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PubMed1996

Several roles of CCKA and CCKB receptor subtypes in CCK-8-induced and LiCl-induced taste aversion conditioning.

Administration of a relatively large IP dose of sulfated cholecystokinin (26-33) (CCK-8; 1.0 mumol/kg) consistently induced moderate taste aversion conditioning (TAC) using a 20-min, one-bottle test in Long-Evans rats. Because CCK-8 has affinity for both CCKA and CCKB receptor subtypes, we wanted to determine the subtype involved in CCK-8-induced TAC. Pretreatment with the selective CCKA antagonist MK-329 (L-364, 718 or devazepide), at doses of 0.1, 1.0, or 10.0 mumol/kg, markedly antagonized (> 70%) CCK-8-induced TAC. Pretreatment with the selective CCKB antagonist L-365,260, at doses of 0.1 or 1.0 mumol/kg, partially antagonized (approximately 50%) CCK-8-induced TAC, although the highest dose of L-365,260. 10.0 mumol/kg, did not. These partial antagonistic effects of L-365,260 on CCK-8-induced TAC were replicated in our second study. In our third study, we observed that another CCKB antagonist, the dipeptoid CI-988, also partially antagonized CCK-8-induced TAC at a dose of 0.1, but not 1.0 or 10.0, mumol/kg. In our final study, pretreatments with a single dose (i.e., 10.0, but not 0.1 or 1.0, mumol/kg) of either MK-329 or L-365,260 were also shown to partially antagonize the formation of moderate TAC induced by treatment with LiCl at 708 mumol/kg. Marked antagonism of LiCl-induced TAC was also observed following pretreatment with the known anxiolytic chlordiazepoxide HCl at 7.4 mumol/kg. Considering the existing data on the induction of TAC by various CCK analogues, we consider an action of CCK-8 on peripheral CCKA, but not CCKB, receptors necessary for the induction of TAC. Our results of partial antagonism of CCK-8- and LiCl-induced TAC by L-365,260, CI-988, or MK-329 suggest, but do not prove, that both CCKA and CCKB mechanisms may be operative during TAC. Because the CCK antagonists affected TAC like chlordiazepoxide, blockade of CCKA and CCKB mechanisms may produce a mild anxiolytic effect.

Animals↗

PubMed2006

Familiarization and cross-familiarization of wheel running and LiCl in conditioned taste aversion.

Familiarization with an unconditioned stimulus (US) interferes with the learning of subsequent Pavlovian conditioned associations. We conducted a series of experiments exploiting this US preexposure effect to elucidate the underlying mechanism of conditioned taste aversion in rats induced by voluntary wheel running. Experiment 1 demonstrated that running-induced taste aversion was alleviated if rats had sufficient experience of running in advance. In Experiments 2A and 2B, preexposure to wheel running had no effect on subsequent taste aversion conditioning by lithium chloride (LiCl) injection. In Experiment 3, however, we observed a weak partial interference from the LiCl injection pretreatment to the subsequent conditioning by wheel running US. This US crossover effect suggests the possibility that wheel running and LiCl injection share a common or similar physiological mechanism in inducing taste aversion.

Analysis of Variance↗

PubMed1999

The suppressive effects of LiCl, sucrose, and drugs of abuse are modulated by sucrose concentration in food-deprived rats.

Suppression of intake of a gustatory conditioned stimulus (CS) occurs when paired with either an aversive or an appetitive unconditioned stimulus (US). Toxic substances, such as lithium chloride (LiCl), induce conditioned taste aversions while rewarding stimuli, such as high a concentration of sucrose, reduce intake through a comparison process referred to as anticipatory contrast. Drugs of abuse also suppress CS intake, but it is not known whether they do so via their rewarding or aversive properties. Using 0.1, 0.3, or 0.5 M sucrose solutions as the gustatory CS, we compared the suppressive effects of LiCl (5.29 mg/kg), morphine (15 mg/kg), cocaine (10 mg/kg), and a 1.0-M sucrose solution in rats that were food deprived. The doses of the three drugs have been equated in terms of their suppressive effects in water-deprived and free-feeding rats. The results showed that in food-deprived rats the sucrose US failed to suppress intake of any of the sucrose CSs, the drugs of abuse failed to suppress intake of the 0.3 and 0.5-M concentration of sucrose, and LiCl failed to suppress intake of the 0.5-M sucrose solution. When taken together, these findings reveal that the suppressive effects of all USs (aversive, appetitive, and drugs of abuse) can be offset by the use of a caloric CS when evaluated in food-deprived rats.

Analysis of Variance↗

PubMed2006

Liquid-liquid transition in supercooled water investigated by interaction with LiCl and Xe.

The hypothesis that supercooled water consists of two distinct liquid phases has been explored on the basis of their ability to hydrate nonpolar (Xe) and electrolytic (LiCl) species. Xe incorporated in the bulk of amorphous solid water survives in the deeply supercooled regime above the glass-transition temperature of 136 K and is finally dehydrated at 165 K, whereas LiCl dissolves only in the liquid phase appearing above 165 K. The second liquid phase connects with normal water as inferred from high (poor) solubility of LiCl (Xe). This result also suggests that decoupling of translational diffusion and viscosity in the deeply supercooled regime is caused by domain structures of the two liquid phases formed during a possible liquid-liquid transition.

Journal Article↗

PubMed1999

Coordinate regulation of Fos and Jun proteins in mouse brain by LiCl.

Expression of the bZIP transcription factor c-Fos in the nucleus tractus solitarius (NTS) of the brain stem may allow for genomic encoding of an unconditioned stimulus (US) during taste aversion learning. Dimerization of c-Fos with other bZIP proteins of the Jun family is necessary to enable transcriptional efficacy at the AP-1 sequence of putative target gene promoter regions. The present study examined the regulation of Fos and Jun proteins by LiCl. Double immunofluorescence labelling revealed that LiCl causes a coordinate upregulation of c-Fos, FosB and JunB, and these proteins are colocalized in a majority of cells examined in NTS, parabrachial nucleus (PBN), and central nucleus of the amygdala (CeA). This study demonstrates that a coordinate signalling response occurs in relevant brain regions in response to LiCl.

Amygdala↗

PubMed1989

LiCl and CCK inhibit gastric emptying and feeding and stimulate OT secretion in rats.

Systemic injection of the nauseogenic agent LiCl is known to increase neurohypophyseal secretion of oxytocin (OT) in rats. The present results indicated that the induced OT secretion was related exponentially to the inhibition of food intake. A similar relation between OT secretion and food intake also was observed after systemic injection of the peptide hormone cholecystokinin (CCK). However, the effects of each agent on food intake lasted much longer than the observed increases in OT secretion. In contrast, both LiCl and CCK produced a dose-dependent inhibition of gastric emptying in rats that was closely related temporally to the inhibition of food intake. The similarity of these three responses to LiCl and CCK suggests that both agents stimulate common central mechanisms, apparently involving both magnocellular and parvocellular neurons in the paraventricular nucleus of the hypothalamus, whereby these neuroendocrine, behavioral, and autonomic functions are integrated.

Animals↗

PubMed2006

[Mechanism of tau hyperphosphorylation in brain cortex of diabetic rats and effect of LiCl].

OBJECTIVE: To explore the mechanism of tau hyperphosphorylation and the effect of LiCl on tau phosphorylation and the memory retention deficits in streptozotocin-induced diabetes mellitus (DM) rats. METHODS: The rats were randomly divided into control, DM, DM + NaCl, and DM + LiCl groups and diabetes was induced by streptozotocin. The activity of glycogen synthase kinase-3 (GSK-3) was measured by 32P-labelling. The level of tau phosphorylated and changes of memory retention were examined by Western blotting and step down test, respectively. RESULTS: Compared with control group, the activity of GSK-3 and tau phosphorylation was increased, and the memory retention was impaired in DM group. When the rats were treated with LiCl, the activity of GSK-3 and hyperphosphorylation of tau were significantly arrested (P < 0.05, P < 0.01), and the memory retention deficit was significantly improved (P < 0.05). CONCLUSION: The hyperphosphorylation of tau can be induced by activation of GSK-3 in diabetic rats. Lithium protects tau from hyperphosphorylation and may rescue memory retention in the rats by inhibiting GSK-3 activity.

Animals↗

PubMed1978

Structure of LiCl core particles of 50 S ribosomal subunits from Escherichia coli by electron microscopy.

The structure of 50 S E. coli ribosomal subunits was studied by electron microscopy as these particles were gradually depleted of proteins by incubation with 0.5 to 6.0 m LiCl. Changes observed in the structure of the depleted subunits were correlated with the location of the deleted ribosomal proteins on the control 50 S particle. These changes were particularly striking in the "crown" region, the site of a considerable number of the proteins necessary for the biological activity of the 50 S subunit. Protein L 16, the first to be removed by the LiCl treatment, was found to be essential for the structural integrity of the large subunit through interactions with ribosomal proteins residing in the left-hand side crest and the interface. Based on electron microscopic evidence, a scheme was proposed for the structural changes accompanying the stepwise unfolding of the 50 S E. coli subunit by LiCl.

Bacterial Proteins↗

PubMed1980

tRNA binding stabilizes rat liver 60 S ribosomal subunits during treatment with LiCl.

