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The pharmacotherapeutic potential of neuropeptide Y for chronic pain
Nie AA, Taylor BK (2025) The pharmacotherapeutic potential of neuropeptide Y for chronic pain. J Intern Med 298(4):280-896. doi: 10.1111/joim.20118 PMID: 40754889
Objective: To evaluate how neuropeptide Y (NPY) and its receptor subtypes (Y1 and Y2) regulate acute and chronic pain, and to explore the therapeutic potential of targeting these pathways for the treatment of neuropathic and inflammatory pain.
Summary: The review highlights that spinal Y1-interneurons contribute to both sensory and affective components of chronic pain and that Y1 receptor activation can inhibit pronociceptive signaling. Prior studies using NPY-SAP demonstrated that ablation of Y1-expressing neurons reduces hypersensitivity in models of nerve injury and inflammation, supporting Y1 modulation as a therapeutic avenue.
Usage: NPY-SAP (IT-28) was referenced in the context of earlier studies employing intrathecal administration to ablate spinal Y1-interneurons.
Related Products: NPY-SAP (Cat. #IT-28)
See Also:
- Nelson TS et al. Facilitation of neuropathic pain by the NPY Y1 receptor-expressing subpopulation of excitatory interneurons in the dorsal horn. Sci Rep 9(1):7248, 2019.
- Lemons LL et al. Neuropeptide Y receptor-expressing dorsal horn neurons: role in nocifensive reflex and operant responses to aversive cold after CFA inflammation. Neuroscience 216:158-166, 2012.
NGF in neuropathic pain: Understanding its role and therapeutic opportunities
García-Domínguez M (2025) NGF in neuropathic pain: Understanding its role and therapeutic opportunities. Curr Issues Mol Biol 47(2):93. doi: 10.3390/cimb47020093 PMID: 39996814
Objective: To determine the use of NGF as an important biomarker and therapeutic target in the management of neuropathic pain
Summary: Taking advantage of the multifaceted dynamics of NGF could provide effective pain management therapies to finally respond to the unmet needs of patients experiencing neuropathic pain. Kras et al. used saporin conjugates targeted to neurons involved in either peptidergic signaling and NGF-induced mechanical and thermal hypersensitivity in the forepaws.
Related Products: Saporin (Cat. #PR-01)
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Descending facilitation from rostral ventromedial medulla mu opioid receptor-expressing neurons is necessary for maintenance of sensory and affective dimensions of chronic neuropathic pain
Dogrul BN, Dogrul BN, Machado Kopruszinski C, Dolatyari Eslami M, Watanabe M, Luo S, Moreira de Souza LH, Vizin RL, Yue X, Palmiter RD, Navratilova E, Porreca F (2025) Descending facilitation from rostral ventromedial medulla mu opioid receptor-expressing neurons is necessary for maintenance of sensory and affective dimensions of chronic neuropathic pain. Pain 166(1):153-159. doi: 10.1097/j.pain.0000000000003360 PMID: 39058958
Objective: To determine whether rostral ventromedial medulla (RVM) mu opioid receptor (MOR)–expressing neurons are required for the expression and maintenance of established neuropathic pain.
Summary: Using chemogenetic silencing of MOR-expressing neurons, the study showed that inhibition of RVM-MOR cells reversibly reduces tactile allodynia and the affective component of neuropathic pain, demonstrating that descending facilitation from these neurons sustains chronic pain. The authors reference earlier findings using Dermorphin-SAP to confirm that complete ablation of MOR-expressing RVM neurons prevents neuropathic pain development without affecting acute surgical pain.
Usage: Dermorphin-SAP (IT-12) was referenced from prior studies as a method for selective ablation of MOR-expressing RVM neurons that prevented mechanical allodynia following spinal nerve ligation.
Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12)
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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)
Repopulated spinal cord microglia exhibit a unique transcriptome and contribute to pain resolution
Donovan LJ, Bridges CM, Nippert AR, Wang M, Wu S, Forman TE, Haight ES, Huck NA, Bond SF, Jordan CE, Gardner AM, Nair RV, Tawfik VL (2024) Repopulated spinal cord microglia exhibit a unique transcriptome and contribute to pain resolution. Cell Rep 43(2):113683. doi: 10.1016/j.celrep.2024.113683 PMID: 38261512
Objective: To study the role of microglia in pain resolution and determine if repopulated microglia actively resolve pain or initiate the transition from acute to chronic pain.
Summary: Pain resolution coincides with microglial repopulation in the spinal cord rather than depletion. Repopulated microglia exhibit unique gene expressions related to phagocytosis and stress response in mice. The study identified potential targets for developing microglial-targeted pain therapeutics by comparing mouse and human spinal cord microglial datasets.
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)
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Locus coeruleus-noradrenergic modulation of trigeminal pain: Implications for trigeminal neuralgia and psychiatric comorbidities
Donertas-Ayaz B, Caudle RM (2023) Locus coeruleus-noradrenergic modulation of trigeminal pain: Implications for trigeminal neuralgia and psychiatric comorbidities. Neurobiol Pain 13:100124. doi: 10.1016/j.ynpai.2023.100124 PMID: 36974102
Objective: To summarize the knowledge about the involvement of noradrenaline in acute and chronic trigeminal pain conditions and how the activity of the locus coeruleus (LC) noradrenergic neurons changes in response to acute and chronic pain conditions and how these changes might be involved in pain-related comorbidities including anxiety, depression, and sleep disturbance.
Summary: LC inhibition of nociceptive transmission in acute pain and in longterm neuropathic pain increases the tonic activity of LC-NA neurons. These changes may contribute to impaired descending pain modulation and pain-related comorbidities such as depression, anxiety, and sleep disorders.
Usage: Elimination of NA neurons via injection of anti-dopamine β-hydroxylase-saporin (Anti-DBH-SAP) into the lateral ventricle and trigeminal brainstem nuclei three weeks after infraorbital nerve injury attenuated mechanical allodynia
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Uncovering central and peripheral pain mechanisms in Alzheimer’s disease
Silva AR (2022) Uncovering central and peripheral pain mechanisms in Alzheimer’s disease. King’s College London Thesis.
Objective: To investigate alterations within the nociceptive pathways, under neuropathic pain conditions.
Summary: The data suggest a disrupted opioidergic tone in TASTPM mice, which followed by peripheral nerve injury, is mediated by peripheral immune cells.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
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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)