J3-2376 — Annual report 2011
1.
Calcitonin gene-related peptide-mediated enhancement of purinergic neuron/glia communication by the algogenic factor bradykinin in mouse trigeminal ganglia from wild-type and R192Q Ca[sub]v2.1 knock-in mice

Crosstalk between neurons and satellite glial cells contributes to trigeminal neuron sensitization and transduction of painful stimuli, including migraine pain. Our findings suggest that ATP receptors on glial cells might be considered as novel players in the cellular processes underlying migraine pathophysiology and might represent new targets for the development of innovative therapeutic agents against migraine pain.

COBISS.SI-ID: 1817851
2.
Lipid rafts control P2X3 receptor distribution and function in trigeminal sensory neurons of a transgenic migraine mouse model

Larger lipid raft compartment of knock-in neurons are enriched in P2X3 pain receptors that exhibited stronger functional responses. These results suggest that the membrane microenvironment of trigeminal sensory neurons is an important factor in determining sensitization of P2X3 receptors and could contribute to a migraine phenotype by enhancing ATP-mediated responses.

COBISS.SI-ID: 2008571
3.
P2X3 receptor expression by HEK cells conditions their survival

In this work, we studied the recovery of recombinant P2X3 receptor expression in HEK cells. Our data demonstrated that HEK cells were not permissive for stable P2X3 expression, while treatment with P2X3 receptor antagonist or the expression P2X3 point mutant Y393A limited the effect.

COBISS.SI-ID: 2061051