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Microgliosis in the spinal dorsal horn early after peripheral nerve injury is associated with damage to primary afferent aβ-fibers
Shibata Y, Matsumoto Y, Kohno K, Nakashima Y, Tsuda M (2025) Microgliosis in the spinal dorsal horn early after peripheral nerve injury is associated with damage to primary afferent aβ-fibers. Cells 14(9):666. doi: 10.3390/cells14090666 PMID: 40358190
Objective: To investigate the spatial relationship between microgliosis and the projections of injured nerves by generating mice that had expressed tdTomato in the fourth lumbar dorsal root ganglion (L4-DRG) neurons via intra-L4-spinal nerve (SpN) injection of adeno-associated viral vectors.
Summary: After transection of the L4-SpN, authors found that microgliosis in the SDH selectively occurred in the innervation territories of the injured primary afferent fibers. However, denervating transient receptor potential vanilloid 1 (TRPV1)-expressing primary afferent fibers in theSDH through intrathecal injection of capsaicin did not trigger microgliosis, nor did it influence the microgliosis induced by L4-SpN injury. Conversely, pharmacological damage to myelinated DRG neurons, including Aβ-fibers, was sufficient to induce microgliosis. Furthermore, L4-SpN injury also induced microgliosis in the gracile nucleus, which primarily receives innervation from Aβ-fibers. These findings suggest that microgliosis in the SDH shortly after peripheral nerve injury is predominantly associated with damage to primary afferent Aβ-fibers.
Usage: WT mice were injected with saporin into the L4-SpN, administering 400 nL of saporin solution [saporin conjugated with cholera toxin B subunit (CTB-SAP), isolectin B4 (IB4-SAP),and unconjugated saporin (Ctrl-SAP)]
Related Products: CTB-SAP (Cat. #IT-14), IB4-SAP (Cat. #IT-10), Saporin (Cat. #PR-01)
T cell death-associated gene 8-mediated distinct signaling pathways modulate the early and late phases of neuropathic pain
Dai SP, Yang CC, Chin Y, Sun WH (2024) T cell death-associated gene 8-mediated distinct signaling pathways modulate the early and late phases of neuropathic pain. iScience 27(10):110955. doi: 10.1016/j.isci.2024.110955 PMID: 39381739
Objective: To elucidate how T cell death-associated gene 8 (TDAG8)-mediated signaling modulates neuron activities in a mouse model of chronic constriction injury-induced neuropathic pain.
Summary: TDAG8 participated alone in mechanical allodynia induced by constriction injury. TDAG8-Nav1.8 signaling in small-diameter isolectin B4-positive [IB4(+)] neurons initiate mechanical allodynia; it also modulated substance P release from IB4(-) neurons to facilitate the development of early mechanical allodynia. TDAG8-mediated signaling increased medium-to large-diameter IB4(-) neuron activity to maintain late mechanical allodynia; it also modulated substance P release in soma to reduce satellite glial number and Nav1.7 expression, thus attenuating chronic mechanical allodynia.
Usage: Mice were intrathecally injected with IB4-saporin (IB4-SAP, 0.06 mg/mL) or Saporin (0.06 mg/mL)
Related Products: IB4-SAP (Cat. #IT-10), Saporin (Cat. #PR-01)
Isolectin B4 (IB4)-conjugated streptavidin for the selective knockdown of proteins in IB4-positive (+) nociceptors
Bogen O, Araldi D, Sucher A, Kober K, Ohara PT, Levine JD (2024) Isolectin B4 (IB4)-conjugated streptavidin for the selective knockdown of proteins in IB4-positive (+) nociceptors. Mol Pain doi: 10.1177/17448069241230419 PMID: 38246917
Objective: To address the need for selective transfection methods, the authors covalently linked isolectin B4 (IB4) to streptavidin and analyzed whether it could be used to study protein function in IB4(+)-nociceptors
Summary: Rats treated intrathecally with IB4-conjugated streptavidin complexed with biotinylated antisense oligonucleotides for protein kinase C epsilon (PKCε) mRNA werefound to have: (a) less PKCε in dorsal root ganglia (DRG), (b) reduced PKCε expression in IB4(+) but not IB4(–) DRG neurons, and (c) fewer transcripts of the PKCε gene in the DRG. This knockdown in PKCε expression in IB4(+) DRG neurons is sufficient to reverse hyperalgesic priming, a rodent model of chronic pain that is dependent on PKCε in IB4(+)- nociceptors.
