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Abstract
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.
Highlights
This study investigated mesencephalic dopamine depletion effects on static mechanical allodynia (SMA) elicited by chronic constriction of the infraorbitary nerve (CCI-IoN)
Dopamine depletion in the substantia nigra As shown in our previous study [25], 6-OHDA injections resulted in a considerable decrease of Tyrosine hydroxylase (TH) staining in the substantia nigra pars compacta (SNc) of CCI-IoN + 6-OHDA when compared to CCI-IoN + saline animals (Additional file 1: Figure S1A and B)
Despite the slight decrease observed along the 12 weeks post-surgery, the SMA score in this group remained significantly increased compared to all other groups
Summary
This study investigated mesencephalic dopamine depletion effects on static mechanical allodynia (SMA) elicited by chronic constriction of the infraorbitary nerve (CCI-IoN). Painful traumatic trigeminal neuropathy (PTTN) following peripheral nerve trauma is a disabling condition clinically characterized by spontaneous and evoked pain mainly experienced as burning and/or shooting pain [1]. It results from dysfunctions of the somatosensory system [2] and remains a therapeutic challenge since the current treatment options are unsatisfactory [3]. Similar results showed that striatal inhibition of nociceptive responses evoked in the trigeminal system [15,16,17] and chronic oro-facial pain conditions in humans were associated with the alteration of the nigrostriatal dopaminergic system [9, 10]. Since the effects of dopamine depletion on the development of PTTN have
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