Studies on vascular permeability in peripheral nerves

Olsson, Yngve

doi:10.1007/bf00686605

Cited by 205 publications

(15 citation statements)

References 72 publications

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“…Wallerian degeneration distal to the sciatic nerve ligature results in interruption of the blood-nerve barrier [61,62], thus allowing diffusion of signaling molecules produced by the Schwann and immune cells into blood flow [63,64]. An absence of blood-nerve barrier in the intact DRG [65-67] supports a possibility for diffusion of circulating signal molecules into the microenvironment of the DRG not associated with injured nerve.…”

Section: Discussionmentioning

confidence: 99%

Bilateral changes of TNF-α and IL-10 protein in the lumbar and cervical dorsal root ganglia following a unilateral chronic constriction injury of the sciatic nerve

Jančálek

Dubový

Svíženská

et al. 2010

J Neuroinflammation

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BackgroundThere is a growing body of evidence that unilateral nerve injury induces bilateral response, the mechanism of which is not exactly known. Because cytokines act as crucial signaling molecules for response of peripheral nerves to injury, they may be induced to mediate the reaction in remote structures.MethodsWe studied levels of tumor necrosis factor α (TNF-α) and interleukin 10 (IL-10) proteins using ELISA in the ipsilateral and contralateral lumbar (L4-L5) and cervical (C7-C8) dorsal root ganglia (DRG) from naïve rats, rats operated on to create unilateral chronic constriction injury (CCI) of the sciatic nerve, and sham-operated rats. Withdrawal thresholds for mechanical allodynia and thermal hyperalgesia were measured in the ipsilateral and contralateral hind and forepaws.ResultsThe ipsilateral hind paws of all rats operated upon for CCI displayed decreased withdrawal thresholds for mechanical allodynia and thermal hyperalgesia, while no significant behavioral changes were found in the contralateral hind paws and both forepaws. Significantly lower baseline levels of TNF-α and IL-10 protein were measured by ELISA in the lumbar than cervical DRG of naïve rats. Bilateral elevation of TNF-α was induced in both the lumbar and cervical DRG by unilateral CCI of the sciatic nerve for 7 and 14 days, while the level of IL-10 protein was increased bilaterally in the lumbar DRG 1 and 3 days after operation. IL-10 levels declined bilaterally even below baseline level in both cervical and lumbar DRG 7 days from CCI and normalized after 14 days. In contrast to no significant changes in TNF-α, level of IL-10 protein was significantly increased in the ipsilateral lumbar DRG after 3 days and bilaterally in the lumbar DRG after 14 days from sham operation.ConclusionsThe results of our experiments show a bilateral elevation of TNF-α and IL-10 not only in the homonymous DRG but also in the heteronymous DRG unassociated with the injured nerve. This suggests that bilaterally increased levels of TNF-α and IL-10 in DRG following unilateral CCI are linked with general neuroinflammatory reaction of the nervous system to injury rather than only to development and maintenance of neuropathic pain.

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Section: Discussionmentioning

confidence: 99%

Bilateral changes of TNF-α and IL-10 protein in the lumbar and cervical dorsal root ganglia following a unilateral chronic constriction injury of the sciatic nerve

Jančálek

Dubový

Svíženská

et al. 2010

J Neuroinflammation

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“…The blood-nerve barrier breaks down uniformly along the nerve within days of injury allowing large molecules to cross and enter the endoneurial space containing axons and Schwann cells (SCs) (Bruck, 1997; Olsson, 1966; Rotshenker, 2003; Seitz et al, 1985; Seitz et al, 1989). Concurrently, SCs dedifferentiate or trans-differentiate into a pro-regenerative phenotype within days.…”

Section: Peripheral Nerve Injury Axonal Regeneration and Functionalmentioning

confidence: 99%

Pathways regulating modality-specific axonal regeneration in peripheral nerve

Wood

Mackinnon

2015

Experimental Neurology

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Following peripheral nerve injury, the distal nerve is primed for regenerating axons by generating a permissive environment replete with glial cells, cytokines, and neurotrophic factors to encourage axonal growth. However, increasing evidence demonstrates regenerating axons within peripheral nerves still encounter axonal-growth inhibitors, such as chondroitin sulfate proteoglycans. Given the generally poor clinical outcomes following peripheral nerve injury and reconstruction, the use of pharmacological therapies to augment axonal regeneration and overcome inhibitory signals has gained considerable interest. Joshi et al (2014) have provided evidence for preferential or modality-specific (motor versus sensory) axonal growth and regeneration due to inhibitory signaling from Rho-associated kinase (ROCK) pathway regulation. By providing inhibition to the ROCK signaling pathway through Y-27632, they demonstrate that motor neurons regenerating their axons are impacted to a greater extent compared to sensory neurons. In light of this evidence, we briefly review the literature regarding modality-specific axonal regeneration to provide context to their findings. We also describe potential and novel barriers, such as senescent Schwann cells, which provide additional axonal-growth inhibitory factors for future consideration following peripheral nerve injury.

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“…The diameters of the continuous, nonfenestrated capillaries are larger than those of capillaries in adjacent skeletal muscle (6–10 vs. 3–6 μm) [11]. In contrast to leaky endoneurial vessels in new-borne mouse sciatic nerve, tight interendothelial junctions in adult endoneurial vessels represent the structural basis for restricted permeability to vascular tracers of various molecular weights [61, 105, 106, 109], while occasional open interendothelial gaps differentiate these vessels from the consistently tight vessels in most regions of the brain [11]. …”

Section: Blood–nerve Interfacementioning

confidence: 99%

Homeostatic regulation of the endoneurial microenvironment during development, aging and in response to trauma, disease and toxic insult

2010

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The endoneurial microenvironment, delimited by the endothelium of endoneurial vessels and a multi-layered ensheathing perineurium, is a specialized milieu intérieur within which axons, associated Schwann cells and other resident cells of peripheral nerves function. The endothelium and perineurium restricts as well as regulates exchange of material between the endoneurial microenvironment and the surrounding extracellular space and thus is more appropriately described as a blood–nerve interface (BNI) rather than a blood–nerve barrier (BNB). Input to and output from the endoneurial microenvironment occurs via blood–nerve exchange and convective endoneurial fluid flow driven by a proximo-distal hydrostatic pressure gradient. The independent regulation of the endothelial and perineurial components of the BNI during development, aging and in response to trauma is consistent with homeostatic regulation of the endoneurial microenvironment. Pathophysiological alterations of the endoneurium in experimental allergic neuritis (EAN), and diabetic and lead neuropathy are considered to be perturbations of endoneurial homeostasis. The interactions of Schwann cells, axons, macrophages, and mast cells via cell–cell and cell–matrix signaling regulate the permeability of this interface. A greater knowledge of the dynamic nature of tight junctions and the factors that induce and/or modulate these key elements of the BNI will increase our understanding of peripheral nerve disorders as well as stimulate the development of therapeutic strategies to treat these disorders.

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Studies on vascular permeability in peripheral nerves

Cited by 205 publications

References 72 publications

Bilateral changes of TNF-α and IL-10 protein in the lumbar and cervical dorsal root ganglia following a unilateral chronic constriction injury of the sciatic nerve

Bilateral changes of TNF-α and IL-10 protein in the lumbar and cervical dorsal root ganglia following a unilateral chronic constriction injury of the sciatic nerve

Pathways regulating modality-specific axonal regeneration in peripheral nerve

Homeostatic regulation of the endoneurial microenvironment during development, aging and in response to trauma, disease and toxic insult

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