We have shown recently that, in the absence of mRNA, 1 molecule of nonacylated tRNA binds to the large ribosomal subunit of rat liver with a high affinity constant (Buisson, M., Reboud, A.M., Dubost, S., and Reboud, J. P. (1979) Biochem. Biophys. Res. Commun. 90,634-640). In this paper, free and tRNA-bound 60 S subunits were treated with increasing concentrations of LiCl to obtain information on tRNA binding site. The rationale for using deacylated tRNA was that it is assumed to bind to the peptidyl donor site. We observed that tRNA has a strong protective effect on subunit modifications produced by LiCl: tRNA prevents subunit inactivation as measured by puromycin reaction and polyphenylalanine synthesis and it shifts the Li+/Mg2+ ratio value needed to reach 50% inactivation, from 60 to 250; it also prevents ribosomal protein and 5 S RNA release and large sedimentation changes of subunits, induced by LiCl. To explain the mechanism of 60 S subunit stabilization by tRNA, two hypotheses are considered: stabilization can be consequent on direct interaction of tRNA with specific proteins, or on maintenance on subunits of essential cations which are otherwise displaced by Li+, or both.

Animals↗

PubMed1976

Purification and properties of a protein factor stimulating peptidoglycan synthesis in toluene- and Licl-treated Bacillus megaterium cells.

A protein factor, called PG-I, can be solubilized from toluene-treated Bacillus megaterium cells by LiCl extraction. After LiCl extraction, peptidoglycan synthesis by the toluene-treated cells is decreased. Protein PG-I can be added back to the extracted cells to stimulate peptidoglycan synthesis. This factor has now been purified 124-fold. It has a molecular weight of 42,000 as estimated by Sephadex gel filtration in the presence of 0.4 M KCl and 52,000 as determined by sodium dodecyl sulfate disc gel electrophoresis. Periodate-Schiff staining of the polyacrylamide gel indicates that factor PG-I is a glycoprotein. The reconstitution of LiCl-extracted cells requires Mg2+ with an apparent Km of 1.9 X 10(-3) M. The Mg2+ ions can be replaced by Ca2+ and by Mn2+ ions to some extent; Zn2+ and Cu2+ ions had no effect. The available data suggest that factor PG-I is essential for peptidoglycan synthesis and requires at least one thiol group for stimulatory activity.

Bacillus megaterium↗

PubMed1997

LiCl-induced malformations of the eyes and the rostral CNS in Xenopus laevis.

Ocular malformations such as synophthalmia and cyclopia occur in all vertebrates including humans. We induced fused eye anlagen by exposure of Xenopus laevis embryos to dissolved LiCl. Three basic forms of malformations were observed in the rostral CNS; these represent major steps in a continuous sequence of ocular abnormalities: (i) "hour-glass eyes", (ii) synophthalmia, and (iii) cyclopia vera. The type of abnormity induced seemed to depend on the time and/or the dosage of LiCl exposure. In all cases studied, the histology of the retinae was normal. We reconstructed olfactory organs, eyes, and rostral portions of the CNS from serial sections of 16 Xenopus larvae. Our results confirm that defective bilateralization affects all parts of the rostral CNS and suggest that the telencephalon displays the weakest, and the eyes have the highest, resistance against midline fusion. Defective bilateralization also involves the pineal anlagen, as duplication or enlargement of the pineal organs occurred in most cases with ocular fusion. We conclude that LiCl-induced interferences with ontogenetic bilateralization of prosencephalic structures are the consequence of an elimination of an, as yet, undefined bilateralization signal from (ventral) midline structures of the neural plate and tube.

Abnormalities, Drug-Induced↗

PubMed2000

LiCl disrupts axial development in mouse but does not act through the beta-catenin/Lef-1 pathway.

Chimera and cell marking studies suggest that axial determination in mouse embryos occurs at postimplantation stages. In contrast, Xenopus laevis axes are determined early due to the asymmetric distribution of maternally derived factors in the one-cell zygote. In our earlier study we used lithium chloride (LiCl) to perturb development of mouse axes. Here we investigate whether the lithium induced axial defects in mouse are being mediated by the beta-catenin/Lef-1 pathway as in Xenopus laevis. In lithium treated embryos we did not observe any changes in the amount or localization of beta-catenin protein. Furthermore, the lack of Lef-1 mRNA in treated and untreated embryos indicates the LiCl induced axial defects in the mouse are not mediated by the beta-catenin/Lef-1 pathway.

Animals↗

PubMed1987

Conditioned enhancement of natural killer cell activity, but not interferon, with camphor or saccharin-LiCl conditioned stimulus.

