ライフサイエンスコーパス: saccharin

1 cose) or did not predict increased calories (saccharin).

2 this effect was replicated by D-fructose or saccharin.

3 tex and striatum, which were unresponsive to saccharin.

4 gonist were able to acquire CTAs to familiar saccharin.

5 increase in sucrose and chow intake but not saccharin.

6 s people more sensitive to the bitterness of saccharin.

7 o the bitterness of an artificial sweetener, saccharin.

8 antly associated with preferences for 1.6 mm saccharin.

9 and also preferred the noncaloric sweetener saccharin.

10 nduced larger increases in FLI than familiar saccharin.

11 rague-Dawley rats were given 5 min access to saccharin.

12 ent of a conditioned taste aversion (CTA) to saccharin.

13 but did not affect elasticity of demand for saccharin.

14 -induced conditioned taste aversion (CTA) to saccharin.

15 y 2 times higher than the average loading of saccharin.

16 t off-target CAs (Ki > 50000 nM) compared to saccharin.

17 tes a so far unknown isomer that we call iso-saccharin.

18 en ethanol (EtOH) (10% v/v), and a palatable saccharin (0.0125% g/v) solution.

19 ver for EtOH (10% v/v) and another lever for saccharin (0.05% or 0.75% g/v), then dose-response and t

20 o, or 5min after, a single pairing of sodium saccharin (0.125%, 10-min access) and LiCl or NaCl (0.15

21 Conditioned place preference (CPP) and saccharin (0.2% w/v) self-administration were also inves

22 Saccharin (0.2% w/v) was subsequently added to the ethan

23 ed by acesulfame (1.22 g/d/1000 people), and saccharin (1.07 g/d/1000 people).

24 f taste compounds (cycloheximide, 10 microm; saccharin, 2 mm; denatonium, 1 mm; SC45647, 100 microm).

25 g/g dw, followed by acesulfame (92 ng/g) and saccharin (49 ng/g).

26 eness to a surrogate nipple providing water, saccharin, 5% ethanol, or 10% ethanol was tested in newb

27 solution compared with a placebo containing saccharin (60.4 +/- 3.7 and 61.6 +/- 3.8 min, respective

28 Significant removal of aspartame (68.2%) and saccharin (90.3%) was found in WWTPs; however, sucralose

29 However, saccharin, a cyclic secondary sulfonamide, has unusually

30 sufficient to inhibit operant responding for saccharin, a measure of motivated behavior.

31 tocol of daily ingestion of a 3% solution of saccharin, a noncaloric sweetener, induced synaptic GluA

32 demonstrating reduced responses to sucrose, saccharin, acesulfame potassium, glucose and NaCl in acu

33 e results showed that rats avoided intake of saccharin after saccharin-cocaine pairings and that grea

34 neurobehavioral consequences of exposure to saccharin alone or saccharin and nicotine for the expose

35 ral-lesions displayed a CTA by rejecting the saccharin, although increases in c-FLI on the side of th

36 nstead given a low value reward (e.g., 0.15% saccharin), an effect termed successive negative contras

37 procedures and the same taste stimuli (0.15% saccharin and 1.0 M sucrose), the authors tested the hyp

38 Approximately, 1180 g of saccharin and 291 g of acesulfame were transformed in or

39 Intake of saccharin and 5% ethanol was high in newborns, far excee

40 small molecule artificial sweeteners such as saccharin and acesulfame K, and proteins such as monelli

41 ctivation of hTAS2R31 (formerly hTAS2R44) by saccharin and acesulfame K, two common artificial sweete

42 precursor cells with artificial sweeteners, saccharin and acesulfame potassium, enhanced adipogenesi

43 The structures of the conjugate bases of saccharin and iso-saccharin were also computed theoretic

44 pared with STDRLO, STDRHI mice consumed more saccharin and less quinine, exhibited greater ethanol-in

45 stered before (but not after) the pairing of saccharin and LiCl resulted in a significantly stronger

46 Rats conditioned with saccharin and LiCl showed a decreased preference for sac

47 s assessed using self-administration of 0.2% saccharin and locomotor activity tests.

48 f OA, because rats given OA and a pairing of saccharin and NaCl did not acquire a CTA.

49 nsequences of exposure to saccharin alone or saccharin and nicotine for the exposed individuals and t

50 We found that co-exposure of male mice to saccharin and nicotine produced significant behavioral i

51 rns about adverse outcomes of co-exposure to saccharin and nicotine.

