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PubMed2000

Food aversion learning induced by lithium chloride in the crayfish Procambarus clarkii.

The ability of the crayfish Procambarus clarkii to develop a food aversion learning was examined. For this purpose, in crayfishes fed with trout, a novel food (chicken) was associated in a single trial with a well-known toxic substance, lithium chloride (LiCl), and food intake was recorded for 10 days afterward using a two-choice protocol. All during the experimental period, a significant effect of treatment was observed that accounted for the lower chicken intake in the LiCl-treated group, compared with the control groups (NaCl-treated group and puncture group). In contrast, LiCl-treated animals had an increased trout intake during the entire period. In addition, it was observed that total food intake was similar among the three groups. These results indicate that the crayfish may develop a food aversion learning when illness is induced by LiCl after the animal accepts and eats a novel food.

Analysis of Variance↗

PubMed2000

Maintenance of retinoic acid receptor alpha pools by granulocyte colony-stimulating factor and lithium chloride in all-trans retinoic acid-treated WEHI-3B leukemia cells: relevance to the synergistic induction of terminal differentiation.

Previous studies have demonstrated that combinations of all-trans retinoic acid (ATRA) with either granulocyte-colony stimulating factor (G-CSF) or lithium chloride (LiCl) produced synergistic terminal differentiation of WEHI-3B myelomonocytic leukemia (D(+)) cells. It was found that steady-state retinoic acid receptor alpha (RARalpha) protein levels were markedly reduced in these cells after exposure to ATRA. Because the presence of receptors for a hormone ligand is required for its action, differentiation therapy with ATRA may be self-limiting. The combination of G-CSF with ATRA significantly attenuated the loss of RARalpha protein, and synergistic terminal differentiation occurred. LiCl was more effective than G-CSF in preserving RARalpha pools and synergized with ATRA more strongly than G-CSF. These findings suggested that the prevention of RARalpha protein loss by G-CSF or LiCl in ATRA-treated cells functioned to extend the differentiation response to the retinoid and was responsible, at least in part, for the observed synergism. D(+) cells transfected with an expression plasmid containing RARalpha cDNA had a 6- to 8-fold increase in steady-state RARalpha mRNA compared with vector-transfected cells and showed a 2- to 3-fold increase in RARalpha protein. ATRA caused a reduction, but not a complete loss, of RARalpha protein in these transfectants, which were considerably more responsive than parental D(+) cells to ATRA as a single agent, supporting the concept that the protection of RARalpha pools results in a heightened differentiation response to ATRA.

Antineoplastic Agents↗

PubMed1983

Lithium chloride and avoidance of novel places.

Rats were exposed to a distinctive chamber (chamber A, part of a two-chamber apparatus), which was novel for half of the rats but familiar for the other half. Each rat was subsequently injected with lithium chloride or saline. In a test trial conducted 24 hr later, all rats were given a choice between chamber A and a second chamber (B), which was novel for all rats. The main result was that the group made familiar with chamber A and then given lithium showed a significant preference for that side or an avoidance of the novel side, a "spatial neophobia." A second experiment confirmed the spatial neophobia effect and demonstrated that it was not dependent on the particular conditioning procedure used in the first experiment. The spatial neophobia effect was related to similar effects in the taste aversion literature, and to the results of research on lithium-induced decreases in exploratory behavior.

Animals↗

PubMed1982

Effects of hepatic denervation on the anorexic response to epinephrine, amphetamine, and lithium chloride: a behavioral identification of glucostatic afferents.

Intraperitoneal injections of epinephrine (20, 40, 80, and 160 microgram/kg) and amphetamine (.1, .2, and .4 mg/kg) were administered to rats with various forms of hepatic denervation. In Experiment 1, destruction of the esophageal trunks of the vagus attenuated epinephrine and amphetamine anorexia, but destruction of the hepatic vagus did not. In Experiment 2, rats with celiac ganglionectomy, subdiaphragmatic vagotomy, or the combined operation all exhibited decreased epinephrine anorexia to the same extent. However, ganglionectomized rats were less responsive to amphetamine anorexia than were vagotomized ones. Vagotomized rats were significantly more reactive to lithium chloride (10, 20, and 30 mg/kg) than were controls. These results suggest that the major component of hepatic metabolic afferent fibers travels from the liver, through the celiac ganglion, and into the esophageal vagal trunks where they ascend to the brain. The anorexic action of amphetamine appears to result from a centrally induced sympathetic action on the liver.

