Agrin Downregulation Induced by Nerve Injury Contributes to Neuropathic Pain

Bazán, Nicolás G.

doi:10.1523/jneurosci.4418-10.2010

Cited by 7 publications

(4 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Activation of GABA interneurons by NR1 phosphorylation was argued to inactivate the postsynaptic relaying neurons, consequently interrupting the pain. Unexpectedly, a decrease of the activation of glia did not suppress the allodynia [57].…”

Section: Controversial Issues Regarding the Role Of Glia In Neuropathmentioning

confidence: 79%

“…Thus, Yaksh et al [56] emphasized the sensitization of central terminals of C-fibers in the substantia gelatinosa of the dorsal horn as the key to hyperalgesia and allodynia induced by peripheral nerve injury, but did not refer to the role of CNS glia. In a recent report [57], the function of agrin (a single geneencoded sulfate proteoglycan which gather up various molecules ensuing specific functions) suppressing neuropathic pain (mechanical allodynia) through phosphorylation of the NMDA receptor (NR1 subunits) on GABA interneurons of the rat dorsal horn was demonstrated after sciatic nerve injury. Activation of GABA interneurons by NR1 phosphorylation was argued to inactivate the postsynaptic relaying neurons, consequently interrupting the pain.…”

Section: Controversial Issues Regarding the Role Of Glia In Neuropathmentioning

confidence: 99%

See 1 more Smart Citation

Roles of Glia, Immune Cells and the Thermo-TRP Channels, TRPV1, TRPA1 and TRPM8, in Pathological Pain

Hiura¹

2012

TONEURJ

View full text Add to dashboard Cite

Studies into the interactions between glia/immune cells and neurons have focused on the induction of pathological (neuropathic or inflammatory) pain. Growing evidence of close relationships between peripheral and central glia and pathological pain has emerged during the last 2 decades. Numerous experimental studies have showed the release of cytokines and inflammatory neuropeptides from peripheral and central terminals of primary sensory neurons and from activated peripheral and central glia after nerve injury (crush, ligation or transection), which in turn act in a paracrine or autocrine manner. Cytokines induce the synthesis of algogens (pain-inducing substances such as prostaglandin) which leads to the primary (peripheral) or secondary (central) sensitization responsible for hyperalgesia or allodynia under inflammatory conditions. The review has also highlighted the role of thermo transient receptor potential (TRP) channels TRPV1, TRPA1 and TRPM8 in the induction of pathological pain. The noxious heat sensor TRPV1 has an overt role in noxious heat hyperalgesia or allodynia, whereas TRPA1 and TRPM8 seem to have roles in noxious cold or mechanical allodynia, although results are inconsistent. Close mutual interrelationships between immune and glial cells and thermoTRP channels via cytokines or pro-inflammatory neuropeptides cannot be ignored when attempting to explain the induction and continuation of pathological pain. Investigations on the initial signals sent to the central area (superficial dorsal horn) remote from injured (or infectious) sites are a key point to clarify the mechanisms of pathological pain.

show abstract

Section: Controversial Issues Regarding the Role Of Glia In Neuropathmentioning

confidence: 79%

Section: Controversial Issues Regarding the Role Of Glia In Neuropathmentioning

confidence: 99%

Roles of Glia, Immune Cells and the Thermo-TRP Channels, TRPV1, TRPA1 and TRPM8, in Pathological Pain

Hiura¹

2012

TONEURJ

View full text Add to dashboard Cite

show abstract

“…Agrin is a heparin sulfate proteoglycan of approximately 220 kDa that plays an important role in development of the neuromuscular junction by inducing the aggregation of acetylcholine receptors during synaptogenesis [12]. Administration of Nano PGE1 led to upregulation of agrin expression in the injured sciatic nerve and in atrophic muscle, which may have facilitated the restoration of neuromuscular transmission.…”

Section: Discussionmentioning

confidence: 99%

Nano PGE1 Enhances Phosphorylation of ERK1/2 and Akt to Promote Recovery from Motor Dysfunction and Muscle Atrophy Induced by Sciatic Nerve Injury