52 ir intake of food and water, and of sucrose, saccharin and quinine solutions, was normal.

53 Most known applications of saccharin and saccharyl derivatives and their potential

54 They were then given brief access to 0.15% saccharin and soon thereafter injected with either cocai

55 er: aspartame (50.4%) > acesulfame (10.9%) > saccharin and sucralose (0.8%).

56 S decreased licking responses to sucrose and saccharin and to NaCl in mice.

57 iable" amides, including bench-stable N-acyl saccharin and various activated amides, from aldehydes b

58 d, sucrose, and ethanol), those that do not (saccharin and water), and those lacking biological relev

59 responsive to natural rewards (in this case saccharin), and the stronger preference for saccharin se

60 he number of meals initiated for water, 0.1% saccharin, and 1.0 M sucrose solutions, but meal size wa

61 The total mass loading of sucralose, saccharin, and acesulfame in the WWTP that served a smal

62 n and LiCl showed a decreased preference for saccharin, and OA administered before (but not after) th

63 (NPY) on licking microstructure for sucrose, saccharin, and water solutions were evaluated.

64 embered ring benzosultams in one step, using saccharin anion as starting material.

65 A wide range of aromatic and aliphatic acyl saccharin are obtained from their respective aldehydes w

66 Using saccharin as a taste stimulus in a taste preference para

67 The same effects occurred with saccharin as the reinforcer in olfactory conditioning.

68 strong conditioning occurred with sucrose or saccharin as the US.

69 es, and environmental emission of sucralose, saccharin, aspartame, and acesulfame were determined bas

70 gative and lower for sucralose compared with saccharin, aspartame, and rebA consumption.

71 Concurrent saccharin availability increased demand for heroin in fe

72 Second, firing evoked by cues signalling saccharin availability shifted from a pattern of primari

73 ophobia, retarded acquisition of conditioned saccharin avoidance and apparently attenuated the magnit

74 A series of novel, saccharin-based antagonists have been identified for the

75 A saccharin-based imine was found to be uniquely suited to

76 tes, as is the case of the recently proposed saccharin-based ionic liquids.

77 e super Lewis acid iron(III) triflimide with saccharin-based thioarylation reagents for the rapid syn

78 The ingestion of saccharin before the OGTT did not alter any of the measu

79 Preexposure to a nipple providing ethanol or saccharin (but not a nipple alone or fluids alone) incre

80 sioned rats displayed a CTA by rejecting the saccharin, but increases in c-FLI were evident only on t

81 t P1 and P2, pups exhibited a preference for saccharin, but not for 5% ethanol.

82 and testing occur in a novel environment, CS saccharin causes an increase in c-Fos expression, and wh

83 TAS2R agonists such as saccharin, chloroquine and denatonium evoked increased i

84 that rats avoided intake of saccharin after saccharin-cocaine pairings and that greater avoidance of

85 voided intake of the saccharin cue following saccharin-cocaine pairings; however, the rats in the yok

86 ed yogurt dietary supplements sweetened with saccharin compared with those fed glucose-sweetened diet

87 Rats decrease intake of a saccharin conditioned stimulus (CS) when followed by: (1

88 uppress intake of a normally preferred 0.15% saccharin conditioned stimulus (CS) when it is paired wi

89 Rats suppress intake of a saccharin conditioned stimulus (CS) when it is paired wi

90 Rats suppress intake of a saccharin conditioned stimulus (CS) when paired with a d

91 ley rats were given 20-min access to a 0.15% saccharin conditioned stimulus (CS).

92 ue-Dawley rats acquired a strong aversion to saccharin (conditioned stimulus; CS) and then underwent

93 sulin sensitivity index independent of prior saccharin consumption (P < 0.025).

94 availability caused an increase in estimated saccharin consumption at no cost (Q(0)), but did not aff

95 Sucrose and saccharin consumption led to increased body weight acros

96 ovelty, morphine had little influence on the saccharin consumption of IC-lesioned rats.

