Overexpressed Na _V 1.7 Channels Confer Hyperexcitability to in vitro Trigeminal Sensory Neurons of Ca _V 2.1 Mutant Hemiplegic Migraine Mice.

ABSTRACT: Trigeminal sensory neurons of transgenic knock-in (KI) mice expressing the R192Q missense mutation in the α1A subunit of neuronal voltage-gated Ca _V 2.1 Ca²⁺ channels, which leads to familial hemiplegic migraine type 1 (FHM1) in patients, exhibit a hyperexcitability phenotype. Here, we show that the expression of Na _V 1.7 channels, linked to pain states, is upregulated in KI primary cultures of trigeminal ganglia (TG), as shown by increased expression of its α1 subunit. In the majority of TG neurons, Na _V 1.7 channels are co-expressed with ATP-gated P2X3 receptors (P2X3R), which are important nociceptive sensors. Reversing the trigeminal phenotype with selective Ca _V 2.1 channel inhibitor ω-agatoxin IVA inhi

SUBMITTER: Mehboob R 

PROVIDER: S-EPMC8185157 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature