Deletion of Tsc2 in nociceptors reduces target innervation, ion channel expression, and sensitivity to heat [PDF]
, 2018 The mechanistic target of rapamycin complex 1 (mTORC1) is known to regulate cellular growth pathways, and its genetic activation is sufficient to enhance regenerative axon growth following injury to the central or peripheral nervous systems.
Carlin, Dan +6 more
core +2 more sources
Pathogenic Role of FGFR3 Autoantibodies in Small Fiber Neuropathy
Advanced Science, EarlyView.Autoantibodies against fibroblast growth factor receptor 3 (FGFR3) are identified as pathogenic drivers of pain in small fiber neuropathy. By binding to sensory neurons in dorsal root ganglia, FGFR3 autoantibodies activate MAPK signaling and induce hyperexcitability and mechanical hypersensitivity, establishing FGFR3 autoantibodies as a therapeutic ...
Lyuba Y. Salih +12 more
wiley +1 more source
A Tac1‐Expressing Brainstem Pathway Underlies the Pathogenesis of Trigeminal Neuralgia
Advanced Science, EarlyView.A critical TG‐Sp5CTac1‐PBNTac1 pathway drives trigeminal neuropathic pain (TNP). Tac1‐expressing parabrachial nucleus (PBNTac1) neurons exhibit heightened responses to innocuous stimuli in TNP, and chemogenetic inhibition of these neurons effectively prevents TNP development.
Liting Sun +11 more
wiley +1 more source
Immune or genetic-mediated disruption of CASPR2 causes pain hypersensitivity due to enhanced primary afferent excitability [PDF]
, 2018 Human autoantibodies to contactin-associated protein-like 2 (CASPR2) are often associated with neuropathic pain, and CASPR2 mutations have been linked to autism spectrum disorders, in which sensory dysfunction is increasingly recognized.
Bennett, David L. +39 more
core +2 more sources
Defining the nociceptor transcriptome [PDF]
Frontiers in Molecular Neuroscience, 2014 Unbiased "omics" techniques, such as next generation RNA-sequencing, can provide entirely novel insights into biological systems. However, cellular heterogeneity presents a significant barrier to analysis and interpretation of these datasets.
Thakur, Matthew +9 more
openaire +4 more sources
Advanced Science, EarlyView.Sensory nerves help bones heal. This study shows that the neuropeptide CGRP, released from sensory nerves, slows down macrophage energy production, preventing excessive bone breakdown. By revealing this nerve–immune–metabolism connection, the work provides new insight into how the body balances bone repair and opens doors to targeted treatments ...
Jiaying Liu +10 more
wiley +1 more source
Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions [PDF]
, 2018 BACKGROUND: Containing a brain for signal processing and decision making, and a peripheral component for sensation and response, the nervous system provides higher organisms a powerful method of interacting with their environment.
Bullock, Daniel
core
Intense isolectin-B4 binding in rat dorsal root ganglion neurons distinguishes c-fiber nociceptors with broad action potentials and high nav1.9 expression [PDF]
, 2006 Binding to isolectin-B4 (IB4) and expression of tyrosine kinase A (trkA) (the high-affinity NGF receptor) have been used to define two different subgroups of nociceptive small dorsal root ganglion (DRG) neurons. We previously showed that only nociceptors
Berry, Carol +6 more
core +1 more source
Depletion of p75NTR in Schwann Cells Driven by Inflammation Mediates Cutaneous Pain in Psoriasis
Advanced Science, EarlyView.Psoriasis‐like inflammation induces proliferation and molecular remodeling of cutaneous Schwann cells, marked by reduced p75NTR and increased NGF expression. IL‐17A promotes this process, whereas Schwann cell‐specific p75NTR overexpression alleviates cutaneous pain in vivo.
Yibo Wang +9 more
wiley +1 more source
Current status and future directions of botulinum neurotoxins for targeting pain processing. [PDF]
, 2015 Current evidence suggests that botulinum neurotoxins (BoNTs) A1 and B1, given locally into peripheral tissues such as skin, muscles, and joints, alter nociceptive processing otherwise initiated by inflammation or nerve injury in animal models and humans.
Pellett, Sabine +2 more
core +2 more sources