97 Sucrose and saccharin consumption significantly increase body weight

98 Notably, water, food, and saccharin consumption was unaltered by either treatment.

99 d taste aversion learning induced by pairing saccharin consumption with LiCl injection, by making the

100 ce consumed less ethanol but were similar in saccharin consumption, sensitivity to ethanol-induced CP

101 One compound also reduced sucrose and saccharin consumption, while the other was selective for

102 he wide variety of interfering UV spectra in saccharin-containing beverage matrices, the same method

103 data suggest that rats suppress intake of a saccharin CS in anticipation of the availability of a pr

104 ructural analysis of licking) for a standard saccharin CS paired with the following: lithium chloride

105 ulus, did not reduce the palatability of the saccharin CS.

106 se animals actually suppressed intake of the saccharin CS.

107 In turn, a single exposure to the saccharin cue also blunted the unconditioned dopamine re

108 In Experiment 3, avoidance of the saccharin cue and the propensity to self-administer coca

109 aFosB in the striatum were given access to a saccharin cue and then injected with saline, 10 mg/kg co

110 d value of drug, but the reward value of the saccharin cue as well.

111 othesis suggests that rats avoid intake of a saccharin cue following pairings with a drug of abuse be

112 Both cocaine groups avoided intake of the saccharin cue following saccharin-cocaine pairings; howe

113 ted controls, all rats reduced intake of the saccharin cue following saccharin-DAMGO pairings.

114 Fischer rats exhibit greater avoidance of a saccharin cue following saccharin-morphine pairings.

115 hibit greater cocaine-induced avoidance of a saccharin cue relative to Fischer 344 rats; while reward

116 Rats suppress intake of a saccharin cue when paired with a drug of abuse such as m

117 Rats avoid intake of a saccharin cue when paired with a drug of abuse.

118 D-glucose, D-fructose, saccharin, D-mannitol, and water were infused for 3 hour

119 educed intake of the saccharin cue following saccharin-DAMGO pairings.

120 on of intraorally infused water, sucrose, or saccharin, demonstrating that ingestion analgesia does n

121 A saccharin-DMAP zwitterion complex was isolated, which pr

122 Artificially sweetened (saccharin) drink reproduces the stress dampening, wherea

123 caused rats to significantly suppress their saccharin drinking (relative to controls) - indicating a

124 AIC firing was not elevated during saccharin drinking, similar to lack of effect of AIC inh

125 eet-tasting molecules as diverse as sucrose, saccharin, dulcin, and acesulfame-K.

126 minister ethanol (10-15%, w/v) in 0.2% (w/v) saccharin during daily 30 min sessions and were surgical

127 However, when switched from sucrose to saccharin during the postshift trials these rats display

128 Spermatazoal DNA was hypermethylated in the saccharin-exposed fathers, especially at dopamine recept

129 e produced motor impulsivity not only in the saccharin-exposed males but also in their offspring.

130 In a mouse model, saccharin exposure produced motor impulsivity not only i

131 t 1, water-deprived rats had 5-min access to saccharin followed by active or yoked intravenous delive

132 ischer rats were given 5 min access to 0.15% saccharin followed by an icv injection of either DAMGO (

133 g of intraoral infusion of 5-ml 0.15% sodium-saccharin followed by injection with LiCl (0.15 M, 20 ml

134 g of intraoral infusion of 5 ml 0.15% sodium-saccharin followed by injection with LiCl (0.15 M, 20 ml

135 al nicotine administration (100 mug/ml in 2% saccharin for 14 days), with special emphasis on amyloid

136 nstrate that the affinity and selectivity of saccharin for CA IX can be further modulated when linked

137 er pairing intake of a palatable glucose and saccharin (G+S) solution with magnetic field exposure.

138 h a fixed amount of a yogurt diet mixed with saccharin gained more weight and showed impaired caloric

139 m ascorbate, like other sodium salts such as saccharin, glutamate, and bicarbonate, produces urinary

140 reference for water flavored with sucrose or saccharin in a two-bottle free-choice drinking paradigm.

141 Suppression of lipolysis by saccharin in adipocytes was also independent of T1R2 and

142 nduced CTA strongly decreased motivation for saccharin in an operant task to obtain the tastant.

143 3 compared demand for saccharin in groups that had or did not have concurrent

144 mmonly used methods to identify and quantify saccharin in non-alcoholic beverages.

