Inositol-1,4,5-trisphosphate Induces Responses in Receptor Neurons in Rat Vomeronasal Sensory Slices

Abstract

Using the whole-cell mode of the patch-clamp technique, we recorded action potentials, voltage-activated cationic currents and putative second messenger-activated currents in receptor neurons in the vomeronasal sensory epithelium of female rats. The resting membrane potential and input resistance were -45.5 +/- 2.5 mV (mean +/- SEM, n = 39) and 1.5 +/- 0.2 G omega (mean +/- SEM, n = 37). Current injection of 1-3 pA induced overshooting action potentials. The firing frequency increased with increasing current injections linearly from 1 to 10 pA and reached a plateau at 30 pA, suggesting that rat vomeronasal receptor neurons sensitively elicit action potentials in response to a small receptor potential. Under voltage clamp, voltage-dependent Na+ inward current, inward Ca2+ current, sustained outward K+ current and Ca-(2+)-activated K(+)-current were identified. Dialysis of D-inositol-1,4,5-trisphosphate (D-IP3) induced inward currents with an increase in membrane conductance in approximately 54% of the cells and inward current fluctuations in 15% of the cell. L-IP3 also induced inward currents and current fluctuations in 53 and 13% of the cells respectively. The mean amplitude of inward currents induced by 100 microM D-IP3 and L-IP3 were 84.6 +/- 14.0 pA (SEM, n = 82) and 66.1 +/- 9.4 pA (SEM, n = 100) respectively. The IP3-induced responses were blocked by elimination of Na+ and Ca2+ in the external solution or application of 10 microM ruthenium red. The present study suggested that IP3-mediated transduction pathways exist in rat vomeronasal receptor neurons.

Pregnancy block by MHC class I peptides is mediatedviathe production of inositol 1,4,5-trisphosphate in the mouse vomeronasal organ

“…Our results suggest that MHC class I peptides stimulate the female VNO via the production of Ins(1,4,5)P 3 . This result complements other studies that show Ins(1,4,5)P 3 levels increase in the VNO membrane preparations during stimulation with urinary pheromones (Sasaki et al, 1999;Kroner et al, 1996;Wekesa and Anholt, 1997;Wekesa et al, 2003;Inamura et al, 1997a;Inamura et al, 1997b). The role of Ins(1,4,5)P 3 in the production of calcium and generation of an action potential is still uncertain along with the role of calcium once it has entered the cell.…”

New Insights into the Roles of cAMP and InsP3 on Odor-Processing and Olfactory-Driven Behaviors

“…There is considerable evidence indicating that some odorants do not induce an increase in cAMP but rather the concentration of inositol, 1, 4, 5-triphosphate (InsP3) is increased [1,10]. InsP3 formation can increase intracellular Ca 2+ [11] and activate Ca 2+ -dependent K + channels or Ca 2+ -dependent non-specific cation channels [1,[12][13], which in turn generate receptor potential and depolarize the olfactory neuron, thus providing a signal for further neuronal processing. In addition to cAMP and InsP3, diverse olfactory transduction pathways, such as the activation of cAMP/cGMP-gated channels [14] reported a fast ionotrophic response and found no evidence of the involvement of G-protein or cAMP, cGMP or InsP3 while Wicher et al [20] showed that insect ORs induce the synthesis of cAMP through a G-protein that in turn activates Or83b, which serves as a cAMP-gated ion channel.…”

Signaling in the Mammalian Vomeronasal Organ

“…They found that the Gα o mutant male mice are less aggressive, and the maternal aggression in females is also severely reduced [13]. Studies have shown that vomeronasal transduction involves release of IP 3 [16][17][18][19]. In the garter snake, a chemo attractant isolated from its prey induced the generation of inositol-1,4,5-trisphosphate in the VNO [18].…”

“…In the garter snake, a chemo attractant isolated from its prey induced the generation of inositol-1,4,5-trisphosphate in the VNO [18]. It has been shown that dialysis of IP 3 into the turtle and rat VNO induces inward currents [17]. The female porcine and mouse VNO can be stimulated by chemosensory cues to cause an increase of IP 3 [16,19].…”

“…Much of the ambiguity and controversy surrounding IP3's role in Ca is coupled to mechanistic description of TRPC2 as a capacitance Ca 2+ entry (CCE) or store-operated (SOC) channel [52,53]. Further review of current literature also indicates that electrophysiological studies provide the bulk of information garnered so far on membrane (or intracellular) Ca 2+ and other ionic currents [17,21,[32][33][34][35][36]48,49,51,[54][55][56][57][58][59], with few direct studies of Ca 2+ to validate and add to the electrophysiological data, especially in the context of internal versus external regulation of Ca 2+ dynamics. Currently, reports of Ca 2+ imaging, particularly in mammalian systems, provide information on VSNs responses to dilute urine or other complex natural stimuli [49,51,58] and in a very few studies of some of the individual volatile constituents of urine or other natural stimuli [53][54][55].…”