1 1 Symposium Chemosensory Receptors Satellite DEVELOPMENT ...

413 Poster Central Taste and Chemosensory BehaviorFUNCTIONAL ANATOMY OF SYNAPTIC PLASTICITYMEDIATING OLFACTORY LEARNINGJones S.V. 1 , Stanek-Rattiner L. 1 , Ressler K. 1 1 Psychiatry & BehavioralSciences, Emory University, Atlanta, GAThis study examined the expression of neural plasticity genes tofurther understand the functional organization of brain regionsmediating olfactory fear learning. Specifically, we examined theexpression of brain-derived neurotrophic factor (BDNF) and thepotassium/chloride cotransporter KCC2. In vitro, BDNF downregulatesKCC2, which may provide a mechanism for learning by altering theeffects of GABAergic signaling via KCC2´s effect on the cellularchloride gradient. For this experiment, adult male C57/B6 mice weredivided into four groups. Mice received 10 pairings of amyl acetate witha 0.4 mA footshock (n = 16), the same number of odors and shocks inan unpaired fashion (n = 8), shock alone (n = 8), or remained in theirhome cage (n = 8). Two hours following training, half of the pairedgroup and all of the other groups were anesthetized and brains wereremoved, frozen and sectioned. The remainder of the paired group wasbehaviorally tested the next day. We then performed in situhybridization to examine relative expression levels of BDNF and KCC2within the olfactory bulb (OB), the anterior piriform cortex (APC), theposterior piriform cortex (PPC), and the basolateral amygdala (BLA).We found increased BDNF mRNA expression and a correspondingdecrease in KCC2 expression within all areas in the paired group. Incontrast, in the unpaired group, there were significant changes in thesegenes in the OB and APC only. No significant changes were found inthe shock only control group. These results are consistent with a modelin which OB and APC respond to olfactory stimuli regardless of thepredictive qualities of shock. In contrast, the PPC and BLA responddifferentially only when there is predictive information to be integrated.414 Poster Central Taste and Chemosensory BehaviorOLFACTORY MASKING IN BEHAVIORALLY-TRAINEDMICESmith D.W. 1 , Culpepper M. 1 , Heil T. 1 1 Department of Psychology,Center for Smell and Taste, University of Florida, Gainesville, FLUnder natural conditions odors are rarely, if ever, experienced inisolation. Yet, surprisingly, little is known about how the olfactorysystem accomplishes this critical task. Here we report on use of abehavioral technique to study olfactory masking in behaviorally-trainedmice. Mice (C57BL/6) were trained to perform a two-odordiscrimination task in an automated liquid-dilution olfactometer(Knosys, Bethesda, MD). Animals were trained to insert their head intoa glass sniffing port to activate a trial sequence. During a trial, either thetarget odorant, Henkels100 (S+), diluted in de-ionized water, or deionizedwater alone (S-) were presented. Water reinforcement wascontingent on the animal reporting the presence of the S+ in the airstream by licking a water spout and activating an electrical switch.Trials were in blocks of 20 (10 S+ and 10 S- in quazi-random order).The concentration of the S+ was decreased in 10-fold steps followingtwo consecutive blocks of ≥85%. Threshold was estimated to be thelowest S+ concentration at which the animal was capable ofdiscriminating the S+ from the S- stimulus with accuracy at ≥85%.Discrimination acquisition was compared for target stimuluspresentations in a null background (no masking odorant) and in thepresence of a continuous supra-threshold level masking odorant (ethylacetate, 10e-5% v/v). Discrimination-acquisition thresholds were, aspredicted, shifted to higher S+ concentrations when measured in thepresence of the masking odorant. The goal of this research program is todevelop psychophysical paradigms to characterize the detection ofcomplex odorants and simple odorants