145 The presence of saccharin in non-diet beverages - a fraud commonly used

146 immunoreactivity than the familiar taste of saccharin in the basolateral region of the amygdala, cen

147 esulfame potassium approximately sucralose > saccharin, in parallel with their ability to increase in

148 of neohesperidin dihydrochalcone (NHDC) and saccharin] included in piglets' feed reduces incidence o

149 Novel saccharin induced larger increases in FLI than familiar

150 charin with lithium or wheel-running reduced saccharin intake as well as lick cluster size, initial l

151 that greater morphine-induced suppression of saccharin intake by the Fischer rats is not likely media

152 infusions of 6% carbohydrate did not affect saccharin intake during the first ingestive bout, but la

153 thium chloride (LiCl)-induced suppression of saccharin intake in Sprague-Dawley rats.

154 reduced both CLAD and AOD, without impacting saccharin intake or locomotion, while aINS inhibition of

155 Saccharin intake was either not altered by RO19-4603 or

156 A/2J mice, exhibit attenuated suppression of saccharin intake when it is paired with cocaine.

157 l rats, morphine caused a rapid reduction in saccharin intake when the taste was novel but not when i

158 Pairing saccharin with amphetamine reduced saccharin intake without reducing the size of licking cl

159 mittent drinking procedure without affecting saccharin intake, ethanol-induced incoordination or etha

160 uced CLAD, with no effect on alcohol-only or saccharin intake, suggesting a specific aINS-brainstem r

161 Ac of mice did not alter water, quinine, and saccharin intake.

162 th attenuated cocaine-induced suppression of saccharin intake.

163 cimol was demonstrated for water, saline, or saccharin intake.

164 MSNs but not iMSNs increases alcohol but not saccharin intake.

165 core reduces methamphetamine SA, as well as saccharin intake.

166 in iMSNs, reduces excessive alcohol but not saccharin intake.

167 Saccharin is a versatile scaffold to build up different

168 Although saccharin is considered safe for human consumption, it p

169 The use of non-nutritive sweeteners such as saccharin is widely prevalent.

170 consumption of an appetitive tastant (e.g., saccharin) is paired to the administration of a malaise-

171 onditionally preferred taste stimulus (e.g., saccharin) is reduced by contingent administration of a

172 less tobacco products, some of which contain saccharin, is on the rise contributing to concerns about

173 Two series of saccharin/isoxazole and saccharin/isoxazoline hybrids we

174 Two series of saccharin/isoxazole and saccharin/isoxazoline hybrids were synthesized by 1,3-di

175 unpaired' controls received a non-contingent saccharin-LiCl presentation.

176 unpaired' controls received a non-contingent saccharin-LiCl presentation.

177 tly reduced EtOH-maintained responding, with saccharin-maintained responding being reduced only with

178 The saccharin-maintained responding was reduced only with th

179 daily prior access to a palatable glucose + saccharin mixture.

180 on transfer (ET) between the triplet excited saccharin moiety and sulfur atom.

181 The results showed that a single saccharin-morphine pairing led to a marked reduction in

182 all rats were exposed to the same number of saccharin-morphine pairings, only half of these animals

183 eater avoidance of a saccharin cue following saccharin-morphine pairings.

184 rences in intake suppression following seven saccharin-morphine pairings.

185 d with sucrose (n = 39), aspartame (n = 30), saccharin (n = 29), sucralose (n = 28), or rebaudioside

186 rent types of stimuli were used: taste (0.5% saccharin), olfactory (0.1% amyl acetate), and trigemina

187 These subjects consumed a higher percent saccharin on test day and their CTAs extinguished more r

188 mice were given MO via the drinking water or saccharin only (SCH) one week prior to mating with DBA m

189 s demonstrated greater nipple attachment for saccharin or 5% ethanol than for water.

190 ive days during adolescence, male rats drank saccharin or alcohol after receiving subcutaneous oil or

191 ng showed that this did not generalize to Na-saccharin or galactose.

192 In Experiment 1, saccharin or salt were either mixed in distilled water,

193 n and preference, with no similar effects on saccharin or sucrose consumption.

194 lution of either 300 parts per million (ppm) saccharin or water with or without the addition of 500 p

195 ation did not impact preference for sucrose, saccharin, or quinine.

196 hat HR rats display a greater preference for saccharin over cocaine compared with ST and HA whereas t

197 ats were then tested on their preference for saccharin over cocaine in a discrete-trial choice proced

198 e, most rats prefer natural rewards, such as saccharin, over cocaine.

199 e frequency was lower for sucralose than for saccharin (P = 0.045).

200 ingestion of water, chocolate, sucrose, and saccharin, pain-related behaviors are suppressed.