Afferent Pathways↗

PubMed1994

Lithium chloride and inescapable, unsignaled tail shock differentially affect meal patterns of rats.

Several motivational states, such as malaise, fear, and satiety, reduce spontaneous food ingestion by rats, and differentiation of these states is often desirable. The present study used the spontaneous meal pattern to this end. The illness-inducing toxin lithium chloride delayed initiation of the first postinjection meal, and that meal was smaller and eaten more slowly (Experiments 1A and 1B). Rats exposed to tail shock also subsequently took longer to initiate meals, but meals were eaten faster and were slightly larger relative to control conditions (Experiment 2). These changes in meal patterns are different from those produced by satiety-related hormones, such as CCK or insulin, which solely reduce meal size in paradigms designed to assess physiological regulation of food intake. Taken together, these findings attest to the ability of meal patterns to distinguish malaise, fear, and satiety from one another.

Animals↗

PubMed1981

Further studies on the potentiating effect of lithium chloride on methamphetamine-induced stereotypy in mice.

To study the mechanism of the potentiating effect of lithium chloride (LiCl) on methamphetamine (MA)-induced stereotypy in mice, effects of various drugs on the action of LiCl on the stereotypy and pharmacokinetics of MA in different brain regions and liver were examined. The potentiating effect of LiCl disappeared in mice pretreated with atropine or scopolamine whereas LiCl potentiated the stereotypy in mice pretreated with p-chlorophenylalanine, alpha-methyl-p-tyrosine, nialamide, physostigmine or butylscopolamine. The concentrations of MA in the striatum, brainstem and liver were increased and the half-life of MA in these tissues was prolonged by LiCl. The effect of LiCl on the kinetics of MA in the brain, but not that in the liver, was blocked by scopolamine. LiCl prolonged the half-life of MA in the brain and liver in mice treated with physostigmine or butylscopolamine. The inhibition of MA elimination from the brain and its blockade by scopolamine seem to explain the potentiating action of LiCl on the stereotypy and the antagonism by scopolamine of the behavioural action of LiCl, respectively.

Animals↗

PubMed2001

Effects of lithium chloride on induction and expression of methylphenidate sensitization.

Repeated administration of psychomotor stimulants produces an enduring and progressively enhanced behavioral response known as behavioral sensitization, which has been implicated as a model for psychiatric disorders such as mania, schizophrenia, and drug addiction. The objective of the study was to determine whether lithium chloride (LiCl), an anti-manic agent, is effective in blocking the development and/or the expression of behavioral sensitization to methylphenidate. Male Sprague-Dawley rats (n=64) weighing 170-190 g were randomly divided into seven treatment groups. A computerized animal activity monitor system continuously recorded locomotor activity for 16 days. Effects of LiCl on induction of methylphenidate sensitization were studied by giving LiCl before or during six daily methylphenidate administrations. Effects of LiCl on the expression of methylphenidate sensitization were studied by injecting LiCl after sensitization to methylphenidate was induced. It was shown that LiCl treatment modulated the acute methylphenidate effects by transiently attenuating the locomotor response to methylphenidate during the six daily methylphenidate administrations but neither single nor multiple treatments with LiCl blocked the development or the expression of behavioral sensitization.

Animals↗

PubMed2006

Progressive postnatal increases in Fos immunoreactivity in the forebrain and brain stem of rats after viscerosensory stimulation with lithium chloride.

Interoceptive signals have a powerful impact on the motivation and emotional learning of animals during stressful experiences. However, current insights into the organization of interoceptive pathways stem mainly from observation and manipulation of adults, and little is known regarding the functional development of viscerosensory signaling pathways. To address this, we have examined central neural activation patterns in rat pups after treatment with lithium chloride (LiCl), a malaise-inducing agent. Rat pups were injected intraperitoneally with 0.15 M LiCl or 0.15 M NaCl (2% body wt) on postnatal day (P)0, 7, 14, 21, or 28, perfused 60 to 90 min postinjection, and their brains assayed for Fos protein immunolabeling. Compared with saline treatment, LiCl increased Fos only slightly in the area postrema, nucleus of the solitary tract, and lateral parabrachial nucleus on P0. LiCl did not increase Fos above control levels in the central nucleus of the amygdala, bed nucleus of the stria terminalis (BNST), or paraventricular nucleus of the hypothalamus on P0 but did on P7 and later. Maximal Fos responses to LiCl were observed on P14 in all areas except the BNST, in which LiCl-induced Fos activation continued to increase through P28. These results indicate that central LiCl-sensitive interoceptive circuits in rats are not fully functional at birth, and show age-dependent increases in neural Fos responses to viscerosensory stimulation with LiCl.

