Modification of learned aversion to LiCl and NaCl by multiple experiences with LiCl.
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Adrenalectomy↗
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Structural and functional response of toad urinary bladder to LiCl.
The physiological and morphological response of toad urinary bladder was examined during mucosal exposure of LiCl both with and without vasopressin (VP). With 20 or 100 mU/ml of VP in the serosal bath there was a decrease in Jv between the first and second VP stimulation in LiCl-treated bladders (VP20, -14 +/- 6%; VP100, -16 +/- 5%) that was not different from that observed without LiCl (VP20, -8 +/- 3%, P = NS). However, with 1 mU/ml of VP, a significant decrease in Jv was evident in LiCl-treated (-30 +/- 10%) versus control sacs (+6 +/- 8%; P less than 0.02). At all VP concentrations tested, a significant decrease in SCC and PD was observed between the first stimulation without LiCl and the second stimulation with LiCl. Both osmotic (Pf) and diffusional water permeability (Pd) were increased significantly with 11 mM LiCl only, while neither basal nor VP-stimulated urea permeability (Pu) was affected. Morphological changes paralleled the physiological alterations induced by LiCl. These data demonstrate that LiCl interferes with the osmotic response of the toad bladder to low concentrations of VP, and increases both Pf and Pd while leaving Pu unaffected. These findings coupled with the cell swelling and intracellular vacuolization suggest the presence of a defect in transepithelial water movement somewhere beyond the apical membrane of the granular cell exposed to LiCl.
Animals↗
Effect of LiCl on gastric acid secretion and mucosal barrier function.
Lithium chloride (LiCl) has been shown to decrease gastric acid secretion and protect against ethanol-induced hemorrhagic gastritis in the rat. To further investigate these properties, two sets of experiments were performed in dogs with chronic Heidenhain pouches to study the effect of LiCl on histamine-stimulated gastric acid secretion and bile-induced disruption of the gastric mucosal barrier. In the first experiments the effect of LiCl on intravenous histamine-stimulated gastric secretion (40 micrograms/kg . hr) was determined. LiCl (30 mg/kg . hr) significantly reduced gastric acid secretion when compared to normal saline control (457 +/- 87 mueq H+/10 min versus 637 +/- 112 mueq H+/10 min, P less than 0.05). Serum and gastric lithium levels were determined and a significant inverse linear correlation existed between acid output and serum and gastric lithium levels. In the second set of experiments the effect of LiCl on bile-induced disruption of the gastric mucosal barrier was determined. Heidenhain pouches were continuously perfused with a pH 2 acid test solution and indices of mucosal barrier function (net acid back-diffusion and potential difference) were determined. LiCl (30 mg/kg . hr) significantly reduced both the increase in acid-back diffusion and the fall in potential difference with bile injury (5 mM taurodeoxycholate). In conclusion, these studies indicate that LiCl (1) decreases histamine-stimulated gastric acid secretion, and (2) diminishes bile-induced disruption of the gastric mucosal barrier in the canine Heidenhain pouch.
Animals↗
Comparison of the interoceptive sensory consequences of CCK, LiCl, and satiety in rats.
In three experiments we assessed the degree to which ad lib feeding, injection of cholecystokinin (CCK), and injection of lithium chloride (LiCl) produce states with similar sensory consequences. In each experiment, two groups of rats were trained to use cues arising from food deprivation and satiation as discriminative signals for shock. One group was shocked when deprived but not when nondeprived. The other group received the reversed discrimination. Testing began when incidence of freezing was greater under the shocked deprivation than under the nonshocked deprivation condition. In Experiment 1, the rats were tested under 24-hr food deprivation after injections of CCK, LiCl, and saline (in counterbalanced order). We reasoned that if either CCK or LiCl induce satiety-like states, they should promote patterns of responding different from those produced by saline but similar to those produced by ad lib feeding. The effects of CCK on freezing did not differ from those of saline, whereas both CCK and LiCl had effects that were different from ad lib feeding. This pattern of results was also obtained when deprivation level during training and testing was reduced to 8 hr (Experiment 1A) and also when rats received small amounts of food in conjunction with CCK (Experiment 2). The intubation of a high-calorie stomach load (Experiment 1A) produced a response profile like that observed after free feeding. Freezing after LiCl treatment differed from that observed after free feeding and from that found after injection of CCK. The results indicate that rats can differentiate between the sensory consequences of the states produced by CCK, by LiCl, and by ad lib feeding.