201 ppressed CS intake and caused a reduction in saccharin palatability.

202 both anions may be relevant in systems where saccharin participates, as is the case of the recently p

203 trains showed the strongest association with saccharin preference at three sites: nucleotide (nt) -79

204 ggest that the polymorphisms associated with saccharin preference do not act by blocking gene express

205 ify Tas1r3 sequence variants associated with saccharin preference in a large number of inbred mouse s

206 ve behavior, and anxiety-like behavior using saccharin preference testing, reward-omission testing, a

207 ssion-like (measured via the forced swim and saccharin preference tests) behaviors in outbred rats re

208 f recent studies suggest that the mouse Sac (saccharin preference) locus is identical to the Tas1r3 (

209 ed by reduced female urine sniffing time and saccharin preference, and behavioral despair in female m

210 m six inbred mouse strains with high and low saccharin preference, including the strains in which the

211 amphetamine hypersensitivity, and increased saccharin preference.

212 ng total fluid intake, locomotor activity or saccharin preference.

213 strains with different Tas1r3 haplotypes and saccharin preferences.

214 ver, those subjects which were preexposed to saccharin prior to CS/US pairing displayed significantly

215 ts showed normal responsivity to sucrose and saccharin prior to the reward downshift.

216 oning and testing occur in the home cage, CS saccharin produces a decrease in c-Fos expression relati

217 eful building blocks in synthesis, including saccharin, pyridones, pyrazoles, and triazoles.

218 After the synthesis, the saccharin removal from the MIP was verified by the UV an

219 ced a synergistic decrease in responding for saccharin, resembling the changes produced by targeting

220 No effects were seen on saccharin responding except with the highest dose level

221 g a dose-dependent increase in the slope for saccharin responding.

222 tal area did not significantly alter EtOH or saccharin responding.

223 ng of the accumbens dopamine response to the saccharin reward cue.

224 uired to find the sweet tastes of sucrose or saccharin rewarding.

225 We report that saccharin's behavioral effects are much more pervasive t

226 2 knockdown reduces methamphetamine, but not saccharin, SA on a progressive ratio schedule of reinfor

227 A was formed through 3 pairings of 0.3% oral saccharin (SAC) and 81 mg/kg i.p. lithium chloride (LiCl

228 The sweeteners saccharin (SAC) and acesulfame K (ACE) recently entered

229 ed a strong CTA [via 3 pairings of 0.3% oral saccharin (SAC; the CS) and 81mg/kg i.p. lithium chlorid

230 itly unpaired (EU) conditioned stimulus (CS; saccharin, SAC) and unconditioned stimulus (US; lithium

231 rats reached 90% reacceptance of a tastant (saccharin: SAC) that had previously been associated with

232 stration at doses that neither affected 0.2% saccharin self-administration nor locomotor activity.

233 Conversely, saccharin self-administration was not affected by NOP de

234 TP-10 also reduced saccharin self-administration, suggesting a general role

235 saccharin), and the stronger preference for saccharin serves to militate against drug.

236 NAcc DA levels during the saccharin sessions tracked the variance of the scheduled

237 also assessed in additional rats during the saccharin sessions.

238 current presentation of EtOH (10% v/v) and a saccharin solution (0.05% w/v).

239 lf of all subjects were preexposed to a 0.2% saccharin solution (CS) for 4 consecutive days prior to

240 ly higher during consumption of the devalued saccharin solution after CTA induction.

241 mulation, rats were again presented with the saccharin solution as we tested for SR of the CTA.

242 -like state, and loss of taste preference in saccharin solution consumption test which pointed to the

243 l infusions of a cocaine-predictive flavored saccharin solution elicited aversive orofacial responses

244 Results revealed that the taste of the novel saccharin solution evoked more Fos immunoreactivity than

245 -like behaviors were assessed by sweet-taste Saccharin solution preference (SSP) and forced swimming

246 red 1.0 M sucrose solution or the same 0.15% saccharin solution.

247 did control subjects that only received the saccharin solution.

248 trient diets as well as saline, sucrose, and saccharin solutions.

249 inking as well as consumption of sucrose and saccharin solutions.