Animals↗

PubMed1995

The effects of lithium chloride on pattern formation in Tetrahymena thermophila.

Lithium ions have long been known to exert dramatic effects on the specification of cell fates in multicellular systems. We have analyzed the effects of Li+ on intracellular patterning in a complex unicellular organism, the ciliate Tetrahymena thermophila. LiCl does not affect the locations of major structural landmarks in the cortical region of wild-type cells and does not modify the phenotype of pattern-mutant cells. However, in all strains studied LiCl differentially affects early stages of oral development. It initially triggers a slow regression of oral primordia, which is followed by an excessive proliferation of basal bodies that leads to a hypertrophy of the ciliature of the cell's feeding organelle. This hypertrophy mimics the effects of the membranellar-pattern-D mutation, the phenotype of which is enhanced in the presence of LiCl. These effects were partially reversed by myo-inositol; however, neomycin failed to mimic the effects of LiCl. Thus, although lithium ions have major cellular effects on Tetrahymena, they do not influence the specification of the body plan in a manner analogous to that observed in multicellular organisms and may work in part through mechanisms other than the now-classical inositol-phosphate cycle.

Animals↗

PubMed1979

The effects of lithium chloride on response to salient and nonsalient stimuli in Carassius auratus.

The exploratory behaviour of 20 goldfish was investigated to see whether it was affected by treatment with lithium chloride. When familiar and novel stimuli were readily discriminable, lithium treatment had no effect on exploration. In a second study, using 20 fish, it was shown that when novel and familiar stimuli were less markedly different from each other, exploratory responses to the novel stimulus were reduced by lithium. The findings may be related to a general suppressant action of lithium on the extent of stimulus generalisation, or to a reduction by lithium of the animals' responsiveness to near-threshold levels of stimulation.

Animals↗

PubMed2004

Flavor aversion learning induced by lithium chloride in reptiles but not in amphibians.

Flavor aversion learning occurs when digestive illness follows ingestion of a novel food. Such learning has been shown to exist in mammals and birds. In this experiment, we looked for flavor aversion learning in amphibians (Bufo paracnemis, Pachytriton breviceps) and reptiles (Basiliscus vitattus, B. basiliscus, Eumeces schneideri, Mabuya multifasciata). After intake of the novel food, the animals received i.p. injection of either lithium chloride (LiCl), an effective illness inducer, or a saline solution. A week later, the LiCl injection had not affected the food intake of the amphibians whereas in the lizards it had produced a strong aversion to the flavor of the novel food. These results are consistent with the hypothesis that specific mental capacities emerged with reptiles.

Amphibians↗

PubMed2006

Onboard determination of submicromolar nitrate in seawater by anion-exchange chromatography with lithium chloride eluent.

Ion-exchange chromatography using a high-capacity anion exchanger with UV detection was applied to the determination of nitrate in seawater. Major ions in seawater samples did not affect the peak shape and the retention time of the nitrate when an alkaline metal cation-chloride solution was used as an eluent at high concentrations (0.5-2 mol/l). At a wavelength of 220 nm, the peak of bromide was very small because of low absorption, while its separation from the nitrate peak was good at high concentrations. Among the eluents tested, lithium chloride gave the best separation of nitrate from bromide. It was estimated that the lithium ion had the least potential for ion-pair formation with nitrate, and its retention time was prolonged compared with the retention times when using other cations; with bromide and nitrite, such an effect was not observed. The results of shipboard seawater nitrate determination by our method in the South Pacific Ocean and Antarctic Sea showed good agreement with those by the conventional photometric method using continuous flow.

Anions↗

PubMed2004

Lithium chloride reinforces the regeneration-promoting effect of chondroitinase ABC on rubrospinal neurons after spinal cord injury.

