OHDA administration into the medial forebrain bundle) effects on CCI-IoN-induced SMA were explored using behavioral (nocifensive behavior score upon non-noxious stimuli using von Frey filament), pharmacological (bromocriptine injections) and immunohistochemical (PKCγ and pERK1/2) techniques.ResultsThe central dopamine depletion increased significantly the SMA score. Intraperitoneal and intracisternal injections of bromocriptine alleviated the allodynic behavior observed in both CCI-IoN and CCI-IoN + 6-OHDA animal groups. At the cellular level, dopamine depletion induced a significant increase in PKCγ expression in the medullary dorsal horn (MDH) in rat with CCI-IoN + 6-OHDA when compared to sham animals (CCI-IoN only). Similarly, after static non-noxious stimuli, the expression of pain marker proteins pERK1/2 within the MDH revealed significantly a higher number of positive cells in CCI-IoN + 6-OHDA rats when compared to the CCI-IoN group.ConclusionThis study demonstrates that nigrostriatal dopamine depletion exacerbates the neuropathic pain resulting from CCI-IoN. This effect is probably due to an action through descending pain inhibitory systems which increased pain sensitization at the MDH level. It demonstrates also an analgesic effect elicited by D2R activation at the segmental level.Electronic supplementary materialThe online version of this article (doi:10.1186/s10194-016-0607-z) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nigrostriatal dopaminergic depletion increases static orofacial allodynia

et al. 2016

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“…PD patients and parkinsonian animal models exhibit accelerated and irregular neuronal firing and abnormal oscillations in the local field potential in the basal ganglia nuclei, including the subthalamic nucleus (STN), globus pallidus interna (GPi), and substantia nigra pars reticulata (SNr), and these abnormalities are correlated with motor deficits (11)(12)(13)(14)(15)(16)(17). As the substantia nigra, striatum, and globus pallidus integrate nociceptive information to render pain avoidance and nocifensive behaviors (2,10,18), neural circuit dysfunction in these regions may lead to the hyperalgesia and shortened nociceptive reflex latencies observed in parkinsonian animal models (19)(20)(21)(22)(23). However, addressing the gap between the dysfunction in basal ganglia circuits and pain sensitization in PD requires experiments using sophisticated neuromodulation techniques.…”

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confidence: 99%

Reversal of hyperactive subthalamic circuits differentially mitigates pain hypersensitivity phenotypes in parkinsonian mice

Luan

Tang

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Although pain is a prevalent nonmotor symptom in Parkinson’s disease (PD), it is undertreated, in part because of our limited understanding of the underlying mechanisms. Considering that the basal ganglia are implicated in pain sensation, and that their synaptic outputs are controlled by the subthalamic nucleus (STN), we hypothesized that the STN might play a critical role in parkinsonian pain hypersensitivity. To test this hypothesis, we established a unilateral parkinsonian mouse model with moderate lesions of dopaminergic neurons in the substantia nigra. The mice displayed pain hypersensitivity and neuronal hyperactivity in the ipsilesional STN and in central pain-processing nuclei. Optogenetic inhibition of STN neurons reversed pain hypersensitivity phenotypes in parkinsonian mice, while hyperactivity in the STN was sufficient to induce pain hypersensitivity in control mice. We further demonstrated that the STN differentially regulates thermal and mechanical pain thresholds through its projections to the substantia nigra pars reticulata (SNr) and the internal segment of the globus pallidus (GPi)/ventral pallidum (VP), respectively. Interestingly, optogenetic inhibition of STN-GPi/STN-VP and STN-SNr projections differentially elevated mechanical and thermal pain thresholds in parkinsonian mice. In summary, our results support the hypothesis that the STN and its divergent projections play critical roles in modulating pain processing under both physiological and parkinsonian conditions, and suggest that inhibition of individual STN projections may be a therapeutic strategy to relieve distinct pain phenotypes in PD.

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