ArticleMolecular pain
Tachykinins modulate nociceptive responsiveness and sensitization: In vivo electrical characterization of primary sensory neurons in tachykinin knockout (Tac1 KO) mice.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Rapid peripheral reprogramming of myelinated afferents drives human hyperalgesia.bioRxiv : the preprint server for biology · 2026Article
- Drug-assisted synthesis of copper nanoparticles and their induction of cuproptosis and necrosis for breast cancer therapy.Journal of Zhejiang University. Science. B · 2025Article
- A multi-omic atlas of human autonomic and sensory ganglia implicates cell types in peripheral neuropathies.bioRxiv : the preprint server for biology · 2025Article
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- Description of Novel Molecular Factors in Lumbar DRGs and Spinal Cord Factors Underlying Development of Neuropathic Pain Component in the Animal Model of Osteoarthritis.Molecular neurobiology · 2024Article
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- Influence of the Peripheral Nervous System on Murine Osteoporotic Fracture Healing and Fracture-Induced Hyperalgesia.International journal of molecular sciences · 2022Article
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- Put in a "CaCells · 2022Review
- Neurokinin-1 receptor is an effective target for treating leukemia by inducing oxidative stress through mitochondrial calcium overload.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Developing Modern Pain Therapies.Frontiers in neuroscience · 2019Review
- Seeding of breast cancer cell line (MDA-MB-231Molecular painArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Since the failure of specific substance P antagonists to induce analgesia, the role of tachykinins in the development of neuropathic pain states has been discounted. This conclusion was reached without studies on the role of tachykinins in normal patterns of primary afferents response and sensitization or the consequences of their absence on the modulation of primary mechanonociceptive afferents after injury. Nociceptive afferents from animals lacking tachykinins (Tac1 knockout) showed a disrupted pattern of activation to tonic suprathreshold mechanical stimulation. These nociceptors failed to encode the duration and magnitude of natural pronociceptive stimuli or to develop mechanical sensitization as consequence of this stimulation. Moreover, paw edema, hypersensitivity, and weight bearing were also reduced in Tac1 knockout mice 24 h after paw incision surgery. At this time, nociceptive afferents from these animals did not show the normal sensitization to mechanical stimulation or altered membrane electrical hyperexcitability as observed in wild-type animals. These changes occurred despite a similar increase in calcitonin gene-related peptide immunoreactivity in sensory neurons in Tac1 knockout and normal mice. Based on these observations, we conclude that tachykinins are critical modulators of primary nociceptive afferents, with a preeminent role in the electrical control of their excitability with sustained activation or injury.
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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.