TY - JOUR
T1 - Intrathecally-administered histamine facilitates nociception through tachykinin NK1 and histamine H1 receptors
T2 - A study in histidine decarboxylase gene knockout mice
AU - Yoshida, Akiko
AU - Mobarakeh, Jalal Izadi
AU - Sakurai, Eiko
AU - Sakurada, Shinobu
AU - Orito, Tohru
AU - Kuramasu, Atsuo
AU - Kato, Masato
AU - Yanai, Kazuhiko
N1 - Funding Information:
This work was supported in part by Grants-in-Aid for scientific research from the Japan Society for the Promotion of Science (JSPS), Goho Life Science Foundation and a 21st Century COE program (Bio-nano-technology) from the Ministry of Education, Culture, Sports, Science and Technology, Japan. We thank Professor Hiroshi Ohtsu for kindly providing the histidine decarboxylase knockout mice.
PY - 2005/10/17
Y1 - 2005/10/17
N2 - Intrathecal injection of histamine elicited behavioral responses consisting of scratching, biting and licking in conscious mice. To study the participation of histamine in pain perception, histidine decarboxylase knockout mice were examined for pain threshold by means of three different kinds of noxious stimuli: thermal nociception (hot-plate, tail-flick, and paw-withdrawal), mechanical nociception (tail-pressure), and chemical nociception (formalin test and capsaicin test). Mutant mice lacking histidine decarboxylase showed significantly fewer nociceptive responses to the hot-plate, tail-flick, paw-withdrawal, tail-pressure, formalin and capsaicin tests. Sensitivity to noxious stimuli in the histidine decarboxylase knockout mice was significantly lower when compared to the wild-type mice. The intrathecally-administered histamine (400 pmol) significantly shortened the latency in the histidine decarboxylase knockout mice, but not in the wild-type mice in tail-flick tests. Pyrilamine, a histamine H1 receptor antagonist, but not ranitidine, a histamine H2 receptor antagonist, produced inhibition of the induced behavioral responses in the tail-flick test when co-administered with histamine. Sendide, a tachykinin NK1 receptor antagonist, inhibited histamine-induced nociceptive behavior in the histidine decarboxylase knockout mice. In contrast, the treatment with d-(-)-2 amino-5-phosponovaleric acid (d-APV), an N-methyl-d-aspartate (NMDA) receptor antagonist, did not prevent the induction of the behavioral responses by histamine. These studies substantiate the evidence that nociceptive behavior induced by intrathecal injection of histamine is largely mediated through tachykinin NK1 and histamine H1 receptors in the spinal cord.
AB - Intrathecal injection of histamine elicited behavioral responses consisting of scratching, biting and licking in conscious mice. To study the participation of histamine in pain perception, histidine decarboxylase knockout mice were examined for pain threshold by means of three different kinds of noxious stimuli: thermal nociception (hot-plate, tail-flick, and paw-withdrawal), mechanical nociception (tail-pressure), and chemical nociception (formalin test and capsaicin test). Mutant mice lacking histidine decarboxylase showed significantly fewer nociceptive responses to the hot-plate, tail-flick, paw-withdrawal, tail-pressure, formalin and capsaicin tests. Sensitivity to noxious stimuli in the histidine decarboxylase knockout mice was significantly lower when compared to the wild-type mice. The intrathecally-administered histamine (400 pmol) significantly shortened the latency in the histidine decarboxylase knockout mice, but not in the wild-type mice in tail-flick tests. Pyrilamine, a histamine H1 receptor antagonist, but not ranitidine, a histamine H2 receptor antagonist, produced inhibition of the induced behavioral responses in the tail-flick test when co-administered with histamine. Sendide, a tachykinin NK1 receptor antagonist, inhibited histamine-induced nociceptive behavior in the histidine decarboxylase knockout mice. In contrast, the treatment with d-(-)-2 amino-5-phosponovaleric acid (d-APV), an N-methyl-d-aspartate (NMDA) receptor antagonist, did not prevent the induction of the behavioral responses by histamine. These studies substantiate the evidence that nociceptive behavior induced by intrathecal injection of histamine is largely mediated through tachykinin NK1 and histamine H1 receptors in the spinal cord.
KW - Histamine
KW - Histamine H receptor
KW - Histidine decarboxylase gene knockout mouse
KW - NMDA receptor
KW - Nociceptive response
KW - Tachykinin NK receptor
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U2 - 10.1016/j.ejphar.2005.08.037
DO - 10.1016/j.ejphar.2005.08.037
M3 - Article
C2 - 16212954
AN - SCOPUS:26844531973
VL - 522
SP - 55
EP - 62
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
SN - 0014-2999
IS - 1-3
ER -