After spinal cord injury, enzymatic digestion of chondroitin sulfate proteoglycans promotes axonal regeneration of central nervous system neurons across the lesion scar. We examined whether chondroitinase ABC (ChABC) promotes the axonal regeneration of rubrospinal tract (RST) neurons following injury to the spinal cord. The effect of a GSK-3beta inhibitor, lithium chloride (LiCl), on the regeneration of axotomized RST neurons was also assessed. Adult rats received a unilateral hemisection at the seventh cervical spinal cord segment (C7). Four weeks after different treatments, regeneration of RST axons across the lesion scar was examined by injection of Fluoro-Gold at spinal segment T2, and locomotor recovery was studied by a test of forelimb usage. Injured RST axons did not regenerate spontaneously after spinal cord injury, and intraperitoneal injection of LiCl alone did not promote the regeneration of RST axons. Administration of ChABC at the lesion site enhanced the regeneration of RST axons by 20%. Combined treatment of LiCl together with ChABC significantly increased the regeneration of RST axons to 42%. Animals receiving combined treatment used both forelimbs together more often than animals that received sham or single treatment. Immunoblotting and immunohistochemical analysis revealed that LiCl induced the expression of inactive GSK-3beta as well as the upregulation of Bcl-2 in injured RST neurons. These results indicate that in vivo, LiCl inhibits GSK-3beta and reinforces the regeneration-promoting function of ChABC through a Bcl-2-dependent mechanism. Combined use of LiCl together with ChABC could be a novel treatment for spinal cord injury.

Adjuvants, Immunologic↗

PubMed2004

Comparing immune activation (lipopolysaccharide) and toxin (lithium chloride)-induced gustatory conditioning: lipopolysaccharide produces conditioned taste avoidance but not aversion.

Feeding and drinking typically involve both appetitive and consummatory behaviors. Appetitive behaviors include those behaviors produced by an animal prior to the actual consumption, such as approach movements, whereas consummatory behaviors (such as licking and chewing) are involved in the actual consumption of food. The present research compared the gustatory conditioning effects of bacterial lipopolysaccharide (LPS) and lithium chloride (LiCl) in two different paradigms, conditioned taste avoidance and conditioned taste aversion which differentially affect the appetitive and consummatory components of feeding. Male rats were implanted with intraoral cannulae and habituated to a water deprivation schedule and afterwards received two conditioning days (Days 1 and 4). Each conditioning day consisted of 1 h access to a novel sucrose solution (0.3 M) immediately followed by a systemic injection of LPS (200 microg/kg), LiCl (0.15 M, 3 meq) or NaCl vehicle. Conditioned taste aversion was assessed using the taste reactivity test on Day 7, where orofacial and somatic responses were videotaped and analyzed during 3 brief (1 min) exposures to the sucrose solution. Conditioned taste avoidance was assessed on Days 8 and 9 using a two-bottle preference test (sucrose versus water). Animals conditioned with LiCl displayed typical aversive-like responses in the taste reactivity paradigm evidenced by significant reductions in positive ingestive responses (P<0.05) and an increase in active aversive responses (P<0.05) relative to controls. Furthermore, LiCl treatment resulted in conditioned avoidance of sucrose in the two-bottle preference test characterized by a decreased sucrose preference (P<0.05). Conditioning with LPS produced a reduced sucrose preference (P<0.05) relative to controls, comparable to the avoidance seen in LiCl-treated rats. In contrast, conditioning with LPS resulted in similar positive ingestive responses to intraorally infused sucrose as seen in controls. The present results demonstrate that LPS treatment produces conditioned avoidance but not aversion and suggest that LPS can selectively condition the appetitive aspects of feeding whereas the consummatory behaviors remain unaffected.

Adjuvants, Immunologic↗

PubMed1992

Effective modulation of the haematopoietic toxicity associated with zidovudine exposure to murine and human haematopoietic progenitor stem cells in vitro with lithium chloride.

The drug zidovudine (AZT), a synthetic thymidine analogue, has been used in the treatment of acquired immunodeficiency syndrome (AIDS). Clinical use of zidovudine has induced haematopoietic toxicity manifested by anaemia, neutropenia, frequent thrombocytopenia, and overall bone-marrow suppression. The monovalent cation lithium has been shown to be an effective agent capable of modulating several aspects of haematopoiesis such as the induction of neutrophilia, thrombopoiesis, and protection against suppression of haematopoietic progenitor stem cells following exposure to anticancer drugs and/or radiation in the treatment of malignant disease. We here report the results of studies designed to evaluate the effectiveness of lithium in reversing and/or protecting against either murine or human bone marrow derived haematopoietic progenitors, i.e. (CFU-GM, CFU-Meg, and BFU-E) when co-cultured in the presence of zidovudine in vitro. Lithium chloride (LiCl) reversed zidovudine toxicity to either murine or human derived CFU-GM and CFU-Meg that was optimal at a concentration of 1 mM (P less than 0.05). However, the addition of lithium failed to influence zidovudine toxicity toward either murine or human BFU-E. In summary, these results support the scant clinical studies that have described the presence of neutrophilia and/or thrombopoiesis in zidovudine-treated AIDS patients receiving lithium. In addition, these data further confirm the need for more detailed evaluation of lithium as an adjuvant agent to reduce the haematopoietic toxicity associated with the use of antiviral therapy in HIV-infected patients.