Animals↗
Odor-aversion learning by rats following LiCl exposure: ontogenetic influences.
The influence of LiCl preexposure on odor-aversion conditioning produced by an odor-LiCl pairing was studied in rats 7-31 days old. LiCl preexposure interfered with the acquisition of the odor aversion in both young and old pups. The time course of this effect depended, however, on the age of the pups. It lasted much longer (over 24 hr) if pups 8-17 days old were preexposed to LiCl than if the pups were preexposed when 30 days old (less 12 hr). Alternative interpretations of these data were discussed, and it was suggested that the age-dependent differences in the time course of the LiCl preexposed effect may be determined in part by age-related differences in the rat's excretory processes that clear lithium from the circulatory system.
Aging↗
Structural transitions of calf thymus DNA in concentrated LiCl solutions.
The solubility, sedimentation, circular dichroism, and absorption spectral characteristics of calf thymus DNA have been examined in concentrated solutions of LiCl (6-13 m) at 25 to 27 degree C. At all concentrations of LiCl, the DNA is base stacked and exhibits normal hypochromicty, At the upper end of this range of LiCl concentrations, DNA aggregates and ultimately precipitates completely from solution between 13 and 14 m LiCl. This aggregation process is dependent on concentration, base composition, and molecular weight of DNA. The sedimentation velocity data taken together with the absorbance spectral data suggest that the aggregation process leading to the formaiton of large structures beings at approximately equal to 9 m. Prior to the onset of aggregation, the circular dichroism (CD) spectra can be adequately fitted by a linear combination of contributions of the B, C, and A forms of DNA (Hanlon, S., Brudno, S., Wu, T. T., and Wolf, B. (1975), Biochemistry 14, 1648). Above 9 m LiCl, both factor analysis and a primitive version of matrix rank order analysis indicate that at least one additional spectral component is required to account for the observed CD spectra above 260 nm. The general shape of this additional component or distortion resembles the psi form of DNA.
Animals↗
Stepwise dissociation of yeast 60S ribosomal subunits by LiCl and identification of L25 as a primary 26S rRNA binding protein.
Treatment of yeast 60S ribosomal subunits with 0.5 M LiCl was found to remove all but six of the ribosomal proteins. The proteins remaining associated with the (26S + 5.8S) rRNA complex were identified as L4, L8, L10, L12, L16 and L25. These core proteins were split off sequentially in the order (L16 + L12), L10, (L4 + L8), L25 by further increasing the LiCl concentration. At 1.0 M LiCl only ribosomal protein L25 remains bound to the rRNA. Upon lowering the LiCl concentration the core proteins reassociate with the rRNA in the reverse order of their removal. The susceptibility of the ribosomal proteins to removal by LiCl corresponds quite well with their order of assembly into the 60S subunit in vivo as determined earlier [Kruiswijk et al. (1978) Biochim. Biophys. Acta 517, 378-389]. Binding studies in vitro using partially purified L25 showed that this protein binds specifically to 26S rRNA. Therefore our experiments for the first time directly identify a eukaryotic ribosomal protein capable of binding to high-molecular-mass rRNA. Binding studies in vitro using a blot technique demonstrated that core proteins L8 and L16 as well as protein L21, though not present in any of the core particles, are also capable of binding to 26S rRNA to approximately the same extent as L25. About nine additional 60S proteins appeared to interact with the 26S rRNA, though to a lesser extent.
Carrier Proteins↗
LiCl induces GSK-3β mediated autophagy, DNA damage, and cell cycle arrest in HPV driven cervical cancer cells.
High-risk HPV infections induce cervical cancer progression by disrupting cellular homeostasis and survival pathways, including autophagy. Targeting autophagy represents a promising therapeutic strategy. Lithium chloride (LiCl), extensively studied for its neuroprotective properties, can be investigated for its potential anticancer effects in HPV-driven cervical cancer cells. Treatment with 30 mM LiCl induced significant phosphorylation of glycogen synthase kinase-3β (GSK-3β) at Ser9, inducing functional inhibition and downstream signal alterations. This modulation of GSK-3β activity compromised genomic integrity, validated by increased double strand DNA breaks, increased oxidative and cellular stress, and reduced antioxidant enzyme activity. Consequently, LiCl treated cells exhibited significant G2/M phase arrest, indicating disruption in cell cycle progression. Interestingly, the observed cytotoxicity occurred independently of classical apoptotic pathways, suggesting the activation of alternative cell death mechanisms. Mechanistic studies revealed a robust autophagic flux, with GSK-3β mediated autophagy, validated through siRNA mediated knockdown experiments. These findings highlight a novel cytotoxic mechanism of LiCl and propose its potential repurposing from neurobiology to targeted cancer therapeutics.
