413 Poster Central Taste and <strong>Chemosensory</strong> 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 <strong>Chemosensory</strong> 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 <strong>Chemosensory</strong> 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 <strong>Chemosensory</strong> 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
417 Poster Central Taste and <strong>Chemosensory</strong> BehaviorRELATIONSHIPS BETWEEN INSULIN RELEASE AND TASTETonosaki K. 1 1 Meikai University, Sakatoshi, JapanIt is known that the food related sensory stimuli induces cephalicphase hormonal release. Thus, tasting sweet food elicits insulin releaseprior to increasing plasma glucose levels, it is called cephalic phaseinsulin release (CPIR). The characteristic of the CPIR is that the plasmainsulin secrets within 2 minutes after oral sensory stimulation, peak at 4minutes and return to baseline in the 8-10 minutes poststimulus timeperiod. The functional role of CPIR is not known clearly. In thisexperiment, we examined any tastes which was placed on the tongueinduced CPIR or not . We used female Wistar rats and five basic tastestimuli: sucrose (sweet), sodium chloride (salty), HCl (sour), quinine(bitter) or monosodium glutamate (umami). Rats reliably exhibit CPIRto sucrose. Sodium chloride, HCl, quinine or monosodium glutamatedoes not elicit CPIR. Sucrose has two typical characters such as `sweet`and `nutritive´. Then, we tested whether `sweet `or `nutritive´ elicitsCPIR. As the results, the non-nutritive sweetener saccharine does elicitCPIR. However, the non-sweetener nutrition starch does not elicitCPIR. In addition, we studied whether the CPIR related with the tastereceptor cell activity. We carried out the experiment that bilaterality cutoff the chorda tympani nerve which is one of the gustatory nerve. Thenthe CPIR could not be recognized for the sweet stimulation. From theseresults, it was proven that CPIR was elicited by the conducted tastenerve sweetness information. It is considered that these results mustinform the important comprehensible information for CPIR.418 Poster Central Taste and <strong>Chemosensory</strong> BehaviorTASTE FUNCTIONS AFTER GASTRIC BYPASS SURGERY INDIETARY AND GENETIC OBESE RATSHajnal A. 1 , Ahmed T.A. 2 , Khokhar S. 1 , Acharya N. 1 , Cooney R.N. 21 Neural and Behavioral Sciences, PennState Univ., College ofMedicine, Hershey, PA; 2 Surgery, PennState Univ. College of Medicine,Hershey, PAWeight loss after gastric bypass surgery (GBP) is caused byrestriction of food intake and malabsorption, but many patients alsonote decreased appetite for palatable meals. To investigate involvementof central taste mechanisms, we performed GBP in diet-induced obese(DIO) and CCK-1 receptor deficient Otsuka Long-Evans TokushimaFatty (OLETF) male rats. After GBP, both DIO and OLETF lost bodyweight similar to that seen in humans (25-30% weight loss) andexhibited improved glucose tolerance compared to both theirpreoperative baseline and pair-fed sham-operated controls. In addition,GBP rats of both strains showed a significantly reduced 24 hr 2-bottlepreference for sucrose (1.0 M) compared to sham-operated controls(preference ratio, DIO: 0.48 ± 0.04 vs. 0.90 ± 0.04, p < 0.001, n = 3/4;OLETF: 0.69 ± 0.02 vs. 0.89 ± 0.06; p < 0.05, n = 6/4). Lick rate (10-s)analysis revealed decreased responsiveness by DIO-GBP to sucroseconcentrations above 0.1M and by OLETF-GBP to sucrose 0.3Mthrough 1.5M and to fructose above 0.4 M (p < 0.05). No differencewas noted in either strain for the non-caloric sweetener saccharin,alanine, aversive taste solutions or trigeminal stimulation withcapsaicin. These findings suggest that (1) GBP may result in alteredtaste function with a reduced preference for palatable sugars in animalmodels of obesity, irrespective to the etiology of obesity, and (2) CCK-1 receptors do not contribute to the beneficial effects of GBP, such asweight reduction and improvement in insulin sensitivity. Supported byNIH grants DK065709, GM55639, and PSU-DFG.419 Poster Central Taste and <strong>Chemosensory</strong> BehaviorTEMPERATURE MODULATES BEHAVIORAL RESPONSESTO SUCROSE TASTE IN THE RATBreza J.M. 1 , Curtis K.S. 1 , Contreras R.J. 1 1 Program in Neuroscience,Florida State University, Tallahassee, FLWe recently showed that temperature modulates the responsivenessof gustatory neurons in the rat geniculate ganglion that respondprimarily to sucrose (sucrose-specialists). Specifically, responses to 0.5M sucrose at 10°C were less than those at 25°C or 40°C, which werenot different from each other. The goal of this study was to investigatewhether temperature modulates behavioral responses to sweet taste inrats. We employed very brief (10-s) trials in a Davis MS80 Riglickometer, modified with individual Peltier heat exchange deviceslocated near the tip of each drinking tube, that allows solutions to bemaintained at constant temperatures. We recorded the number oflicks/10 s to 0.2 M sucrose and to 0.05 M sucrose at 10, 25, and 40°C.Lick rates to 0.2 M sucrose were greater than those to 0.05 M sucrose atall temperatures. For a given concentration of sucrose, licking waslowest at 10°C, most robust at 25°C, and intermediate at 40°C. Lickingto 0.2 M sucrose at 10°C was 33% less at than that at 25°C, whereaslicking to 0.05 M sucrose at 10°C was 58% less than that at 25°C. Thefinding that lick rates to sucrose at 10°C decreased is consistent withour previous observation of reduced responses from sucrose-specialistneurons in the geniculate ganglion to sucrose at 10°C, and suggests thatcold temperature modulates sweet taste perception and thereby affectsbehavioral responses to sweet taste. Supported by NIH Grant DC04875420 Poster Central Taste and <strong>Chemosensory</strong> BehaviorEVALUATING THE LIMITS OF CANINE OLFACTIONSeward M.K. 1 , Latchney S.E. 1 , Hornung D.E. 1 1 St. LawrenceUniversity, Canton, NYTo assess the limits of a canine´s ability to identify a specific humanscent, a golden-retriever was trained to pick a T-shirt impregnated witha target human´s scent from T-shirts worn by the target´s relatives andnon-related persons. After sampling three test boxes (one of whichcontained the target), the dog was trained to exhibit a sit/stay responsewhen the target was identified. Correct responses were rewarded 90%of the time. The first series of experiments introduced olfactory “noise”to the testing environment by placing beakers containing increasingconcentrations of pure olfactory and olfactory/trigeminal odors betweenthe T-shirts and the sampling ports of the test boxes. The dog was ableto correctly identify the target even when the air concentrations of theseadded distracter odors were at their highest vapor concentrations. Asecond series of experiments reduced the concentration of the targetscent by covering the three beakers containing the T-shirts with platesthat decreased the exposed surface area, thus reducing the number ofmolecules present for detection. The dog was able to detect the targetscent when the surface area of the beaker was reduced by 93%.Combined, these two series of experiments illustrate the specificity andsensitivity with which a canine is able to detect a target human scentand discriminate between this scent and that of competingenvironmental odors. The first series of experiments provides somehints as to the chemical nature of this particular type of detection taskand the second series of experiments allows for an estimation of theminimum number of molecules necessary for detection.105
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