2009 Abstracts - Association for Chemoreception Sciences

hodamine dye and measured the fluorescent intensity in theVNO. In WT mice the fluorescent intensity of the VNO wasnegatively correlated with the concentrations of the exposedirritants indicating the stronger the irritants the lesser amountdrawn into the VNO. In KO mice the fluorescent intensity wassignificantly higher for both control and irritant stimuli indicatinggreater chemical access to the VNO. In addition the pH of thesolution affected chemical access to the VNO, decreasing as thepH deviates from neutral. This pH dependent pattern is distortedin TRPM5KO mice. Our data strongly indicate that TRPM5expressed in SCCs of the VNO is involved in monitoring andcontrolling chemical access to the VNO.#P202 Poster session IV: Chemosensory transductionand perireceptor eventsTransient receptor potential V1 is directly activated bynickel ionsMatthias Luebbert 1 , Debbie Radtke 1,2 , Hanns Hatt 1 ,Christian H. Wetzel 11Department of Cellular Physiology Ruhr University BochumBochum, Germany, 2 Ruhr University Research School Bochum,GermanyTRPV1 is a member of the transient receptor potential (TRP)family of cation channels. It is expressed in sensory neurons oftrigeminal and dorsal root ganglions, as well as in a wide range ofnon neuronal tissues, including cells of the immune system. As apolymodal receptor, TRPV1 can be activated by various chemicaland physical stimuli, including divalent cations in concentrations>10 mM. Searching for further activators and modulators ofTRPV1, we were interested in the effect of Ni 2+ ions (NiSO 4 ),known to induce allergic contact dermatitis. Using Ca 2+ -imagingand whole-cell voltage-clamp recordings we observed thatmicromolar doses of NiSO 4 induced Ca 2+ transients in culturedcapsaicin-sensitive trigeminal neurons of mice. Moreover NiSO 4led to an activation of recombinant rat and human TRPV1heterologously expressed in CHO-cells, inducing significantoutwardly rectifying currents. Outside out recordings revealed anincrease in open probability paralleled by a decrease in singlechannelconductance. Both events resulted in an increased netactivity of TRPV1 which became manifest in macroscopiccurrents. The effect of Ni 2+ on capsaicin-induced currentsdepended on the capsaicin concentration. Outward currentsinduced by low doses of capsaicin were sensitized by NiSO 4 inlow concentrations, whereas currents induced by higher doses ofcapsaicin were inhibited. Using TRPV1-mutants with specificpoint mutations, we identified several positively charged aminoacids localized at the channels pore region which are apparentlyinvolved in the TRPV1 activation by Ni 2+ . Future experimentswill focus on the detailed molecular mechanisms of TRPV1activation and modulation by Ni 2+ and the impact of TRPV1 inthe development of pathophysiological changes in neuronal andnon-neuronal tissues.#P203 Poster session IV: Chemosensory transductionand perireceptor eventsCetylpyridinium Chloride Effects on Sodium and PotassiumTaste Stimulus Sensing in HamsterClara C. McClenon, Brooke L. Reidy, Victoria M. Stevens, RobertE. StewartWashington and Lee University Lexington, VA, USAWe sought to obtain neuropharmacological evidence for theexistence of a general salt-sensing pathway in taste receptor cellsof the hamster anterior tongue. Previous work has suggested thatsalty taste in rat depends partly on detection of sodium andpotassium by a variant form of the type I vanilloid receptor(VR1). We recorded integrated hamster chorda tympani nervetaste responses to sodium and potassium solutions (100 and 250mM) in the presence and absence of VR1 agonist-antagonistligands cetylpyridinium chloride (CPC) and SB-366791. Lingualapplication of CPC modestly, but significantly, inhibited chordatympani nerve taste responses to salts of sodium and potassium ina concentration-dependent, reversible manner. While 2 and 5 mMCPC caused significant suppression of 100 and 250 mM sodiumchloride (NaCl), sodium gluconate (NaGlu), and potassiumresponses (KCl) (ts ³ -.7.08, ps