Bilateral tactile hypersensitivity and neuroimmune responses after spared nerve injury in mice lacking vasoactive intestinal peptide

Gallo, Alessandro; Leerink, Marjolein; Michot, B.; Ahmed, Eman; Forget, Patrice; Mouraux, André; Hermans, Emmanuel; Deumens, Ronald

doi:10.1016/j.expneurol.2017.03.019

Cited by 15 publications

(15 citation statements)

References 68 publications

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“… 15 , 52 The presence of contralateral sensory deficits have also been reported in various genetic knockout animals, included vasoactive intestinal peptide and tumor necrosis factor alpha receptor knockouts. 18 , 39 Together, these studies suggest that the causes of contralateral effects of nerve injury may stem from multiple mechanisms, and may depend on the type and severity of the injury or disease state.…”

Section: Discussionmentioning

confidence: 94%

Acute hyperalgesia and delayed dry eye after corneal abrasion injury

Hegarty

Hermes

Morgan

et al. 2018

PR9

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Introduction:Corneal nerves mediate pain from the ocular surface, lacrimation, and blinking, all of which protect corneal surface homeostasis and help preserve vision. Because pain, lacrimation and blinking are rarely assessed at the same time, it is not known whether these responses and their underlying mechanisms have similar temporal dynamics after acute corneal injury.Methods:We examined changes in corneal nerve density, evoked and spontaneous pain, and ocular homeostasis in Sprague-Dawley male rats after a superficial epithelial injury with heptanol. We also measured changes in calcitonin gene-related peptide (CGRP), which has been implicated in both pain and epithelial repair.Results:Hyperalgesia was seen 24 hours after abrasion injury, while basal tear production was normal. One week after abrasion injury, pain responses had returned to baseline levels and dry eye symptoms emerged. There was no correlation between epithelial nerve density and pain responses. Expression of both ATF3 (a nerve injury marker) and CGRP increased in trigeminal ganglia 24 hours after injury when hyperalgesia was seen, and returned to normal one week later when pain behavior was normal. These molecular changes were absent in the contralateral ganglion, despite reductions in corneal epithelial nerve density in the uninjured eye. By contrast, CGRP was upregulated in peripheral corneal endings 1 week after injury, when dry eye symptoms emerged.Conclusion:Our results demonstrate dynamic trafficking of CGRP within trigeminal sensory nerves following corneal injury, with elevations in the ganglion correlated with pain behaviors and elevations in peripheral endings correlated with dry eye symptoms.

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Section: Discussionmentioning

confidence: 94%

Acute hyperalgesia and delayed dry eye after corneal abrasion injury

Hegarty

Hermes

Morgan

et al. 2018

PR9

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“…It should be noted that microglial activation is also observed following standard CCI. Previous reports have suggested that elevated microglial activation plays a greater role in the induction of contralateral allodynia [ 72 ]. Therefore, a combination of both astrocyte and microglial activation may be required to generate robust bilateral allodynia observed following standard unilateral sciatic nerve injury.…”

Section: Discussionmentioning

confidence: 99%

Prenatal alcohol exposure is a risk factor for adult neuropathic pain via aberrant neuroimmune function

