Cox-2 inhibitor attenuates NO-induced nNOS in rat caudal trigeminal nucleus

Hedvig Varga, A. Párdutz, E. Vámos, Imola Plangar, Eszter Egyud, J. Tajti, F. Bari, L. Vécsei

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Objective - The aim of the present study was to determine which isoform of the cyclooxygenase (COX) enzyme plays a role in the neuronal nitric oxide synthase (nNOS) activation caused by nitroglycerin (NTG), in the most caudal part of the trigeminal caudal nucleus (TNC) of the rat. Background - Nitric oxide donor, NTG, can trigger migraine attack in migraineurs, but not in healthy persons. In rats, subcutaneous administration of NTG (10 mg/kg) increases significantly the number of nNOS-immunoreactive neurons in the TNC after 4 hours, which could be attenuated by acetyl-salicylate (Aspirin), a nonselective COX-inhibitor. Methods - SPRD rats were divided into 3 groups: (1) control group (no drug administration), (2) NS398 (selective COX-2 inhibitor) administration (1, 3, or 5 mg/kg), and (3) SC560 (selective COX-1 inhibitor) administration (1, 5, or 10 mg/kg). Thirty minutes after drug administration, the animals received NTG (10 mg/kg) or placebo injection. Four hours later the animals were transcardially perfused and the cervical part of the TNC was removed for immunohistochemistry. Results - The selective COX-2 inhibitor NS398 in contrast to the selective COX-1 inhibitor SC560 attenuates the NTG-induced nNOS expression dose-dependently. Conclusion - These findings suggest that metabolites deriving from COX-2 (but not COX-1) may be the most important factors in the NTG-induced nNOS expression. These data could help to better understand the pathogenesis of headaches and the action of antimigraine drugs.

Original languageEnglish
Pages (from-to)1319-1325
Number of pages7
JournalHeadache
Volume47
Issue number9
DOIs
Publication statusPublished - Oct 2007

Fingerprint

Trigeminal Caudal Nucleus
Nitric Oxide Synthase Type I
Nitroglycerin
Cyclooxygenase 1
Cyclooxygenase Inhibitors
Cyclooxygenase 2 Inhibitors
Pharmaceutical Preparations
Nitric Oxide Donors
Salicylates
Cyclooxygenase 2
Prostaglandin-Endoperoxide Synthases
Migraine Disorders
Aspirin
Headache
Protein Isoforms
Immunohistochemistry
Placebos
Neurons
Control Groups
Injections

Keywords

  • Caudal spinal trigeminal nucleus
  • Cyclooxygenase-inhibitors
  • Nitric oxide synthase
  • Nitroglycerin
  • Rat

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Cox-2 inhibitor attenuates NO-induced nNOS in rat caudal trigeminal nucleus. / Varga, Hedvig; Párdutz, A.; Vámos, E.; Plangar, Imola; Egyud, Eszter; Tajti, J.; Bari, F.; Vécsei, L.

In: Headache, Vol. 47, No. 9, 10.2007, p. 1319-1325.

Research output: Contribution to journalArticle

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T1 - Cox-2 inhibitor attenuates NO-induced nNOS in rat caudal trigeminal nucleus

AU - Varga, Hedvig

AU - Párdutz, A.

AU - Vámos, E.

AU - Plangar, Imola

AU - Egyud, Eszter

AU - Tajti, J.

AU - Bari, F.

AU - Vécsei, L.

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N2 - Objective - The aim of the present study was to determine which isoform of the cyclooxygenase (COX) enzyme plays a role in the neuronal nitric oxide synthase (nNOS) activation caused by nitroglycerin (NTG), in the most caudal part of the trigeminal caudal nucleus (TNC) of the rat. Background - Nitric oxide donor, NTG, can trigger migraine attack in migraineurs, but not in healthy persons. In rats, subcutaneous administration of NTG (10 mg/kg) increases significantly the number of nNOS-immunoreactive neurons in the TNC after 4 hours, which could be attenuated by acetyl-salicylate (Aspirin), a nonselective COX-inhibitor. Methods - SPRD rats were divided into 3 groups: (1) control group (no drug administration), (2) NS398 (selective COX-2 inhibitor) administration (1, 3, or 5 mg/kg), and (3) SC560 (selective COX-1 inhibitor) administration (1, 5, or 10 mg/kg). Thirty minutes after drug administration, the animals received NTG (10 mg/kg) or placebo injection. Four hours later the animals were transcardially perfused and the cervical part of the TNC was removed for immunohistochemistry. Results - The selective COX-2 inhibitor NS398 in contrast to the selective COX-1 inhibitor SC560 attenuates the NTG-induced nNOS expression dose-dependently. Conclusion - These findings suggest that metabolites deriving from COX-2 (but not COX-1) may be the most important factors in the NTG-induced nNOS expression. These data could help to better understand the pathogenesis of headaches and the action of antimigraine drugs.

AB - Objective - The aim of the present study was to determine which isoform of the cyclooxygenase (COX) enzyme plays a role in the neuronal nitric oxide synthase (nNOS) activation caused by nitroglycerin (NTG), in the most caudal part of the trigeminal caudal nucleus (TNC) of the rat. Background - Nitric oxide donor, NTG, can trigger migraine attack in migraineurs, but not in healthy persons. In rats, subcutaneous administration of NTG (10 mg/kg) increases significantly the number of nNOS-immunoreactive neurons in the TNC after 4 hours, which could be attenuated by acetyl-salicylate (Aspirin), a nonselective COX-inhibitor. Methods - SPRD rats were divided into 3 groups: (1) control group (no drug administration), (2) NS398 (selective COX-2 inhibitor) administration (1, 3, or 5 mg/kg), and (3) SC560 (selective COX-1 inhibitor) administration (1, 5, or 10 mg/kg). Thirty minutes after drug administration, the animals received NTG (10 mg/kg) or placebo injection. Four hours later the animals were transcardially perfused and the cervical part of the TNC was removed for immunohistochemistry. Results - The selective COX-2 inhibitor NS398 in contrast to the selective COX-1 inhibitor SC560 attenuates the NTG-induced nNOS expression dose-dependently. Conclusion - These findings suggest that metabolites deriving from COX-2 (but not COX-1) may be the most important factors in the NTG-induced nNOS expression. These data could help to better understand the pathogenesis of headaches and the action of antimigraine drugs.

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