损毁大鼠杏仁中央核对不同味觉溶液摄入的影响

目的:研究大鼠杏仁中央核在味觉欣快感受中的作用,以探讨其在味觉指导下进行摄食行为调节的可能机制.方法:采用双瓶选择实验(味觉溶液vs水),观察电解损毁大鼠双侧CeA后对四种基本味觉溶液摄入的影响.结果:与对照组相比,CeA损毁明显降低了大鼠对0.03、0.1和0.3 mol/L氯化钠溶液,0.01、0.1和1.0 mmol/L柠檬酸溶液及10、20和50 μmol/L盐酸奎宁溶液的摄入,且其对相邻浓度的氯化钠、柠檬酸和盐酸奎宁的分辨能力也明显降低.但两组动物总的摄入量(味觉溶液和水)在各组实验中均无显著性差异.结论:CeA损毁可降低大鼠对味觉溶液的摄入,但对不同浓度溶液的影响不同.结果提示CeA可能通过影响中枢味觉评估机制,改变大鼠对不同味觉刺激的欣快阈值,从而参与摄食行为的调控.     

运动对高脂膳食雌鼠性发育和瘦素受体mRNA表达的影响

目的：探讨运动干预对高脂膳食雌性大鼠肥胖与性发育不良的影响及其作用的机制。方法：雌性Wister大鼠,按体重随机分为正常对照组（C组）、高脂膳食对照组（HC组）、高脂膳食运动组（HE组）,采用无负重递增负荷游泳训练8周,观察其肥胖、性发育与脂肪瘦素受体的关系。结果：8周的高脂饮食导致大鼠肥胖,卵巢重量、血清雌二醇、瘦素水平明显升高（P〈0．01,P〈0．05,P〈0．05）,脂肪的Leptin mRNA和体长显著下降（P〈0．01）;8周的游泳训练使卵巢重量、血清雌二醇水平和瘦素水平明显下降（P〈0．05;P〈0．01）,脂肪Leptin mRNA表达和体长显著上升（P〈0．01）;且血清雌二醇与肥胖度各指标呈正相关,与体长呈负相关;血清瘦素与肥胖度各指标和反映性发育水平各指标均呈正相关。结论：①高脂膳食可诱导雌性大鼠肥胖,使血瘦素水平升高,瘦素受体的基因表达下调。出现了瘦素抵抗,性发育增强。②耐力训练可明显降低体脂和血瘦素水平,上调脂肪的瘦素受体的基因表达,有效的缓解了瘦素抵抗和性发育增强。     

氨基酸等化学刺激物对异育银鲫摄食行为的影响

实验采用撞球法中的双球法研究异育银鲫对氨基酸等刺激物的摄食行为的反应,运用实验鱼对实验球和空白球啄咬次数不同判断刺激物是否具有促摄食作用,运用刺激物与10-5mol/L丙氨酸啄咬次数的比值来比较不同刺激物间的反应。实验鱼体重为(46.5±9.3)g,刺激物为10-6-10-2mol/L的天冬氨酸、蛋氨酸、赖氨酸、精氨酸、丙氨酸、组氨酸、甜菜碱和乳酸,以及10-6-10-2g/L的鱿鱼提取物复合物。实验记录从第2分钟到第10分钟的数据。结果发现,异育银鲫对多数刺激物的刺激没有反应。天冬氨酸在10-6-10-4mol/L浓度范围内具有明显的促摄食作用,但10-3-10-2mol/L浓度范围内则具有微弱的摄食抑制作用。10-5mol/L和10-4mol/L的天冬氨酸溶液、10-4mol/L的精氨酸溶液对异育银鲫的促摄食作用最强,分别为10-5mol/L丙氨酸刺激作用的4.86、5.15和4.6倍。精氨酸、甜菜碱和乳酸的反应具有明显的浓度-反应效应,平均相对啄咬率分别在10-4mol/L、10-5mol/L、10-5mol/L浓度下达到最高,其他刺激物引起的反应在各浓度下差异不显著。蛋氨酸和乳酸在10-6-10-2mol/L各浓度下显著性地抑制异育银鲫的摄食行为。10-4mol/L精氨酸、10-5mol/L丙氨酸以及10-6、10-3和10-2mol/L赖氨酸对异育银鲫的撞球反应具明显的刺激作用。除甜菜碱和天冬氨酸外,多数刺激物引起摄食行为反应在2-9min期间非常稳定。甜菜碱和天冬氨酸刺激异育银鲫所产生的摄食行为反应有随记录时间的延长逐渐适应的趋势,特别是在10-6-10-4mol/L。       