Sanchez

Noor

Davies

et al. 2017

J Neuroinflammation

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BackgroundClinical studies show that prenatal alcohol exposure (PAE) results in effects that persist into adulthood. Experimental animal models of moderate PAE demonstrate that young adults with PAE display potentiated sensitivity to light touch, clinically termed allodynia, following sciatic nerve chronic constriction injury (CCI) that coincides with heightened spinal glial, spinal macrophage, and peripheral immune responses. However, basal touch sensitivity and corresponding glial and leukocyte activation are unaltered. Therefore, the current study explored whether the enduring pathological consequences of moderate PAE on sensory processing are unmasked only following secondary neural insult.MethodsIn middle-aged (1 year) Long Evans rats that underwent either prenatal saccharin exposure (control) or moderate PAE, we modified the well-characterized model of sciatic neuropathy, CCI, to study the effects of PAE on neuro-immune responses in adult offspring. Standard CCI manipulation required 4 chromic gut sutures, while a mild version applied a single suture loosely ligated around one sciatic nerve. Spinal glial immunoreactivity was examined using immunohistochemistry. The characterization and functional responses of leukocyte populations were studied using flow cytometry and cell stimulation assays followed by quantification of the proinflammatory cytokines interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Data were statistically analyzed by ANOVA and unpaired t tests.ResultsThe current report demonstrates that mild CCI generates robust allodynia only in PAE rats, while the pathological effects of PAE following the application of a standard CCI are revealed by enhanced allodynia and elevated spinal glial activation. Additionally, mild CCI increases spinal astrocyte activation but not microglia, suggesting astrocytes play a larger role in PAE-induced susceptibility to aberrant sensory processing. Leukocyte populations from PAE are altered under basal conditions (i.e., prior to secondary insult), as the distribution of leukocyte populations in lymphoid organs and other regions are different from those of controls. Lastly, following in vitro leukocyte stimulation, only PAE augments the immune response to antigen stimulation as assessed by heightened production of TNF-α and IL-1β.ConclusionsThese studies demonstrate PAE may prime spinal astrocytes and peripheral leukocytes that contribute to enduring susceptibility to adult-onset neuropathic pain that is not apparent until a secondary insult later in life.

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“…Compared with VIP, several preproVIP-derived peptides did not cause a significant inhibition of smooth muscle activity of human female genital tract [25]. VIP also plays important role in somatic pain sensation [26].…”

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confidence: 85%

Megaloneurite, a giant neurite of vasoactive intestinal peptide and nitric oxide synthase in the aged dog and identification by human sacral spinal cord

Hou

Jia

et al. 2019

Preprint

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Megaloneurite of NADPH diaphorase (NADPH-d) positivity is a new kind of aging-related neurodegeneration and also co-localized with vasoactive intestinal peptide (VIP) in the sacral spinal cord of aged dog and monkey. However, no immunocytochemistry of VIP was exclusively tested in the aged dog and no evidence has been reported in the aged human spinal cord. Aged dogs were used to examine the distribution of VIP immunopositivity in the sacral spinal cord. Immunocytochemistry of VIP and alpha-synuclein were also examined in the aged human spinal cord. The VIP immunopositivity in aged dog was reconfirmed our previous finding illustrated by immunofluorescent study. Megalogneurite was also identified by nitric oxide synthase (NOS) immunoreaction in aged dog. The VIP positive megaloneurites both in age dog and human were detected in dorsal root entry zoon, Lissauer's tract, dorsal commissural nucleus and anterior commissural gray as well as in the lateral funiculus of the sacral spinal cord exclusive of other segments of spinal cord. Alpha-synuclein positivity was present mini-aggregation and Lewy body in the sacral spinal cord of aged human, that also occurred in the lumber, thoracic and cervical spinal cord. It was firstly tested that VIP megaloneurites occurred in the aged human sacral spinal cord, especially in the white matter. Megaloneurites identified by NADPH-d-VIP-NOS immunoreaction could implicate for the dysfunction of pelvic organs in the aged human being. Vasoactive intestinal peptide (VIP) acts on neuronal cells to support physiological condition and protect neurons survival in pathological condition[1-3]. Different from other neuropeptides, the distribution of VIP is restricted to the sacral cord[4]. Or it is majorly distributed in the sacral spinal cord and a few of VIP positivity is detected in the other segment of the spinal cord in cat[5].VIP neurons are small-size neurons and central original source for peripheral innervation[6]. VIP-ergic afferent neurons projected to the pelvic organs are bigger proportion that the other segments, while the lower lumbosacral segments of the neuropeptide innervation was also more priority to the upper lumber segment[7]. VIP fibers are majorly found in the Lissauer's tract (LT), superficial lamina,

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Bilateral tactile hypersensitivity and neuroimmune responses after spared nerve injury in mice lacking vasoactive intestinal peptide

Cited by 15 publications

References 68 publications

Acute hyperalgesia and delayed dry eye after corneal abrasion injury

Acute hyperalgesia and delayed dry eye after corneal abrasion injury

Prenatal alcohol exposure is a risk factor for adult neuropathic pain via aberrant neuroimmune function

Megaloneurite, a giant neurite of vasoactive intestinal peptide and nitric oxide synthase in the aged dog and identification by human sacral spinal cord

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