Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Nociception01:44

Nociception

29.3K
Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.
29.3K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

2.5K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
2.5K
Analgesia and Pain Management01:25

Analgesia and Pain Management

764
Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
764
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

7.8K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.8K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Corneal Innervation Research at a Crossroads: A Tool-Driven Roadmap for the Future.

Investigative ophthalmology & visual science·2026
Same author

The production of the chemokine CCL2 by corneal sensory neurons initiates anti-viral immunity at the cornea and trigeminal ganglion.

Cell reports·2025
Same author

Distinct human small intestinal microbiome communities underlie visceral hypersensitivity in a humanized mouse model.

The Journal of clinical investigation·2025
Same author

Rethinking relief: Targeting sensory neurons to combat cancer and pain.

Cancer cell·2025
Same author

Prostaglandin E2 as a Mechanistic Biomarker of Chronic Pancreatitis.

Clinical and translational gastroenterology·2025
Same author

Clinical and Economic Correlates of Pharmacotherapy in Patients with Essential Tremor.

Tremor and other hyperkinetic movements (New York, N.Y.)·2024

Related Experiment Video

Updated: Aug 29, 2025

Teasing Out the Interplay Between Natural Killer Cells and Nociceptor Neurons
09:40

Teasing Out the Interplay Between Natural Killer Cells and Nociceptor Neurons

Published on: June 30, 2022

2.3K

Neuronally expressed PDL1, not PD1, suppresses acute nociception.

Kimberly A Meerschaert1, Brian S Edwards2, Ariel Y Epouhe1

  • 1Pittsburgh Center for Pain Research, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Center for Neuroscience, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.

Brain, Behavior, and Immunity
|September 11, 2022
PubMed
Summary
This summary is machine-generated.

Programmed death-ligand 1 (PDL1) is expressed in neurons and influences pain perception. Activating neuronal PDL1 with soluble PD1 reduces pain responses by modulating TRPV1 channels, suggesting a role in pain regulation.

Keywords:
AnalgesiaDRGNeuroimmuneNociceptor sensitizationReverse signalingSex difference

More Related Videos

Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies
08:16

Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies

Published on: October 6, 2022

6.5K
Author Spotlight: Magnetic Fluorescent Bead-Based Dual-Reporter Flow Analysis of PDL1-Vaxx Peptide Vaccine-Induced Antibody Blockade of the PD-1/PD-L1 Interaction
10:18

Author Spotlight: Magnetic Fluorescent Bead-Based Dual-Reporter Flow Analysis of PDL1-Vaxx Peptide Vaccine-Induced Antibody Blockade of the PD-1/PD-L1 Interaction

Published on: July 7, 2023

1.4K

Related Experiment Videos

Last Updated: Aug 29, 2025

Teasing Out the Interplay Between Natural Killer Cells and Nociceptor Neurons
09:40

Teasing Out the Interplay Between Natural Killer Cells and Nociceptor Neurons

Published on: June 30, 2022

2.3K
Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies
08:16

Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies

Published on: October 6, 2022

6.5K
Author Spotlight: Magnetic Fluorescent Bead-Based Dual-Reporter Flow Analysis of PDL1-Vaxx Peptide Vaccine-Induced Antibody Blockade of the PD-1/PD-L1 Interaction
10:18

Author Spotlight: Magnetic Fluorescent Bead-Based Dual-Reporter Flow Analysis of PDL1-Vaxx Peptide Vaccine-Induced Antibody Blockade of the PD-1/PD-L1 Interaction

Published on: July 7, 2023

1.4K

Area of Science:

  • Neuroimmunology
  • Pain research
  • Molecular biology

Background:

  • Programmed death-ligand 1 (PDL1) typically mediates immunosuppression by binding to PD1 on immune cells.
  • Previous research indicates PD1 is mainly on immune cells, not neurons.
  • Neuronal PDL1 expression and its signaling pathways (reverse signaling) are largely uncharacterized.

Purpose of the Study:

  • To investigate the expression and function of neuronal PDL1.
  • To explore the role of neuronal PDL1 in pain modulation.
  • To elucidate the intracellular signaling mechanisms of PDL1 reverse signaling in neurons.

Main Methods:

  • Single neuron qPCR, immunolabeling, and flow cytometry to assess PD1 and PDL1 expression in neurons.
  • Administration of soluble PD1 to mice to study its effects on nociception.
  • Calcium imaging in dissociated sensory neurons to examine TRPV1 activity.
  • Behavioral tests in wild-type and PDL1 knockout mice to assess pain responses.

Main Results:

  • Widespread PDL1 expression was found in sensory and sympathetic neurons, while PD1 was absent.
  • Administration of soluble PD1 reduced pain behaviors induced by capsaicin.
  • Exogenous PD1 decreased TRPV1-dependent calcium transients and TRPV1 membrane expression in sensory neurons.
  • PD1 administration had no effect on pain in sensory neuron-specific PDL1 knockout mice.

Conclusions:

  • Neuronal PDL1 is expressed and functional, playing a role in modulating pain sensitivity.
  • Activation of neuronal PDL1 by soluble PD1 can reduce nociception via TRPV1.
  • Neuronal PDL1 represents a potential homeostatic mechanism for regulating acute pain.