Neuropathic and cAMP-induced pain behavior is ameliorated in mice lacking CNGB1.

Abstract:

:Cyclic nucleotide-gated (CNG) channels, which are directly activated by cAMP and cGMP, have long been known to play a key role in retinal and olfactory signal transduction. Emerging evidence indicates that CNG channels are also involved in signaling pathways important for pain processing. Here, we found that the expression of the channel subunits CNGA2, CNGA3, CNGA4 and CNGB1 in dorsal root ganglia, and of CNGA2 in the spinal cord, is transiently altered after peripheral nerve injury in mice. Specifically, we show using in situ hybridization and quantitative real-time RT-PCR that CNG channels containing the CNGB1b subunit are localized to populations of sensory neurons and predominantly excitatory interneurons in the spinal dorsal horn. In CNGB1 knockout (CNGB1-/-) mice, neuropathic pain behavior is considerably attenuated whereas inflammatory pain behavior is normal. Finally, we provide evidence to support CNGB1 as a downstream mediator of cAMP signaling in pain pathways. Altogether, our data suggest that CNGB1-positive CNG channels specifically contribute to neuropathic pain processing after peripheral nerve injury.

journal_name

Neuropharmacology

journal_title

Neuropharmacology

authors

Kallenborn-Gerhardt W,Metzner K,Lu R,Petersen J,Kuth MS,Heine S,Drees O,Paul M,Becirovic E,Kennel L,Flauaus C,Gross T,Wack G,Hohmann SW,Nemirovski D,Del Turco D,Biel M,Geisslinger G,Michalakis S,Schmidtko A

doi

10.1016/j.neuropharm.2020.108087

subject

Has Abstract

pub_date

2020-07-01 00:00:00

pages

108087

eissn

0028-3908

issn

1873-7064

pii

S0028-3908(20)30155-6

journal_volume

171

pub_type

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