Neuropathic and cAMP-induced pain behavior is ameliorated in mice lacking CNGB1.
Neuropharmacology
; 171: 108087, 2020 07.
Article
en En
| MEDLINE
| ID: mdl-32272140
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.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Dolor
/
AMP Cíclico
/
Canales Catiónicos Regulados por Nucleótidos Cíclicos
/
Proteínas del Tejido Nervioso
/
Neuralgia
Límite:
Animals
Idioma:
En
Revista:
Neuropharmacology
Año:
2020
Tipo del documento:
Article