Different Involvement of ASIC and TRPA1 in Facial and Hindpaw Allodynia in Nitroglycerin-Induced Peripheral Hypersensitivities in Mice

The pathophysiological mechanism underlying migraine-associated peripheral hypersensitivity remains unclear. Acid-sensing ion channels (ASICs) and transient receptor potential ankyrin 1 (TRPA1) are known to be causative pathogenic factors of mechanical and cold allodynia, respectively. Here, we soug...

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Bibliographic Details
Published in:Life (Basel, Switzerland) Switzerland), 2022-08, Vol.12 (9), p.1294
Main Authors: Kim, Sol-Ji, Yeo, Ji-Hee, Yoon, Seo-Yeon, Roh, Dae-Hyun
Format: Article
Language:English
Subjects:
acid-sensing ion channel
Acidity
Amiloride
Angina pectoris
Animals
Ankyrins
c-Fos protein
Cold
Drug withdrawal
Filaments
Headache
Headaches
Hypersensitivity
Immunohistochemistry
Ion channels
Laboratories
Mechanical properties
Migraine
Nitroglycerin
nitroglycerine
Pain
Pain perception
Protein expression
Proteins
Sodium channels
Spinal cord
transient receptor potential ankyrin type 1
Transient receptor potential proteins
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Summary:The pathophysiological mechanism underlying migraine-associated peripheral hypersensitivity remains unclear. Acid-sensing ion channels (ASICs) and transient receptor potential ankyrin 1 (TRPA1) are known to be causative pathogenic factors of mechanical and cold allodynia, respectively. Here, we sought to investigate their involvement in cold and mechanical allodynia of the face and hindpaws, respectively, in a mouse model of repetitive nitroglycerin (NTG)-induced migraine. NTG (10 mg/kg) was administered to the mice every other day for 9 days, followed 90 min later by HC-030031 (a TRPA1 blocker) or amiloride (a non-selective ASIC blocker). Mechanical or cold sensitivity of the hindpaw and facial regions was quantified using von-Frey filaments or acetone solution, respectively. Immunohistochemistry revealed that c-Fos expression was significantly increased in the trigeminal nucleus caudalis region but not in the spinal cord. Amiloride treatment only reduced NTG-induced hindpaw mechanical allodynia, whereas HC-030031 treatment only improved facial cold allodynia. Interestingly, the number of c-Fos positive cells decreased to a similar level in each drug treatment group. These findings demonstrate that facial cold allodynia and hindpaw mechanical allodynia are differentially mediated by activation of TRPA1 and ASIC, respectively, in mice with repetitive NTG-induced hypersensitivity.
ISSN:2075-1729
2075-1729
DOI:10.3390/life12091294