in the presence of backgroundmasking odors.415 Poster Central Taste and Chemosensory BehaviorTHE ROLE OF THE CELLULAR PRION PROTEIN PRPC INAN OLFACTORY-DRIVEN BEHAVIORLe Pichon C.E. 1 , Glithero K.J. 1 , Aguzzi A. 2 , Firestein S. 1 1 ColumbiaUniversity, New York, NY; 2 University Hospital of Zürich, Zürich,SwitzerlandDespite over a decade of research, the normal physiological functionof the cellular prion protein (PrP C ), encoded by the Prnp gene, remainsunknown. We found PrP C to be highly expressed in murine olfactorytissues and have used the olfactory system as a model in which to studyPrP C function. We observed the behavior of Prnp knockout mice andother Prnp-related transgenics in the hidden cookie test. A mouse wasplaced in a novel cage in which a cookie had been buried under freshbedding. The time the animal took to find the cookie was recorded.Each individual was given two trials, the first (T1) lasting 10 mins andthe second (T2) 5 mins. Zürich I (ZI) Prnp knockout mice (medians:T1 = 233 s, T2 = 127.5 s, n = 20) scored lower than wild type controlanimals (medians: T1 = 73 s, T2 = 20 s, n = 9). In addition, asignificant proportion of the ZI knockouts (n = 6/20) failed to find thecookie altogether, whereas none of the control mice failed the test.Further testing on numerous transgenic lines in which Prnp had beenplaced under control of various promoters showed cell-type specificrequirements for PrP C function. In particular, mice in the ZI knockoutbackground expressing PrP C only in neurons were rescued (medians: T1= 68 s, T2 = 22 s, n = 9). Thus, the presence of PrP C in neuronsrestored wild type behavior in this olfactory-driven test. In conclusion,we have demonstrated neuronal expression of Prnp is necessary forwild type performance in the hidden cookie test. These results are afirst step towards the elucidation of a function for PrP C . Support:EMBO and NIDCD.416 Poster Central Taste and Chemosensory BehaviorEFFECTS OF THE MGLUR4 ANTAGONIST CPPG ON ALEARNED TASTE AVERSION IN RATSEschle B.K. 1 , Eddy M.C. 1 , Watson J.P. 1 , San Antonio C.M. 1 , DelayE.R. 1 1 Department of Biology, University of Vermont, Burlington, VTUmami stimuli such as monosodium glutamate (MSG) and L-aminoacid taste stimuli are believed to be detected by broadly-tuned, Gprotein-coupled T1R1+T1R3 taste receptors (Nelson et al., 2002;Damak et al., 2003; Zhao et al., 2003). However, studies with T1R3knockout mice have reported contradictory findings about the functionof this receptor. Zhao et al. (2003) found that T1R3 knockout mice lackthe ability to detect umami taste. Others with independently developedT1R3 knockout mice report only a reduction in umami taste preferenceand nerve recordings (Damak et al., 2003; Nie et al. 2005), no loss oftaste thresholds and some ability to discriminate between MSG andsucrose (Delay et al., submitted), suggesting other receptors such astaste-mGluR4 (Chaudhari et al., 2000) may be involved. We usedconditioned taste aversion methods in brief access testing (Heyer et al.,2003) to determine if: (1) an aversion to L-MSG generalizes to L-arginine and (2) if that generalization is effected by 1 mM CPPG, an m-GluR4 antagonist. Rats were presented with 100 mM MSG (withamiloride to reduce Na + taste) and then injected with NaCl or LiCl.Three days later, the rats were presented with two bottles of (1) water,(2) 100 mM L-MSG and (3) 50 mM L-arginine. CPPG (1 mM) wasadded to one of the two bottle of each substance. Amiloride was in allsolutions, including water rinse trials. Lick rates emitted in 10-secondtrials were counted. CPPG reduced the aversion to MSG but did notalter generalization of the aversion to arginine. These findings suggestthat MSG may be detected by a combination of T1R and mGluR4receptors while L-arginine is detected only by the T1R1+T1R3heterodimer. Supported by NSF grant IOB-0450350 to ERD.104