瘦素诱导体外培养大鼠脂肪间充质干细胞凋亡

为观察瘦素诱导体外培养大鼠脂肪间充质干细胞凋亡的作用, 采用胶原酶消化法分离培养大鼠附睾脂肪垫间充质干细胞, 第3代细胞用于实验。细胞免疫荧光化学方法鉴定CD105、Vimentin表达阳性率约80%以上, 10-6 mol/L的瘦素作用细胞48 h、72 h后激光共聚焦显微镜观察分别可见早期及中晚期特征表现; 0 mol/L、10-8 mol/L、10-7 mol/L、10-6 mol/L瘦素分别作用于细胞48 h后, 应用AnnexinⅤ/PI双染色法流式细胞仪检测早期凋亡率分别为2.50%±0.72%、6.78%±1.99%、11.99%±1.58%、17.93%±4.82% (P<0.05); 随着瘦素浓度的增加和作用时间的延长, Caspase-3的活性逐渐增高, 至48 h时达到高峰。说明瘦素可以直接诱导脂肪间充质干细胞凋亡, 从数量上减少脂肪组织的含量。     

有氧运动对老年大鼠胃肠动力及血清中胃促生长素、瘦素水平的影响

目的：探讨有氧运动对老年大鼠胃肠动力以及血清中胃促生长素（ghrelin）和瘦素（leptin）的影响。方法：雄性SD大鼠45只,分为青年对照组、老年对照组以及老年有氧运动组（n=15）。老年有氧运动组采用递增负荷的方式进行8周跑台运动。实验过程中连续观察并记录各组大鼠的摄食量、体重以及行为学特征;实验结束测定各组大鼠胃排空速率以及小肠推进比,血清Ghre-lin和Leptin。结果：与青年对照组相比,老年对照组大鼠摄食量、胃排空速率、小肠推进比、血清Ghrelin水平明显降低,体重、体脂和Leptin水平显著升高;与老年对照组相比,老年有氧运动组大鼠摄食量、胃排空速率、小肠推进比、血清Ghrelin水平明显升高,体重、体脂和Leptin水平明显降低。结论：有氧运动能促进老年大鼠食欲、提高胃肠动力、改善身体成分,其保护机制可能与血清中Ghrelin含量升高和Leptin含量降低有关。     

营养状态影响大鼠味蕾甘丙肽及其受体mRNA的表达

机体的营养代谢状态参与调制外周味觉信息的整合,影响外周味觉感受和食物摄入。味蕾上的味觉受体及神经递质都是营养状态调节味觉感知的重要靶点。本文旨在探讨营养状态对味蕾上的重要神经递质甘丙肽及其受体表达的影响。我们比较了高脂饮食诱导的肥胖大鼠、慢性限制性饮食大鼠、以及正常膳食大鼠味蕾水平甘丙肽及其受体2 (galanin receptor 2,GalR2)mRNA表达水平的差异,以探讨机体营养代谢状态是否通过调控味蕾水平甘丙肽的表达来影响味觉感知。分别给予各组大鼠6周的高脂饮食、半量饮食和正常饮食,检测其体重、血糖、血脂等代谢相关指标,用real-time PCR方法检测其味蕾甘丙肽与GalR2 mRNA的表达变化。结果显示:与对照组相比,高脂饮食大鼠的体重显著增加,血清甘油三酯及血糖水平显著增高,味蕾水平甘丙肽与GalR2的mRNA表达水平显著降低,而慢性限制性饮食大鼠味蕾甘丙肽的mRNA表达增高,是对照组的2.3倍。结合以前的研究,我们可以得出初步结论:高脂饮食诱导的肥胖大鼠味觉感受行为学的变化可能与味蕾甘丙肽及其受体的表达变化存在相互关系。味蕾水平的甘丙肽及其受体GalR2参与营养状态调控大鼠味觉感知及摄食行为的外周机制。     

