ArticleeNeuro
Optogenetic Silencing of Nav1.8-Positive Afferents Alleviates Inflammatory and Neuropathic Pain.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 119 citations in OpenAlex.
- Sensing the skeleton: sensorineural regulation in bone.Nature reviews. Neuroscience · 2026Review
- Targeting Microglia-Neuron Crosstalk to Regulate Neuronal Excitability: Novel Translational Approaches for Chronic Pain Intervention.International journal of molecular sciences · 2026Review
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- Genetic identification of mouse trigeminal afferents responsible for mechanical allodynia.Cell reports · 2026Article
- Light-induced analgesia provides a drug-free optical method for pain relief via activation of TRAAK kNature communications · 2026Article
- Optogenetic modulation of peripheral nociceptive neurons with biocompatible optoelectronic implants.Bioengineering & translational medicine · 2025Article
- Loss of Glutaminase 1 in Small Sensory Neurons Prevents Nerve Injury Induced Mechanical Allodynia: Insights From Conditional Knockout Mice.European journal of pain (London, England) · 2025Article
- Review
- Central terminals of primary afferents coordinate the spontaneous activity of dorsal horn neurons.The Journal of physiology · 2025Article
- Nav1.8 and Chronic Pain: From Laboratory Animals to Clinical Patients.Biomolecules · 2025Review
- Article
- Article
- TRPC3/6 Channels Mediate Mechanical Pain Hypersensitivity via Enhancement of Nociceptor Excitability and of Spinal Synaptic Transmission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Optogenetic Activation of Peripheral Somatosensory Neurons in Transgenic Mice as a Neuropathic Pain Model for Assessing the Therapeutic Efficacy of Analgesics.ACS pharmacology & translational science · 2024Article
- Emerging optogenetics technologies in biomedical applications.Smart medicine · 2023Review
- Optogenetic and Chemogenic Control of Pain Signaling: Molecular Markers.International journal of molecular sciences · 2023Review
- The insulin receptor regulates the persistence of mechanical nociceptive sensitization in flies and mice.Biology open · 2023Article
- Persistent nociceptor hyperactivity as a painful evolutionary adaptation.Trends in neurosciences · 2023Review
- Peripheral mechanisms of peripheral neuropathic pain.Frontiers in molecular neuroscience · 2023Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
We report a novel transgenic mouse model in which the terminals of peripheral nociceptors can be silenced optogenetically with high spatiotemporal precision, leading to the alleviation of inflammatory and neuropathic pain. Inhibitory archaerhodopsin-3 (Arch) proton pumps were delivered to Nav1.8(+) primary afferents using the Nav1.8-Cre driver line. Arch expression covered both peptidergic and nonpeptidergic nociceptors and yellow light stimulation reliably blocked electrically induced action potentials in DRG neurons. Acute transdermal illumination of the hindpaws of Nav1.8-Arch(+) mice significantly reduced mechanical allodynia under inflammatory conditions, while basal mechanical sensitivity was not affected by the optical stimulation. Arch-driven hyperpolarization of nociceptive terminals was sufficient to prevent channelrhodopsin-2 (ChR2)-mediated mechanical and thermal hypersensitivity in double-transgenic Nav1.8-ChR2(+)-Arch(+) mice. Furthermore, prolonged optical silencing of peripheral afferents in anesthetized Nav1.8-Arch(+) mice led to poststimulation analgesia with a significant decrease in mechanical and thermal hypersensitivity under inflammatory and neuropathic conditions. These findings highlight the role of peripheral neuronal inputs in the onset and maintenance of pain hypersensitivity, demonstrate the plasticity of pain pathways even after sensitization has occurred, and support the involvement of Nav1.8(+) afferents in both inflammatory and neuropathic pain. Together, we present a selective analgesic approach in which genetically identified subsets of peripheral sensory fibers can be remotely and optically inhibited with high temporal resolution, overcoming the compensatory limitations of genetic ablations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.