Expression of Tight and Gap Junctional Proteins in the Perineurial Window Model of the Rat Sciatic Nerve

Ohta, Mituhiko; Okajima, Seiichiro; Hirakawa, Hisanori; Tokunaga, Daisaku; Fujiwara, Hiroyoshi; Oda, Ryo; Kobashi, Hiroaki; Hirata, Miyuki; Kubo, Toshikazu

doi:10.1080/00207450591001871

Cited by 6 publications

(4 citation statements)

References 21 publications

(28 reference statements)

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“…Detectable signs of recovery process, such as thin perineurial cell layer and first evidence of tight junctions appear within one week, and by three weeks perineurium has tight junction strands and gap junctions. Perineurial window model emphasizes the role of tight junctions in perineurial repair process 51 - 53 . Corresponding results have been shown in the nerve injury model in which ligating rat sciatic nerve for 24h resulted in the recovery of claudin-1 expression in perineurium within two days.…”

Section: Clinical Aspects Of the Peripheral Nerve Barrierssupporting

confidence: 55%

Barriers of the peripheral nerve

2013

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This review introduces the traditionally defined anatomic compartments of the peripheral nerves based on light and electron microscopic topography and then explores the cellular and the most recent molecular basis of the different barrier functions operative in peripheral nerves. We also elucidate where, and how, the homeostasis of the normal human peripheral nerve is controlled in situ and how claudin-containing tight junctions contribute to the barriers of peripheral nerve. Also, the human timeline of the development of the barriers of the peripheral nerve is depicted. Finally, potential future therapeutic modalities interfering with the barriers of the peripheral nerve are discussed.

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Section: Clinical Aspects Of the Peripheral Nerve Barrierssupporting

confidence: 55%

Barriers of the peripheral nerve

2013

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“…Although plasticity of peripheral gap junctions has been observed following nerve injury (Chandross et al, 1996;Nagaoka et al, 1999;Lin et al, 2002;Ohta et al, 2005), the evidence of their contribution to pain is very limited. A study by Lin et al (2002) suggested a role for Cx37 in neuropathic pain hypersensitivity following peripheral nerve injury through a correlation between the levels of sciatic nerve Cx37 mRNA and the extent of thermal hyperalgesia.…”

Section: Involvement Of Gap Junctions Inmentioning

confidence: 99%

Role of gap junctions in chronic pain

Green

Rupenthal

et al. 2011

J of Neuroscience Research

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Gap junctions are specialized transmembrane channels that allow rapid electrical signalling and direct intercellular communication for maintenance and coordination of normal cellular activities and homeostasis. Although gap junction channels in the nervous system mediate intercellular coupling between glial cells and between neurons, they also contribute to the spread of secondary damage and inflammation under pathological conditions. There is now evidence of the involvement of gap junctions in chronic pain caused by nervous system damage or tissue inflammation. In this Mini-Review, we highlight recent studies demonstrating the dynamic plasticity of gap junctions in response to nervous system injury and the effects of gap junction blockade on neuronal survival and modulation of pain in animal models of neuropathic and inflammatory pain. The involvement of dorsal root ganglia and spinal cord gap junctions in mediating chronic pain and the potential for targeting connexins as a novel modality for the treatment of intractable pain syndromes arising from nervous system injury and disorders are discussed.

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“…Tight junction proteins occludin and ZO-1 as well as gap junction protein connexin 43 were not detectable at 3 days after perineurial window, a surgery method that caused limited peripheral nerve injury. Tight junction proteins occludin and ZO-1 were recovered and re-observed at 7 days after injury while gap junction protein connexin 43 were re-observed after 21 days (Ohta et al, 2005). Gene and protein expressions of claudin-5 and occludin were found to be decreased starting from 3 h after chronic constriction injury of rat sciatic nerves (Moreau et al, 2016).…”

Section: Barrier Alternations Following Peripheral Nerve Injurymentioning

confidence: 99%

Pathophysiological Changes of Physical Barriers of Peripheral Nerves After Injury

Liu

Wang

2018

Front. Neurosci.

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Peripheral nerves are composed of complex layered anatomical structures, including epineurium, perineurium, and endoneurium. Perineurium and endoneurium contain many physical barriers, including the blood-nerve barrier at endoneurial vessels and the perineurial barrier. These physical barriers help to eliminate flux penetration and thus contribute to the establishment of a stable microenvironment. In the current review, we introduce the anatomical compartments and physical barriers of peripheral nerves and then describe the cellular and molecular basis of peripheral physical barriers. We also specifically explore peripheral nerve injury-induced changes of peripheral physical barriers, including elevated endoneurial fluid pressure, increased leakage of tracer, decreased barrier-type endothelial cell ratio, and altered distributions and expressions of cellular junctional proteins. The understanding of the pathophysiological changes of physical barriers following peripheral nerve injury may provide a clue for the treatment of peripheral nerve injury.

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Expression of Tight and Gap Junctional Proteins in the Perineurial Window Model of the Rat Sciatic Nerve

Cited by 6 publications

References 21 publications

Barriers of the peripheral nerve

Barriers of the peripheral nerve

Role of gap junctions in chronic pain

Pathophysiological Changes of Physical Barriers of Peripheral Nerves After Injury

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