胍丁胺对离体大鼠主动脉张力的影响及其受体机制

采用离体血管环灌流方法,观察了胍丁胺（agmatine,Agm)对大鼠胸主动脉张力的影响,并探讨其受体机制,实验结果如下：（1）在苯肾上腺素PE,10^-6mol/L)引起血管预收缩的 基础上,Agm(10^-7-10^-2mol/L)剂量依赖性地舒张大鼠胸主动脉。（2）上述舒张反应在去除内皮和应用NOS抑制剂N^-G-mnitro-L-arginine methyl ester(L-NAME,0.5mmol/L)后依然存在,提示Agm的舒血管作用为非内皮依赖性,并无NO的参与。（3）在高Ca^2 (3mmol/L)引起血管预收缩的基础上,Agm也可剂量依赖性地舒张大鼠主动脉。（4）预先应用α2－肾上腺素能受体（α2－adrenergic receptor,α2－AR）和咪唑啉受体（IR）阻断剂idazoxan(10^-4mol/L)则可完全阻断Agm的上述作用。（5）应用α2－AR拮抗剂yohimbine(10^-4mol/L)可部分阻断Agm对大鼠主动脉的舒张反应,以上结果表明,Agm对大鼠主动脉血管的舒张作用是由α2－AR和IR共同介导。     

电损毁大鼠杏仁中央核对脑桥臂旁核味觉神经元的影响

应用细胞外记录的电生理学方法,在乌拉坦麻醉的大鼠观察了电损毁双侧杏仁中央核前后脑桥臂旁核味觉神经元对四种基本味觉刺激(即氯化钠、盐酸、奎宁和蔗糖)反应的变化。根据对味觉刺激的优势反应,29个记录的味觉神经元中,有14个NaCl优势、9个HCl优势、3个QH2SO4优势和3个蔗糖优势反应神经元。损毁杏仁中央核明显增强臂旁核味觉神经元对盐酸和硫酸奎宁的反应(P＜0．01)。氯化钠优势、盐酸优势和奎宁优势反应神经元对盐酸和硫酸奎宁的反应在电损毁杏仁中央核后也明显增强。在破坏杏仁中央核后,臂旁核味觉神经元对氯化钠和硫酸奎宁苦味的分辨能力降低。以上结果提示,杏仁中央核在大鼠脑桥水平的味觉编码中发挥重要作用,它可能是通过参与对味觉的影响来调节机体的摄食行为。     

瘦素受体基因敲除SD大鼠的表型及病理观察

目的观察CRISPR/Cas9技术建立的肥胖、代谢综合征和糖尿病前期特征的瘦素受体基因敲除大鼠模型的多种参数,为代谢性疾病的分子机制研究和新药研发提供更为理想的动物模型。方法1)定期测定Lepr^-/-大鼠的体重、摄食量、随机血糖和空腹血糖;葡萄糖耐量试验和胰岛素耐量试验;血清血脂参数;2)观察14周和18周Lepr^-/-大鼠主要脏器的病理学改变;3)观察脏器脂质沉积情况。结果Lepr^-/-大鼠表现明显肥胖、高摄食量、葡萄糖耐量受损、胰岛素抵抗和血脂异常;14周和18周出现胰岛增生和心脏肌细胞肥大、脂肪肝、肥胖相关性肾病;肝细胞、肾小管上皮细胞和骨骼肌纤维内脂质沉积。结论Lepr^-/-大鼠是代谢性疾病的病因研究和新药研发的理想动物模型。     

肠道味觉受体细胞及其甜味感受

味觉是人和动物的一种基本生理感觉,用来识别食物的性质、调节食欲、控制摄食量.味觉不仅仅存在于口腔中,同样存在于胃肠道中.最近研究表明,动物肠道的粘膜上存在着表达味觉受体和味觉相关因子的细胞,调控着肠道激素如GLP-1和GIP的分泌以及糖转运体SGLT-1和GLUT-2的表达.甜味剂的刺激影响这些激素的分泌及载体的表达,从而影响机体对葡萄糖的吸收和利用.肠道味觉的研究有助于揭示肠道消化吸收功能的调控机理,同时为糖尿病、肥胖、代谢失调及其它饮食相关疾病的治疗提供新的切入点.主要介绍了肠道粘膜上的味觉受体细胞、味觉的信号转导途径以及甜味感受对肠道激素的分泌和葡萄糖吸收的影响,最后讨论了味觉细胞生物学的发展方向.     

