Contribution of Histamine to Nociceptive Behaviors Induced by Intrathecally Administered Cholecystokinin-8
Autor: | Soh Katsuyama, Yasuyuki Agatsuma, Tsukasa Sakurada, Damiana Scuteri, Giacinto Bagetta, Takafumi Hayashi, Shinobu Sakurada, Chizuko Watanabe |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
medicine.drug_class Pharmacology digestive system 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine nociceptive behaviors medicine Pharmacology (medical) Receptor tachykinin neurokinin-1 receptor Cholecystokinin Original Research lcsh:RM1-950 digestive oral and skin physiology Antagonist spinal cord Receptor antagonist histamine 030104 developmental biology Nociception lcsh:Therapeutics. Pharmacology chemistry 030220 oncology & carcinogenesis NMDA receptor N-methyl-D-aspartate receptor Histamine H3 receptor Histamine hormones hormone substitutes and hormone antagonists cholecystokinin-8 |
Zdroj: | Frontiers in Pharmacology Frontiers in Pharmacology, Vol 11 (2020) |
ISSN: | 1663-9812 |
DOI: | 10.3389/fphar.2020.590918 |
Popis: | The involvement of spinal release of histamine in the nociceptive behaviors induced by cholecystokinin-8 (CCK-8) was investigated in mice. Intrathecal (i.t.) injection of CCK-8 elicited the nociceptive behaviors consisting of scratching, biting, and licking. The nociceptive behaviors induced by i.t. treatment with CCK-8 showed two bell-shaped patterns. The histamine H3 receptor antagonist significantly promoted the nociceptive behaviors induced by CCK-8 at doses of 1–100 fmol and 100 pmol. The nociceptive behaviors elicited by CCK-8 was inhibited by i.t. administration of the CCK-B receptor antagonist in a dose-dependent manner, but not by the CCK-A receptor antagonist. The nociceptive behaviors induced by CCK-8 were markedly suppressed by i.t. pretreatment with antiserum against histamine and were abolished in histidine decarboxylase-deficient mice. In histamine H1 receptor-deficient mice, the nociceptive behaviors induced at both 10 amol and 10 pmol of CCK-8 were not affected. The tachykinin neurokinin-1 (NK1) receptor antagonists inhibited CCK-8 (10 pmol)-induced nociceptive behaviors in a dose-dependent manner. No significant reduction in CCK-8 (10 amol)-induced nociceptive behaviors was detected after co-administration of the tachykinin NK1 receptor antagonists. The nociceptive behaviors elicited by CCK-8 were inhibited by i.t. administration of the antagonist for the N-methyl-D-aspartate (NMDA) receptor in a dose-dependent manner. Our results suggest that the nociceptive behaviors induced by i.t. administration of CCK-8 (10 pmol) are mediated through the spinal release of histamine and are elicited via activation of the tachykinin NK1 and NMDA receptors, whereas the nociceptive behaviors induced by i.t. administration of CCK-8 (10 amol) are mediated through the spinal release of histamine and elicited via NMDA receptor activation. |
Databáze: | OpenAIRE |
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