Humans↗
Effects of acute swim stress on LiCl-induced conditioned taste aversions.
The present study examined the effects of a 5-min period of swim stress experienced between a flavor (saccharin) and illness (LiCl) on conditioned taste aversion learning. Experiment 1 obtained a stress-induced attenuation of learning. Experiment 2 replicated the findings of Experiment 1, and also obtained a similar attenuation when stress was administered 30 min prior to the saccharin presentation. Experiment 3 examined the effects of swim stress either 15 min or 90 min after the LiCl had been administered. It was found that swim stress 15 min after LiCl significantly attenuated CTA, but swim stress 90 min after LiCl did not. These results are discussed with regard to current views of the relationship between external events and conditioned taste aversions.
Animals↗
Behavioral conditioned responses to contextual and odor stimuli paired with LiCl administration.
The present experiments examined whether behavioral conditioned responses (CRs) develop to LiCl-paired contextual and odor stimuli, and whether these CRs are similar to the behaviors observed following the administration of the drug. During conditioning, a novel context (Experiment 1) or a novel odor (Experiment 2) was paired with LiCl injections, and the CRs which developed to these stimuli were assessed during testing. Suppression of general activity occurred after LiCl exposure and after exposure to the lithium-paired context and odor. However, the actual behaviors which emerged as conditioned responses were distinctly different from those which were elicited by the drug itself. Lying on belly was the predominant unconditioned response to LiCl. Freezing was the predominant CR to the context, whereas gaping was the predominant CR to the odor. These outcomes are discussed and compared to previous results using a taste stimulus.
Animals↗
NaCl and LiCl efficacy in the induction of aversion for quinine and saccharin solutions immediately following injection.
Rats 24-hr water deprived were injected IP with a fixed amount (10 ml/kg) of solution of various concentrations of LiCl and NaCl in dosage ranges which in previous experiments either increased or had no effect on water intake. Intake of 0.01% QHCl decreased with increasing concentrations of both NaCl and LiCl. On a molar basis, LiCl was more effeictive. LiCl also produced an aversion to a palatable solution, 0.1% sodium saccharin; however, NaCl produced no aversion over the dosage range which can be tolerated by the animals.
Animals↗
LiCl-induced selective depression of saccharin drinking in the mouse.
Water-deprived mice were injected with various concentrations of LiCl or NaCl 15 min before they were allowed to drink either water or 0.1% saccharin. The NaCl injections produced a dose-dependent increase in intake of both fluids: however, the higher dosages of LiCl produced a selective depression of fluid intakes. Saccharin intakes were depressed for less than one hr but water intakes were not affected. LiCl injections also depressed general activity and produced an apparent shift of water from blood into cells. The LiCl-induced depression of saccharin was not significantly influenced by extensive previous experience with the drinking fluid.
Animals↗
Effects of anterior basolateral amygdala lesions on taste aversions produced by high and low oral doses of LiCl and lactose in the rat.
Adult male hooded rats (n = 12) with bilateral electrolytic lesions centered on the anterior basolateral amygdala (BLA) were given training using procedures meant to produce two different types of conditioned taste aversions (CTAs) to test whether the disruptive effects of such lesions on this form of learning were dependent upon the dosages of the illness-inducing agents used as unconditioned stimuli (UCSs). The CTAs were produced by either LiCl-induced toxicosis or lactose malabsorption. Comparison with sham-operated control subjects (n = 8) indicated that the disruptive effects of the lesions were inversely related to the dosage level of LiCl but not lactose: whilst the lesions disrupted CTAs produced by a low i.p. dose of LiCl and by a low, but not a high, oral dose of LiCl, they did not alter CTA learning produced by either high or low oral doses of lactose. These results were interpreted as providing further evidence that BLA mediates only certain types of CTA learning.
Administration, Oral↗
Effect of LiCl pretreatment on cholinomimetic-induced seizures and seizure-induced brain edema in rats.