Monosodium glutamate and sweet taste: generalization of conditioned taste aversion between glutamate and sweet stimuli in rats

Even though monosodium glutamate (MSG) is a prototypical umami substance, previous studies reported that a conditioned taste aversion (CTA) to MSG, mixed with amiloride to block the taste of sodium, generalizes to sucrose. These findings suggest that the taste of glutamate mimics the taste of sucrose and raise the question of whether glutamate has a broadly tuned sweet taste component. To test this hypothesis, CTA experiments were conducted to test for generalization between MSG and several sweet stimuli: sucrose, glucose, maltose, saccharin and SC-45647. Strong bidirectional generalization was seen between MSG mixed with amiloride and sucrose, glucose, saccharin and SC-45647. Weak generalization was seen between MSG and maltose, and sucrose and maltose. None of the CTAs generalized to NMDA. These findings support the hypothesis that the taste of MSG has broadly tuned, sweet-like characteristics, possibly due to the convergence of afferent signals for MSG, natural sugars and artificial sweeteners.     

Monosodium glutamate and sweet taste: discrimination between the tastes of sweet stimuli and glutamate in rats

Generalization of a conditioned taste aversion (CTA) is based on similarities in taste qualities shared by the aversive substance and another taste substance. CTA experiments with rats have found that an aversion to a variety of sweet stimuli will cross-generalize with monosodium glutamate (MSG) when amiloride, a sodium channel blocker, is added to all solutions to reduce the taste of sodium. These findings suggest that the glutamate anion elicits a sweet taste sensation in rats. CTA experiments, however, generally do not indicate whether two substances have different taste qualities. In this study, discrimination methods in which rats focused on perceptual differences were used to determine if they could distinguish between the tastes of MSG and four sweet substances. As expected, rats readily discriminated between two natural sugars (sucrose, glucose) and two artificial sweeteners (saccharin, SC45647). Rats also easily discriminated between MSG and glucose, saccharin and, to a lesser extent, SC45647 when the taste of the sodium ion of MSG was reduced by the addition of amiloride to all solutions, or the addition of amiloride to all solutions and NaCl to each sweet stimulus to match the concentration of Na+ in the MSG solutions. In contrast, reducing the cue function of the Na+ ion significantly decreased their ability to discriminate between sucrose and MSG. These results suggest that the sweet qualities of glutamate taste is not as dominate a component of glutamate taste as CTA experiments suggest and these qualities are most closely related to the taste qualities of sucrose. The findings of this study, in conjunction with other research, suggest that sweet and umami afferent signaling may converge through a taste receptor with a high affinity for glutamate and sucrose or a downstream transduction mechanism. These data also suggest that rats do not necessarily perceive the tastes of these sweet stimuli as similar and that these sweet stimuli are detected by multiple sweet receptors.     

The sweet-bitter taste of alcohol: aversion generalization to various sweet-quinine mixtures in the rat

Rats were trained to avoid a 5% alcohol solution and then testedwith either sweet + quinine hydrochloride solutions (Experiment1) or sweet + hydrochloric acid solutions (Experiment 2). Thesweet stimuli used were sucrose, glucose, fructose and saccharin.Significant aversion generalization was found only in Experiment1 where trained rats generalized to all four test stimuli, thussuggesting that alcohol has a sweet taste (in combination withbitter) not specific to one sweetener. No significant aversiongeneralization was noted in Experiment 2 when sweet + hydrochloricacid solutions were tested. In Experiment 3, rats were trainedto avoid 6% alcohol and tested with sucrose + quinine hydrochloridemixtures with varying concentrations of each component. In general,rats showed generalization of the alcohol aversions across thevarious concentrations of sucrose and quinine hydrochloridetested.     

Sweetness intensity enhancement by pulsatile stimulation: effects of magnitude and quality of taste contrast

Upon stimulation with continuously alternating (pulsatile) taste concentrations, humans report higher average taste intensities than for continuous stimulation with the same average tastant concentration. We investigated the effect of the magnitude of concentration changes (concentration contrast) and the effect of taste quality changes (quality contrast) between alternating tastants on sweet taste enhancement. The perceived sweetness intensity increased with the magnitude of the sucrose concentration contrast: The pulsatile stimulus with the highest concentration difference (average sucrose concentration: 60 g/L) was rated as the sweetest in spite of the fact that the gross sucrose concentrations were identical over stimuli. Moreover, this stimulus was rated equally sweet as a continuous reference of 70 g/L sucrose. On alternation of sucrose with the qualitatively different citric acid, sweet taste enhancement remained at the level observed for alternation with water at citric acid concentration levels up to 3 times its detection threshold. Alternation of a sucrose solution with a citric acid solution at 9 times its threshold concentration, resulted in an attenuation of the pulsation-induced enhancement effect. Upon alternation of citric acid pulses at concentrations around the threshold with water intervals only, no taste enhancement was observed compared with continuous citric acid stimuli of the same net concentration. We propose that the magnitude of pulsation-induced taste enhancement is determined by the absolute rather than relative change of tastant concentration. This explains why 1) pulsation-induced sweet taste enhancement is determined by the magnitude of the sucrose pulse-interval contrast and 2) the alteration of citric acid with water does not enhance taste intensity at detection threshold level.     