Takenaga¹,

Ishihara²,

Niimi³

et al. 2019

Preprint

View full text Add to dashboard Cite

The effect of prostaglandin E1 (PGE1) encapsulated in nanoparticles (Nano PGE1) on motor dysfunction and muscle atrophy induced by sciatic nerve injury (SNI) was investigated in rats, and was compared with PGE1 encapsulated in lipid microspheres (Lipo PGE1) or PGE1 clathrated in cyclodextrin (PGE1-CD). The hind limb muscle weight ratio decreased until 2 weeks after SNI. All 3 PGE1 formulations significantly improved SNI-induced motor dysfunction. Nano PGE1 significantly promoted recovery from muscle atrophy at 2 and 3 weeks after SNI. Lipo PGE1 was also effective, but multiple doses were required. Compared with the SNI control group, the Nano PGE1 group showed upregulation of vascular endothelial growth factor (VEGF) and agrin expression in the injured sciatic nerve and atrophic muscles. Nano PGE1 accumulated prominently at the site of nerve injury and persisted for longer than Lipo PGE1 or PGE1-CD. Expression of all EP receptors was detected in the normal sciatic nerve, and EP2 expression increased after SNI. Finally, Nano PGE1 promoted ERK1/2 and Akt phosphorylation. These findings suggest that PGE1 released from nanoparticles accumulates at sites of nerve injury and increases VEGF production by augmenting ERK1/2 phosphorylation via EP receptor signaling, thus promoting tissue repair and regeneration.

show abstract

“…AAV2 vectors were injected through a needle inserted into the superficial lamina of L4–5 DH along with the root entry at a depth of 220–250 µm with a micromanipulator (Cui and Bazan, ). Changes of behavior started only 48 hr after injection and lasted for 7 days.…”

Section: Delivery Methods Of Aav Vectors Into Spinal Cordmentioning

confidence: 99%

Lentiviral Vectors and Adeno‐Associated Virus Vectors: Useful Tools for Gene Transfer in Pain Research

Zheng

Wang

Bai

et al. 2018

The Anatomical Record

View full text Add to dashboard Cite

Pain, especially chronic pain, has always been a heated point in both basic and clinical researches since it puts heavy burdens on both individuals and the whole society. A better understanding of the role of biological molecules and various ionic channels involved in pain can shed light on the mechanism under pain and advocate the development of pain management. Using viral vectors to transfer specific genes at targeted sites is a promising method for both research and clinical applications. Lentiviral vectors and adeno-associated virus (AAV) vectors which allow stable and long-term expression of transgene in non-dividing cells are widely applied in pain research. In this review, we thoroughly outline the structure, category, advantages and disadvantages and the delivery methods of lentiviral and AAV vectors. The methods through which lentiviral and AAV vectors are delivered to targeted sites are closely related with the sites, level and period of transgene expression. Focus is placed on the various delivery methods applied to deliver vectors to spinal cord and dorsal root ganglion both of which play important roles in primary nociception. Our goal is to provide insight into the features of these two viral vectors and which administration approach can be chosen for different pain researches. Anat Rec,

show abstract

Agrin Downregulation Induced by Nerve Injury Contributes to Neuropathic Pain

Cited by 7 publications

References 47 publications

Roles of Glia, Immune Cells and the Thermo-TRP Channels, TRPV1, TRPA1 and TRPM8, in Pathological Pain

Roles of Glia, Immune Cells and the Thermo-TRP Channels, TRPV1, TRPA1 and TRPM8, in Pathological Pain

Nano PGE1 Enhances Phosphorylation of ERK1/2 and Akt to Promote Recovery from Motor Dysfunction and Muscle Atrophy Induced by Sciatic Nerve Injury

Lentiviral Vectors and Adeno‐Associated Virus Vectors: Useful Tools for Gene Transfer in Pain Research

Contact Info

Product

Resources

About