• Inflammation is proposed as a key mechanism
underlying the pathogenesis of migraine.
• NLRP2 may play a role in migraine pathogenesis.
• NLRP2 may also express in neuronal cells besides
astrocytes.
• NLRP2 immunreactivity decreases very early time after
CSD.
Introduction: The objective of this study is to elucidate the expression
pattern and alterations of NLRP2 following a single cortical spreading
depolarization (CSD).
Method: Brain tissue was obtained by cardiac perfusion at the 15th
minute after CSD in optogenetically inducible Thy1-ChR2-YFP (n=3)
mice. NLRP2 expression was examined in the obtained brain tissue
sections by immunofluorescence staining and compared with NLRP2
expression pattern in the sections obtained from the control group (n=3)
and naive mice (n=1). The cellular source of NLRP2 is demonstrated by
dual staining with NeuN and S100β.
Results: Cellular immunoreactivity of NLRP2 was evident in the
cortical and subcortical regions of sham and naive group brains. This
immunoreactivity exhibited a notable reduction in CSD-induced brains.
The the majority of cells expressing NLRP2 exhibited colocalization with
NeuN, a neuronal marker, while a smaller subset demonstrated merging
with S100β, an astrocyte marker.
Conclusion: This study revealed the decreased immunoreactivity of
NLRP2 after single CSD in early period.
Keywords: Cortical spreading depolarization, inflammasome,
inflammation, migraine, NLRP2