Low serum leptin predicts mortality in patients with chronic kidney disease stage 5

Objective: Leptin, secreted from adipose tissue, regulates food intake, energy expenditure, and immune function. It is unknown whether leptin predicts mortality in patients with chronic kidney disease stage 5 on hemodialysis therapy. Research Methods and Procedures: We performed a prospective cohort study of 71 patients with chronic kidney disease stage 5 in an outpatient hemodialysis center. Subjects were recruited in June 1998 and followed for 83 months. Survival was compared by the Kaplan‐Meier method. Results: After 83 months of follow‐up, 48 patients (68%) had died. Serum leptin concentrations at study entry were lower among all deceased patients compared with those patients who survived (5.2 ± 9.0 μg/L; n = 48; vs. 7.7 ± 7.8 μg/L; n = 23; p = 0.005). Baseline serum leptin concentrations were significantly lower in patients who died from cardiovascular diseases (4.7 ± 9.4 μg/L, n = 32) or infections (4.0 ± 2.7 μg/L; n = 10; each p < 0.05), but not cancer (9.4 ± 7.9 μg/L; n = 6), than in survivors (7.7 ± 7.8 μg/L; n = 23; p = 0.003). The relative risk for mortality in patients with serum leptin concentrations below the median (<2.6 μg/L) compared with patients above the median was 1.96 (95% confidence interval, 1.01 to 3.79; p = 0.04). Survival was shorter in patients with leptin concentrations below the median compared with those whose leptin concentrations were above the median (all‐cause mortality, χ² = 5.05; p = 0.02). Discussion: Low serum leptin concentration is an independent predictor of mortality in patients with chronic kidney disease stage 5 on hemodialysis therapy.     

Inhibition of hamster chorda tympani neural response by copper chloride

Copper chloride was evaluated as a specific inhibitor of neuralresponses to sweet taste stimuli in the goldern hamster (Mesocricetusauratus). The chorda tympani whole-nerve response to taste stimuliwas recorded before and after the tongue was treated for 30s with 0.01, 0.1 and 1 mM CuCl₂. Sweet stimuli [sucrose, fructose,saccharin (calcium salt), D-phenylalanine], which primarilystimulate chorda tympani S fibers, and non-sweet stimuli (NaCl,NH₄Cl) were used. At 0.01 mM, copper chloride had little effect.At 0.10 mM it partially inhibited responses to sucrose and saccharin,but had little effect on responses to D-Phe, fructose, NaCl,NH₄Cl, or a mixture of sucrose plus L-Phe. L-Phe, which hasthe same chelating properties as D-Phe, is not an S-fiber stimulusand likely reduced sucrose inhibiton by chelating the cupricion.Analysis of concentration–response functions revealedthat 0.1 mM copper chloride inhibited the neural response tolow concentrations of sucrose by about 25%, but did not significantlyinhibit high concentrations of surcrose, suggesting competitiveinhibition. In contrast, 0.1 mM CuCl₂ reduced saccharin responsesby 25% throughtout the effective range, suggesting non-competitiveinhibition. Occupation of a saccharide receptor site by coppermay interfere with dimer but not monomer reception and distortthe saccharin receptor site. At 1 mM, CuCl₂ non-competitivelyinhibited responses to sucrose, fructose, saccharin and thenon-sweet NaCl (an N-fiber stimulus), but not NH₄Cl (an H-fiberstimulus). The mechanisms of copper chloride inhibition aredifficult to establish because its effects are weak at concentrationswhere they are specific.     

