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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.
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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...
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  11. A Short-chain Fatty Acid, Butyrate, Suppresses The Hyperexcitability Of Rat Nociceptive Primary Neurons Involved In Inflammatory Hyperalgesia.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Neurosciences
  9. Sensory Systems
  11. A Short-chain Fatty Acid, Butyrate, Suppresses The Hyperexcitability Of Rat Nociceptive Primary Neurons Involved In Inflammatory Hyperalgesia.

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A Short-Chain Fatty Acid, Butyrate, Suppresses the Hyperexcitability of Rat Nociceptive Primary Neurons Involved in Inflammatory Hyperalgesia.

Yukito Sashide1, Syogo Utugi1, Mamoru Takeda1

  • 1Laboratory of Food and Physiological Sciences, Department of Life and Food Sciences, School of Life and Environmental Sciences, Azabu University, 1-17-71 Fuchinobe, Chuo-ku, Sagamihara 252-5201, Kanagawa, Japan.

Molecules (Basel, Switzerland)
|June 13, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

Butyrate, a gut microbe product, reduces nerve hyperexcitability and pain from inflammation. This study shows butyrate alleviates trigeminal nerve inflammation and mechanical hyperalgesia in rats.

Keywords:
COX-2SCFAsbutyrateextracellular single-unit recording

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Area of Science:

  • Neuroscience
  • Microbiology
  • Pharmacology

Background:

  • Gut microbiota-derived short-chain fatty acids (SCFAs) modulate pain by reducing inflammation.
  • The neurophysiological mechanisms of butyrate in reducing primary nociceptive neuron hyperexcitability during inflammation are not fully understood.

Purpose of the Study:

  • To investigate if systemic butyrate administration can reduce inflammation-induced hyperexcitability in trigeminal ganglion (TG) primary neurons.
  • To determine if butyrate attenuates mechanical inflammatory hyperalgesia in vivo.

Main Methods:

  • Rats received Complete Freund's Adjuvant (CFA) injections to induce whisker pad inflammation.
  • Systemic butyrate administration was given to CFA-inflamed rats.
  • Mechanical stimulation-induced escape thresholds and TG neuron discharge frequencies were measured.
gut microbiota
inflammation
peripheral sensitization

Main Results:

  • CFA-induced inflammation significantly lowered mechanical pain thresholds.
  • Butyrate administration restored mechanical thresholds to normal levels within four days.
  • Butyrate significantly decreased spontaneous and stimulus-evoked discharge frequency in TG neurons of inflamed rats.

Conclusions:

  • Butyrate effectively reduces inflammatory hyperexcitability in nociceptive primary TG neurons.
  • Butyrate alleviates inflammatory hyperalgesia, suggesting therapeutic potential.
  • Butyrate may prevent trigeminal inflammatory mechanical hyperalgesia and its clinical symptoms.