Usage: For each intrathecal injection 2.3μL IB4-streptavidin (30 pmol of conjugate with 120 pmol of biotin binding sites), 1.2μL biotinylated ODN (c = 100 pmol/μl) and 16.5μL PBS were mixed (injection volume = 20μL),
Related Products: Streptavidin-ZAP (Cat. #IT-27), IB4-SAP (Cat. #IT-10)
Featured Article: Selective ablation of IB4+ primary afferent neurons reduces mechanical and cold hyperalgesia in an EAE mouse model of multiple sclerosis
Nguyen KL, Lamerand SR, Deshpande RP, Taylor BK (2021) Featured Article: Selective ablation of IB4+ primary afferent neurons reduces mechanical and cold hyperalgesia in an EAE mouse model of multiple sclerosis. Targeting Trends 22
Related Products: IB4-SAP (Cat. #IT-10), Blank-SAP (Cat. #IT-21)
Read the featured article in Targeting Trends.
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A spinal microglia population involved in remitting and relapsing neuropathic pain
Kohno K, Shirasaka R, Yoshihara K, Mikuriya S, Tanaka K, Takanami K, Inoue K, Sakamoto H, Ohkawa Y, Masuda T, Tsuda M (2022) A spinal microglia population involved in remitting and relapsing neuropathic pain. Science 376(6588):86-90. doi: 10.1126/science.abf6805
Objective: To investigate pain recovery mechanisms.
Summary: The authors reveal a mechanism for the remission and recurrence ofneuropathic pain, providing potential targets for therapeutic strategies.
Usage: The dose of CTB-SAP and IB4-SAP was 8 ug/10 uL, diluted in PBS.
Related Products: CTB-SAP (Cat. #IT-14), IB4-SAP (Cat. #IT-10)
Contribution of small diameter non-peptidergic primary afferent neurons to central neuropathic pain in a new, more clinically relevant mouse model of multiple sclerosis
Nguyen KL, Lamerand SR, Deshpande RP, Taylor BK (2021) Contribution of small diameter non-peptidergic primary afferent neurons to central neuropathic pain in a new, more clinically relevant mouse model of multiple sclerosis. Neuroscience 2021 Abstracts P377/07. Society for Neuroscience, Virtual.
Summary: Over 50% of multiple sclerosis (MS) patients suffer from neuropathic pain (MSNP). Current treatments give inadequate relief due to incomplete understanding of underlying mechanisms. Recent electrophysiological recordings of primary afferent neurons (PAN) in the dorsal root ganglion (DRG) following experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, revealed increased afterhyperpolarization in small-diameter fibers. These data form the premise of our goal to understand the contribution of small-diameter (peptidergic or non-peptidergic) PANs to MSNP. Arguably the most common method to induce EAE is administration of myelin oligodendrocyte glycoprotein (MOG) to generate an autoimmune response targeting the myelin sheath. A MOG fragment is typically given with two adjuvants: complete Freund’s adjuvant (CFA) to boost immunogenicity and pertussis toxin (PTX) to breakdown the blood-brain barrier and facilitate CNS immune cell infiltration. However, PTX can disrupt G-protein coupled receptors, cause pain, and alter autoimmune response gene expression. In 10-week-old C57BL/6 mice, we conducted the first rigorous comparison of a classic PTX EAE model with the novel non-PTX (nPTX) EAE model. We found that both PTX and nPTX EAE mouse models showed the same degree of: 1) motor deficits; 2) plantar hindpaw mechanical and cold hypersensitivity (except cold hypersensitivity resolved more