Modulation of NR1 receptor by CaMKIIα plays an important role in chronic itch development in mice.

Abstract:

:Intractable scratching is the characteristic of chronic itch, which represents a great challenge in clinical practice. However, the mechanism underlying chronic itch development is largely unknown. In the present study, we investigated the role of NMDA receptor in acute itch and in development of chronic itch. A mouse model was developed by painting DNFB to induce allergic contact dermatitis (ACD). We found that the expression of pNR1, which is a subunit of NMDA receptor, was significantly increased in the dorsal root ganglion in the DNFB model. The DNFB-evoked spontaneous scratching was blocked by the NMDA antagonist D-AP-5, the calcium-calmodulin-dependent protein kinase (CaMK) inhibitor KN-93, a CaMKIIα siRNA and the PKC inhibitor LY317615. Moreover, activation of PKC did not reverse the CaMKIIα knockdown-induced decrease in scratching, suggesting that PKC functions upstream of CaMKIIα. Thus, our study indicates that modulation of NR1 receptor by CaMKIIα plays an important role in the development of chronic itch.

journal_name

Brain Res Bull

journal_title

Brain research bulletin

authors

Li NQ,Tang Y,Huang ST,Liu XT,Zeng LP,Li H,Wan L

doi

10.1016/j.brainresbull.2020.02.011

subject

Has Abstract

pub_date

2020-05-01 00:00:00

pages

66-76

eissn

0361-9230

issn

1873-2747

pii

S0361-9230(19)31003-2

journal_volume

158

pub_type

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