Animals↗

PubMed2006

Taste aversion in rats induced by forced swimming, voluntary running, forced running, and lithium chloride injection treatments.

The present experiment compared the strengths of taste aversion learning in rats induced by forced swimming in a water pool (5, 15, 30, or 60 min), voluntary running in an activity wheel (15, 30, 60, or 120 min), forced running in a motorized wheel (60 min at the speed of 8 m/min), optional running in the apparatus consisting of an activity wheel and a side room (120 min), and a lithium chloride (LiCl, 0.15 M LiCl at 2% of body weight) injection. The rats were given an access to saccharin solution immediately followed by one of the above treatments or simply returned back to the home cages for the control group. On the next 2 days, aversion to the saccharin solution was assessed by two-bottle choice testing between it and tap water. The following results were obtained. (1) The saccharin aversion was a positive function of exercise durations in the forced swimming and voluntary running rats, and the exercise of more than 30 min induced statistically significant saccharin aversion, compared with the control rats. (2) The forced running caused relatively strong saccharin aversion. The group of forced running rats acquired the numerically strongest saccharin aversion on average among all exercised rats. (3) The optional running treatment had little effect. (4) The LiCl injection resulted in the strongest aversion among the all treatments explored here.

Animals↗

PubMed1976

[Effects of lithium chloride administered in combination with methamphetamine or a reserpine- like drug on brain norepinephrine and dopamine metabolism in rats].

Lithium chloride (LiCl) was injected acutely (2.4 mEq/kg, i.p.) or subacutely (2.5 mEq/kg X 2/day for 4.5 days, i.p.) in rats treated concurrently with methamphetamine (MAPT) or a reserpine-like drug (Ro4-1284), and effects of LiCl on behavior as well as metabolism of brain norepinephrine (NE) and dopamine (DA) were investigated. Acute administration of LiCl suppressed the MAPT-induced hyper-locomotor activity but did not affect the Ro4-1284-induced behavioral depression. LiCl administered subacutely increased the MAPT-induced stereotyped behavior, and it reduced the Ro4-1284-induced initial transient excitation in spontaneous locomotor activity and tended to facilitate the recovery from behavioral depression. As for NE and DA metabolism, LiCl administered subacutely inhibited the MAPT-induced decrease of the deaminated NE metabolites and Ro4-1284-induced decrease of DA metabolism and the Ro4-1284-induced alterations in NE metabolism. From these results, it is likely that the inhibitory effect of LiCl on the MAPT and Ro-1284-induced changes in NE and DA metabolism may to some extent be involved in the therapeutic effects on manic-depressive illness.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗

PubMed2004

Differential effects of the selective orexin-1 receptor antagonist SB-334867 and lithium chloride on the behavioural satiety sequence in rats.

Recent studies have shown that acute systemic administration of the selective orexin-1 receptor antagonist SB-334867 significantly reduces food intake in rats. Although this anorectic action of orexin-1 receptor blockade is associated with an acceleration in the transition from eating to resting, it is widely recognised that the behavioural indices of satiety are not dissimilar to those of illness. In this context, Experiment 1 confirmed a significant anorectic effect of 90 (but not 60) mg/kg lithium chloride (LiCl) in male rats presented with palatable mash in the home-cage environment. Experiment 2 employed a continuous monitoring technique to contrast the effects of LiCl (90 mg/kg) and SB-334867 (10 and 30 mg/kg) on food intake and behaviour during a 1-h test with palatable mash. SB-334867 dose-dependently inhibited food intake, with the higher dose producing a comparable degree of appetite suppression (approximately 40%) to that seen with LiCl. Despite equivalent anorectic action, the two compounds produced very different effects on behaviour. LiCl reduced active behaviours (locomotion, rearing, grooming and sniffing), slowed the rate of eating and disrupted the behavioural satiety sequence (BSS). In contrast, SB-334867 (30 mg/kg) decreased the duration of feeding and grooming, and modestly accelerated the transition between eating and resting. Furthermore, whereas LiCl failed to alter posttreatment bodyweight gain, SB-334867 (30 mg/kg) produced a significant weight loss in the 24-h period immediately following injection. Overall, the divergent profiles obtained with equianorectic doses of LiCl and SB-334867 provide convincing evidence for the behavioural selectivity of SB-334867-induced anorexia.

Animals↗