quickly after PTX EAE than nPTX EAE); and 3) lumbar spinal cord demyelination. Unlike most rodent models of MS including PTX EAE, the nPTX EAE group exhibited somatosensory cortex demyelination, a core feature of MS in human patients and cold hypersensitivity. We suggest nPTX EAE to be the most clinically relevant rodent model available to study not only MSNP, but MS in general. To evaluate the contribution of peptidergic and non-peptidergic neurons to MSNP, we induced nPTX EAE. After 12 days we administered capsaicin (10µg/mouse, i.t.) or IB4-saporin (1.5µg/mouse, i.t.) to primarily ablate peptidergic or nonpeptidergic C-fibers, respectively. Ablation efficacy was successfully confirmed with dramatic loss in DRG of TRPV1/CGRP immunoreactivity (peptidergic C-fibers) following capsaicin, and IB4 immunoreactivity (nonpeptidergic C-fibers) following IB4-saporin. IB4-saporin, but not capsaicin, partially reduced mechanical hypersensitivity and reversed cold hypersensitivity within 9 days. These data suggest nonpeptidergic but not peptidergic C-fibers contribute to MSNP. Our next studies will use genetic knockout, chemogenetic, and optogenetic strategies using MrgprdCreER mice to modulate the activity of nonpeptidergic C-fibers.
Related Products: IB4-SAP (Cat. #IT-10)
Nociception impedes grasping recovery in the spinal cord injured rat.
Walker J, Kim T, Giszter S, Detloff MR (2021) Nociception impedes grasping recovery in the spinal cord injured rat. Neuroscience 2021 Abstracts P372.04. Society for Neuroscience, Virtual.
Related Products: IB4-SAP (Cat. #IT-10)
TRP channels in cancer pain
de Almeida AS, Bernardes LB, Trevisan G (2021) TRP channels in cancer pain. Eur J Pharmacol 904:174185. doi: 10.1016/j.ejphar.2021.174185 PMID: 34015320
Objective: To describe the role of TRP vanilloid 1 (TRPV1) and TRP ankyrin 1 (TRPA1) involved in cancer pain mechanisms.
Summary: Several studies have revealed that the administration of TRPV1 or TRPA1 agonists/antagonists and TRPV1 or TRPA1 knockdown reduced sensitivity to nociception in cancer pain models. Thus, TRP channels are potential targets for managing cancer-related pain syndromes.
Usage: Ablation of IB4 (+) neurons.
Related Products: IB4-SAP (Cat. #IT-10)
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Studying human nociceptors: from fundamentals to clinic
Middleton SJ, Barry AM, Comini M, Li Y, Ray PR, Shiers S, Themistocleous AC, Uhelski ML, Yang X, Dougherty PM, Price TJ, Bennett DL (2021) Studying human nociceptors: from fundamentals to clinic. Brain 144(5):1312-1335. doi: 10.1093/brain/awab048
Summary: The authors injected 5 µg of IB4-SAP into the sciatic nerve in the left thigh. Lesioned animals displayed attenuated NGF-induced hyperalgesia, as well as differences in other pain-model markers.
Related Products: IB4-SAP (Cat. #IT-10)
Antiplexin D1 antibodies relate to small fiber neuropathy and induce neuropathic pain in animals
Fujii T, Lee EJ, Miyachi Y, Yamasaki R, Lim YM, Iinuma K, Sakoda A, Kim KK, Kira JI (2021) Antiplexin D1 antibodies relate to small fiber neuropathy and induce neuropathic pain in animals. Neurol Neuroimmunol Neuroinflamm 8(5):e1028. doi: 10.1212/NXI.0000000000001028
Summary: NeP patient-derived plexin D1-IgG selectively binds to isolectin B4-positive unmyelinated C-fiber type small DRG neurons that sense mechanical pain.
Related Products: IB4-SAP (Cat. #IT-10)