Local subcutaneous injection of chlorogenic acid inhibits the nociceptive trigeminal spinal nucleus caudalis neurons in rats

• Published in: Neuroscience research Vol. 134; pp. 49 - 55
• Main Authors: Kakita, Kaede, Tsubouchi, Hirona, Adachi, Mayu, Takehana, Shiori, Shimazu, Yoshihito, Takeda, Mamoru
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.09.2018
• Subjects: Chlorogenic acids; Extracellular single unit recording; Local anesthetic agents; Nociception; Trigeminal spinal nucleus caudalis; Nociception; Trigeminal spinal nucleus caudalis; Local anesthetic agents; Chlorogenic acids; Extracellular single unit recording
• ISSN: 0168-0102; 1872-8111
• DOI: 10.1016/j.neures.2017.11.009

•Local CGA injection suppresses nociceptive SpVc WDR neuronal excitability.•Neuronal firing rates were dose-dependently inhibited by CGA.•The inhibitory effect of CGA lasted for 30min and was reversible.•The potency of inhibition by CGA almost equaled that by 1% lidocaine.•CGA may be an effective treatment option for trigeminal pain. Acute administration of chlorogenic acid (CGA) in vitro was recently shown to modulate potassium channel conductance and acid-sensing ion channels (ASICs) in the primary sensory neurons; however, in vivo peripheral effects of CGA on the nociceptive mechanical stimulation of trigeminal neuronal activity remains to be determined. The present study investigated whether local administration of CGA in vivo attenuates mechanical stimulation-induced excitability of trigeminal spinal nucleus caudalis neuronal (SpVc) activity in rats. Extracellular single-unit recordings were made of SpVc wide-dynamic range (WDR) neuronal activity elicited by non-noxious and noxious orofacial mechanical stimulation in pentobarbital anesthetized rats. The mean number of SpVc WDR neuronal firings responding to both non-noxious and noxious mechanical stimuli were significantly and dose-dependently inhibited by local subcutaneous administration of CGA (0.1–10mM), with the maximal inhibition of discharge frequency revealed within 10min and reversed after approximately 30min. The mean frequency of SpVc neuronal discharge inhibition by CGA was comparable to that by a local anesthetic, the sodium channel blocker, 1% lidocaine. These results suggest that local CGA injection into the peripheral receptive field suppresses the excitability of SpVc neurons, possibly via the activation of voltage-gated potassium channels and modulation of ASICs in the nociceptive nerve terminal of trigeminal ganglion neurons. Therefore, local injection of CGA could contribute to local anesthetic agents for the treatment of trigeminal nociceptive pain.