Vzg-1/lysophosphatidic acid-receptor involved in peripheral pain transmission.

The nociception by intraplantar (i.pl.) lysophosphatidic acid (LPA) injection was significantly, but partially blocked when mice received intrathecal (i.t.) antisense oligodeoxynucleotide treatment for the vzg-1 type LPA-receptor. The residual LPA-nociception observed under the condition of pertussis toxin-treatment, which is expected to block presynaptic contribution, was abolished by diphenhydramine (i.pl.), an H1-type histamine receptor antagonist. Taking into account that vzg-1 mRNA was detected in the dorsal root ganglion by RT-PCR method, these findings suggest that the LPA-induced nociception is attributed to the mechanism through vzg-1 receptor on nociceptor endings, and to that through unidentified LPA-receptor on peripheral, possibly mast cells.