Suprasternal gland secretion of male short-tailed opossum induces IP 3 generation in the vomeronasal organ

Abstract

Chemical communication is an important component of mammalian social behaviors. Gray short-tailed opossums ( Monodelphis domestica) communicate by scent marking. The male opossum possesses a prominent suprasternal scent gland, extracts of which strongly attract female opossums. This attractivity remains unaltered following repeated lyophilization. The suprasternal gland secretion functions in a sexually dimorphic manner, i.e., it elicits elevated levels of IP 3 in the vomeronasal (VN) sensory epithelium of female opossums, but suppressed the levels of IP 3 in the VN sensory epithelium of male opossums. The elevated levels of IP 3 induced by suprasternal gland secretion in female vomeronasal sensory epithelium is inhibited by the G i/o specific inhibitor, NF023, but not its inactive analogue, NF007. It is also suppressed by specific antibodies to the alpha subunits of G i and G o proteins, by the phospholipase C inhibitor, U73122, as well as by GDPβS. Surprisingly, GDPβS itself enhances basal levels of IP 3 in female VN sensory epithelium. This GDPβS-induced increase in levels of IP 3 is reduced by the PLC inhibitor, U73122, but not by the G i/o inhibitor, NF023. In addition, GDP also enhances basal levels of IP 3. GDPβS, a known inhibitor of G-protein activation, thus appears to have dual functions: as both stimulator and inhibitor of IP 3 production in the VN sensory epithelium of opossums. In contrast, this nucleotide analogue functions as an inhibitor in the VN sensory epithelium of mice. The mechanism of signal transduction underlying the suprasternal gland secretion-elicited signals in the VN sensory epithelium of opossums appears to involve signals that are generated through activation of G-protein-coupled receptors and transduced via activation of G i/o-proteins and the effector, phospholipase C, resulting in an increased production of the second messenger, IP 3. The extracellular signals are thus amplified.