Publication:
5-HT2A receptor activation and nitric oxide synthesis: A possible mechanism determining migraine attacks

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Issued Date

2002

Resource Type

Article

File Type

application/pdf

ISSN

178748

DOI

10.1046/j.1526-4610.2002.02142.x

Other identifier(s)

2-s2.0-0036651874

Rights Holder(s)

มหาวิทยาลัยศรีนครินทรวิโรฒ

Bibliographic Citation

Headache. Vol 42, No.7 (2002), p.566-574

Suggested Citation

Srikiatkhachorn A., Suwattanasophon C., Ruangpattanatawee U., Phansuwan-Pujito P. 5-HT2A receptor activation and nitric oxide synthesis: A possible mechanism determining migraine attacks. Headache. Vol 42, No.7 (2002), p.566-574. doi:10.1046/j.1526-4610.2002.02142.x Retrieved from: https://hdl.handle.net/20.500.14740/6726

Title

5-HT2A receptor activation and nitric oxide synthesis: A possible mechanism determining migraine attacks

Author(s)

Srikiatkhachorn A.
 Suwattanasophon C.
 Ruangpattanatawee U.
 Phansuwan-Pujito P.

Abstract

Objective. To determine the effect of the 5-HT2A receptor in control of spinal nociception, cerebral circulation, and nitric oxide synthase (nNOS) expression in trigeminovascular neurons. Background. The plasticity of the 5-HT2A receptor is a possible factor determining the course of migraine. Up-regulation of this receptor has been demonstrated to correlate with the increasing frequency of migraine attacks and may underlie the development of chronic daily headache. Methods. Adult male Wistar rats were divided into groups receiving the 5-HT2A agonist, 1,2,5-dimethoxy-4-iodophenyl-2-aminopropane (DOI), nitroglycerin, or normal saline. The tail flick test and chemical nociception-evoked Fos-expression in dorsal horn neurons were used as indicators of nociception. Regional cerebral blood flow was monitored using laser Doppler flowmetry. Expression of Fos and nNOS was studied using immunohistochemical method. Results. Administration of DOI led to the shortening of tail flick latency (1.3 ± 0.2 and 7.2 ± 0.6 seconds for DOI-treated and control groups, respectively). The number of Fos-immunoreactive neurons was also greater in the DOI-treated group compared with the control group. DOI also produced long-lasting cerebral hyperemia (123% of baseline value) associated with the enlargement of perivascular nNOS-immunoreactive nerve fibers and increased nNOS-immunoreactive neurons in trigeminal ganglia and trigeminal nucleus caudalis. These findings resembled those observed in the rats exposed to nitroglycerin. Conclusion. Our results suggest that activation of the 5-HT2A receptor leads to an enhancement of NO production in trigeminovascular pathway. NO may trigger migraine attacks by inducing cerebral vasodilation and sensitizing the perivascular nociceptors and central nociceptive neurons in trigeminovascular system. Up-regulation of this pronociceptive receptor can increase headache attacks and contributes to the development of chronic daily headache.

Subject(s)

1,2,5 dimethoxy 4 iodophenyl 2 aminopropane
 Biological marker
 Glyceryl trinitrate
 Nitric oxide
 Nitric oxide synthase
 Protein fos
 Serotonin 2A agonist
 Serotonin 2A receptor
 Sodium chloride
 Unclassified drug
 Nitric oxide
 Serotonin receptor
 Animal experiment
 Animal model
 Animal tissue
 Article
 Blood vessel innervation
 Brain blood flow
 Brain circulation
 Chronicity
 Controlled study
 Correlation analysis
 Disease course
 Doppler flowmetry
 Drug exposure
 Evoked response
 Headache
 Hyperemia
 Immunohistochemistry
 Immunoreactivity
 Male
 Migraine
 Nerve fiber
 Neuromodulation
 Nociception
 Nociceptive receptor
 Nonhuman
 Pain assessment
 Priority journal
 Protein determination
 Protein expression
 Rat
 Regulatory mechanism
 Spinal cord dorsal horn
 Spinal nerve
 Synthesis
 Tail flick test
 Trigeminal nucleus
 Trigeminus ganglion
 Vasodilatation
 Animal
 Biosynthesis
 Human
 Metabolism
 Migraine
 Pathophysiology
 Physiology
 Randomization
 Wistar rat
 Animals
 Cerebrovascular Circulation
 Humans
 Male
 Migraine Disorders
 Nitric Oxide
 Nociceptors
 Random Allocation
 Rats
 Rats, Wistar
 Receptors, Serotonin

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URI

https://hdl.handle.net/20.500.14740/6726

Collections

Scopus: Year 1983-2021

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