Pavlovian conditioning of the natural killer (NK) cell response has been demonstrated by pairing camphor with polyinosinic:polycytidylic acid (poly I:C) in nine association trials. The NK cell response could be conditioned also by using combined saccharin and lithium chloride (LiCl) as the conditioned stimulus. The camphor and saccharin-LiCl paradigms were tested to determine if the conditioned NK cell activity was the result of conditioning of the interferon response. Interferon levels were measured at 6 hr and NK cell activity at 24 hr after application of the conditioned stimulus. The interferon levels measured in separate experiments were not uniformly elevated in conditioned animals compared with controls.

Animals↗

PubMed1990

Changes in cerebral inositol-1-phosphate concentrations in LiCl-treated rats: regional and strain differences.

LiCl-induced (5 mEq/kg) regional differences in the cerebral phosphoinositide (PI) cycle were studied by measuring inositol-1-phosphate (Ins-1-P), an intermediate in the PI cycle, in male Sprague Dawley and Han/Wistar rats by gas chromatography/mass spectrometry. Control Ins-1-P levels were higher frontally than caudally in both rat strains. LiCl increased Ins-1-P levels 1.8 to 7.4 fold in different regions of brain of Sprague Dawley rats but only 1.2 to 1.8 fold in Han/Wistar rats. This strain difference offers a way to compare the effects of lithium on PI metabolism versus receptor-G protein-phospholipase C coupling mechanisms.

Animals↗

PubMed1982

Disruption of conditioned taste aversion by the combined effects of LiCl and ECS.

Rats were taught a conditioned taste aversion by allowing them to drink sucrose (CS) for 5 min and 30 min later poisoning them with LiCl (UCS). Experimental animals were given ECS (80 mA for 250 msec) at 0, 15, 20, 25, 27.5, 30, 32.5, 35, 40, or 45 min after the CS. Only animals given ECS both within the CS-UCS interval and in close temporal proximity to the UCS (within 5 min) showed a significant, although limited, disruption of learning. At least two explanations are possible. The first is that apart from its toxicity, LiCl may also possess amnesic properties which interact with those of the ECS. Alternatively, ECS may have impaired the ability of the animals to fully experience the lithium-induced illness.

Animals↗

PubMed1992

Defensive burying following injections of cholecystokinin, bombesin, and LiCl in rats.

Past research indicates that feeding is reduced for animals injected with cholecystokinin and bombesin. One explanation for this effect suggests that these peptides act as natural satiety signals; an opposing view asserts that bombesin and cholecystokinin reduce feeding through malaise. The present experiment tested the basic assumptions associated with these positions using the defensive burying procedure. Groups of rats were given sweetened condensed milk followed by IP injections of bombesin (6, 16, and 32 micrograms/kg), cholecystokinin (0.7, 1.4, and 2.9 micrograms/kg), LiCl (6.4 mg/ml), or saline. The results showed that animals injected with cholecystokinin, bombesin, and LiCl developed learned aversions to the milk and actively buried the milk spout with their bedding. The findings provide further support for the view that bombesin and cholecystokinin induce malaise rather than satiety.

Animals↗

PubMed1992

LiCl aversive conditioning has transitory effects on pheromonal responsiveness in male house mice (Mus domesticus).

Appetitive and aversive experiences influence whether odors elicit precopulatory behavior from male rodents. A role for aversive experience in odor-elicited reproductive behaviors had been demonstrated for hamsters and rats, but similar work on house mice had not been performed. Four experiments examined whether lithium chloride (LiCl) aversive conditioning would alter two precopulatory behaviors (ultrasonic vocalizations and olfactory preference) that male house mice normally exhibit to female urine. Lithium chloride was used to aversively condition male house mice to either female urine odor, female urine in drinking water, the female herself, or a novel odor. Independent tests of taste aversion establishment were also conducted. In these experiments, LiCl aversive conditioning produced robust taste aversions to water adulterated with either female urine or a novel odorant/tastant (isoamylacetate), but only transitory decrements in odor-elicited, male-typical precopulatory behaviors. We conclude that aversive conditioning is unlikely to be a significant factor affecting male mouse precopulatory behavior.

Animals↗

PubMed1980

The effects of various barbiturates on LiCl induced taste aversion.

The effects of various barbiturates on LiCl induced taste aversion were examined. Rats were adapted to a 23 hr and 50 min water deprivation schedule. On the Treatment Day, animals were offered a novel 0.125% saccharin solution and then administered 3.0 mEq/kg LiCl. The saccharin solution was presented again on three subsequent Test Days. Fifteen minutes prior to drinking on the first Test Day animals were injected subcutaneously with either 10, 30, and 50 mg/kg Amobarbital, 3, 9, and 15 mg/kg Pentobarbital, 40, 80, and 120 mg/kg Barbital, or 1, 3, and 9 mg/kg Hexobarbital. Results indicate that only 30 mg/kg of Amobarbital and 15 mg/kg of Pentobarbital significantly attenuated the magnitude of taste aversion.

Animals↗