Male Sprague-Dawley rats received LiCl (5 mEq/kg; sc) or saline 24 h prior to injection of cholinomimetics. Physostigmine (PHY, 0.54-0.80 mg/kg), diisopropylfluorophosphate (DFP, 1.3-2.5 mg/kg), pilocarpine (PIL, 23-30 mg/kg), or saline was injected subcutaneously at time 0. Rats were observed for seizure activity for 2 h, survivors were killed 24 h later and edema was measured in samples from parietal and piriform cortices, dorsal thalmus, and hippocampus. None of the rats pretreated with saline had seizures when given doses of cholinomimetics alone. However, rats pretreated with LiCl had the following incidence of seizures: PHY 68%, DFP 71% and PIL 100%. Rats given cholinomimetic agents alone did not have brain edema. In contrast, all LiCl-pretreated rats that seized had pronounced brain edema which was greatest in the piriform cortex. Thus, these studies demonstrate that LiCl pretreatment potentiates cholinomimetic-induced seizures. Further, cholinomimetic-induced seizures produce brain changes resulting in edema.
Animals↗
Role of brain amines in the fetal hyperpyrexia caused by tranylcypromine in LiCl-pretreated rats.
Tranylcypromine (TCP), a monoamine oxidase inhibitor, caused a fatal hyperpyrexia in rats pretreated with LiCl once a day for 4 days. Pretreatment with LiCl alone did not alter the level of serotonin (5-HT), dopamine (DA) and norepinephrine (NE) in the brain. In fatal hyperpyrexia caused by LiCl plus TCP, the brain 5-HT and DA levels were increased, whereas the brain NE level was decreased. Reserpine and alpha-methyl-p-tyrosine completely prevented the hyperpyrexia, but FLA-63 did not show any effect. The hyperpyrexia was completely prevented by p-chlorophenylalanine (PCPA) given 72 hours before TCP but not by PCPA given 24 hours before TCP. Haloperidol and chlorpromazine, DA receptor blockers, inhibited the fatal hyperpyrexia, while cyproheptadine and methysergide, 5-HT receptor blockers, did not. These results suggest that DA plays an essential role in the hyperpyrexia induced by the combination of TCP and LiCl in rats, but the involvement of 5-HT is inconclusive.
Amines↗
Suppression of adult copulatory behaviors following LiCl-induced aversive contingencies in juvenile male rats.
Sexually immature juvenile male rats received an injection of .3 M (20 ml/kg) lithium chloride (LiCl) during each of 8-10 pairings (spaced at 2-3-day intervals) with an estrous female. Approximately seven weeks later, these males displayed fewer copulatory behaviors in pairings with estrous females than saline control rats. Noncontingent .3 M LiCl injections administered to juvenile males did not affect adult copulatory behaviors. Males that were either group or individually housed during the retention interval displayed comparable suppression, which suggests that copulatory suppression does not represent a generalized aversion to social interactions with another animal. Males housed during the retention interval in an environment that contained the odors of estrous females also displayed suppression comparable to that of males housed in the absence of such odors. This suggests that the associations that mediate copulatory suppression are not elicited solely by the odor cues of estrous females. These data demonstrate that LiCl-induced aversive contingencies in juvenile male rats subsequently suppress adult copulatory behaviors.
Animals↗
Learned aversion and rearing movement in rats given LiCl, PbCl2 or NaCl.
The effects of an i.p. injection of 0.15 M LiCl resembled closely the effects of another toxic substance, 0.005 M PbCl2, on conditioned aversion to saccharin and rearing movements in male rats. The findings suggest that nonspecific aversive after-effects of a LiCl injection can account fully for prompt effects of LiCl on rearing behavior.
Animals↗
Morphine antinociception is mediated through a LiCl-sensitive, IP3-restorable pathway.
Pretreatment (18 h) of mice with a single s.c. injection of LiCl (10 mmol/kg) reduced the antinociceptive action of centrally administered (i.c.v.) morphine in the tail-flick test (ED50 = 7.7 micrograms) compared to vehicle-treated controls (ED50 = 1.8 micrograms). The coadministration of inositol-1,4,5-trisphosphate (IP3; 20 micrograms) with morphine restored the morphine-induced antinociception (ED50 = 2.4 micrograms) in LiCl-pretreated mice to control levels. These finding implicate a LiCl-sensitive (possibly phosphoinositide) second messenger pathway in the mediation of morphine-induced analgesia.
Analgesics↗