间歇性低氧对肥胖小鼠瘦素及其受体表达的影响

为探讨适度低氧环境对体重的影响及其作用机制,明确瘦素在其中的作用,用高脂饮食建立小鼠肥胖模型并观察间歇性低氧的干预效果。健康昆明小鼠随机分为4组（每组20只）,正常对照组：喂正常食物,不进行间歇性低氧训练;低氧组：喂正常食物,并进行间歇性低氧训练;肥胖组：喂高脂、高糖食物,但不进行间歇性低氧训练;低氧＋肥胖组,喂高脂、高糖食物,并进行间歇性低氧训练。40d后,测量小鼠体重,用酶联免疫吸附法测定血清瘦素水平,免疫组织化学检测肝脏瘦素受体表达,苏丹Ⅲ染色检测肝脏脂肪细胞分布和密度。结果显示,与正常对照组相比,肥胖组小鼠平均体重和平均血清瘦素水平显著升高,肝脏分布大量脂肪细胞,提示高脂模型建立成功;经过间歇性低氧训练后,低氧组和低氧＋肥胖组小鼠的平均体重及肝脏脂肪细胞分布密度和范围分别较对照组和肥胖组低,而血清瘦素水平明显增高;低氧＋肥胖组小鼠肝脏瘦素受体的表达高于肥胖组。结果提示,适度的间歇性低氧可以通过提高血清瘦素水平和增强肝脏瘦素受体表达而使体重减轻,并有效防止肝细胞脂肪变。     

The obesity in bilateral ovariectomized rats is related to a decrease in the expression of leptin receptors in the brain.

We investigated the expression levels of leptin receptors in the brain of ovariectomized (OVX) rats. The mean expression level of ob mRNA in adipose tissues of OVX rats was significantly (P < 0.01) lower than that in the SHAM operation group rats, and the mean body weight of OVX rats was significantly (P < 0.01) greater than that in the SHAM group rats. However, there were no differences between serum leptin concentrations in these two groups. The mean level of leptin receptor (OB-R) mRNA expression in the brain tissue and the mean level of long form type OB-R (OB-RL) mRNA expression in the hypothalamus of the OVX rats were significantly (P < 0.05) lower than those in the SHAM group rats. These changes were cancelled by supplementation with 17 beta-estradiol in OVX rats. These results suggested that not only changes in the expression level of ob mRNA in adipose tissue and the serum leptin concentration but also changes in the OB-R mRNA in the brain are involved in the body weight increase in OVX rats and that a decrease in OB-R makes transmission of signals to suppress the amount of food intake difficult, thus leading to an increase in body weight.     

Dysregulation of leptin signaling in Alzheimer disease: evidence for neuronal leptin resistance

Leptin signaling has received considerable attention in the Alzheimer disease (AD) field. Within the past decade, the peptide hormone has been demonstrated to attenuate tau hyperphosphorylation in neuronal cells and to be modulated by amyloid‐β. Moreover, a role in neuroprotection and neurogenesis within the hippocampus has been shown in animal models. To further characterize the association between leptin signaling and vulnerable regions in AD, we assessed the profile of leptin and the leptin receptor in AD and control patients. We analyzed leptin levels in CSF, and the concentration and localization of leptin and leptin receptor in the hippocampus. Significant elevations in leptin levels in both CSF and hippocampal tissue of AD patients, compared with age‐matched control cases, indicate a physiological up‐regulation of leptin in AD. However, the level of leptin receptor mRNA decreased in AD brain and the leptin receptor protein was localized to neurofibrillary tangles, suggesting a severe discontinuity in the leptin signaling pathway. Collectively, our results suggest that leptin resistance in the hippocampus may play a role in the characteristic changes associated with the disease. These findings are the first to demonstrate such dysregulated leptin‐signaling circuitry and provide novel insights into the possible role of aberrant leptin signaling in AD.

     

Whole nerve chorda tympani responses to sweeteners in C57BL/6ByJ and 129P3/J mice

The C57BL/6ByJ (B6) strain of mice exhibits higher preferences than does the 129P3/J (129) strain for a variety of sweet tasting compounds. We measured gustatory afferent responses of the whole chorda tympani nerve in these two strains using a broad array of sweeteners and other taste stimuli. Neural responses were greater in B6 than in 129 mice to the sugars sucrose and maltose, the polyol D-sorbitol and the non-caloric sweeteners Na saccharin, acesulfame-K, SC-45647 and sucralose. Lower neural response thresholds were also observed in the B6 strain for most of these stimuli. The strains did not differ in their neural responses to amino acids that are thought to taste sweet to mice, with the exception of L-proline, which evoked larger responses in the B6 strain. Aspartame and thaumatin, which taste sweet to humans but are not strongly preferred by B6 or 129 mice, did not evoke neural responses that exceeded threshold in either strain. The strains generally did not differ in their neural responses to NaCl, quinine and HCl. Thus, variation between the B6 and 129 strains in the peripheral gustatory system may contribute to differences in their consumption of many sweeteners.