250 d food (15% sucrose), and non-nutrient (0.2% saccharin) solutions following intraperitoneal (i.p.) ad

251 ocity values for aqueous solutions of sodium saccharin (SS) has been measured as a function of concen

252 Surprisingly, neither saccharin-stimulated adipogenesis nor Thr-308 phosphoryl

253 Saccharin-stimulated Akt phosphorylation at Thr-308 occu

254 iment 2 established that a safe and familiar saccharin stimulus supports substantially weaker conditi

255 than does a potentially dangerous and novel saccharin stimulus.

256 ately recognize the novelty of the postshift saccharin stimulus.

257 veral synthetic sweeteners (e.g., aspartame, saccharin, sucralose) are becoming less popular due to h

258 e strains of mice in their responsiveness to saccharin, sucrose and other sweeteners.

259 hronic LPS also reduced licking responses to saccharin, sucrose, and NaCl in mice.

260 id not cause a conditioned taste aversion to saccharin, suggesting that the anorexic effect of NAc co

261 t study examined whether a novel taste (0.5% saccharin) supports a different pattern of c-Fos express

262 sucralose (Splenda), aspartame (Equal), and saccharin (Sweet'N Low), only erythritol negatively affe

263 tassium; AceK) as well as in animals given a saccharin-sweetened base diet (refried beans) that was c

264 creased weight gain in response to consuming saccharin-sweetened compared with glucose-sweetened supp

265 ntake, weight gain, and adiposity when given saccharin-sweetened compared with glucose-sweetened yogu

266 tional weight when subsequently exposed to a saccharin-sweetened diet.

267 g that body weight differences persist after saccharin-sweetened diets are discontinued and following

268 However, in male rats fed an HE diet, saccharin-sweetened supplements produced extra weight ga

269 were observed in the self-administration of saccharin-sweetened water.

270 After repeated pairings of a saccharin taste (conditioned stimulus, CS) with injectio

271 ion of the bile duct (BDL) was paired with a saccharin taste developed a persistent conditioned taste

272 esponse to cue presentation, lever press and saccharin taste.

273 l, i.p.) conditioned taste aversion (CTA) to saccharin taste.

274 rials these ICX rats consistently drank more saccharin than the ICX rats maintained on saccharin thro

275 ss for an unexpected low-value reward (0.15% saccharin) than did control subjects that only received

276 nded most positively to the nipple providing saccharin, the longest time spent on an empty nipple was

277 highest dose with the formulation containing saccharin, these adverse events were reported by 41%, 14

278 re saccharin than the ICX rats maintained on saccharin throughout the experiment.

279 ption coefficients of ASWs ranged from 4.10 (saccharin) to 4540 L/kg (aspartame).

280 Saccharin treatment of 3T3-L1 cells and primary mesenchy

281 fferent groups were trained to nose-poke for saccharin under certain [fixed-ratio (FR)] or uncertain

282 Here, we show that saccharin undergoes structural rearrangement when subjec

283 ly effective method to identify and quantify saccharin using HPLC with fluorescence detection (HPLC-F

284 sion could not be classically conditioned to saccharin using WRYamide as the unconditioned stimulus.

285 ehaving rats learned to dislike the taste of saccharin [via conditioned taste aversion (CTA)].

286 Photocyclization of N-(thioalkyl)-saccharin was carried out to obtain different polycyclic

287 Monomeric saccharin was isolated in low-temperature argon matrices

288 Sodium saccharin was shown to produce a low incidence of bladde

289 of the conjugate bases of saccharin and iso-saccharin were also computed theoretically.

290 sweeteners such as aspartame, cyclamate, and saccharin were not enhanced by SE-1 whereas sucrose and

291 es to NaCl, HCI, quinine-HCl, sucrose and Na saccharin were recorded simultaneously in pairs of singl

292 study are similar to those seen with sodium saccharin when administered in a two-generation bioassay

293 rienced CS/US pairing displayed aversions to saccharin when given a two bottle choice test.

294 Rodents suppress intake of saccharin when it is paired with a drug of abuse.

295 Pairing saccharin with amphetamine reduced saccharin intake with

296 rolled CuF(2)-catalyzed Chan-Lam coupling of saccharin with arylboronic acids is reported, enabling t

297 By contrast, pairing saccharin with lithium or wheel-running reduced sacchari

298 ering consumption of quinine-free alcohol or saccharin with or without quinine.

299 eward value of the available solution (0.15% saccharin) with respect to the memory of the preferred s

300 Irradiation of matrix-isolated saccharin, with a narrow-band source (290 nm), generates