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PubMed1977

[Effect of lithium chloride on the rat hypothalamus neurosecretory system].

Methods of quantitative cytochemical analysis were applied to the study of the reaction of the hypothalamohypophysial neurosecretory system (HHNS) to single and course administrations of lithium chloride (in doses of 200 mg/kg). Reaction of the HHNS proved to depend directly on the amount of lithium administered and was characteriaed by the activation of the synthesis and elemination of the neurosecretion with a single administration on the preparation, or depression of the hormonopoiesis in the hypothalamus and exhaustion of the neurosecretion stores in the neurohypophysis in its course application. During the restoration (7 to 30 days after stopping the drug administration) the state of the HHNS gradually approached the initial level. The authors came to the conclusion that the changes in the central mechanisms of the neuro-endocrine regulation at the hypothalamic level caused by lithium were significant in the pathogenesis of the side-action of its salts

Animals↗
PubMed1996

c-Fos induction in the rat nucleus of the solitary tract by intraoral quinine infusion depends on prior contingent pairing of quinine and lithium chloride.

Intraoral infusions of sucrose or saccharin induce c-Fos-like immunoreactivity (c-FLI) in the intermediate nucleus of the solitary tract (iNTS) of rats after acquisition of a conditioned taste aversion (CTA). The induction of c-FLI in the iNTS may be a consequence of the shift in behavioral response from ingestive to aversive behaviors that characterize acquisition and expression of a CTA. To test this hypothesis, rats were intraorally infused with 0.3 mM quinine sulfate, an aversive taste, 1. prior to conditioning, 2. after 3 noncontingent (unpaired) infusions of quinine and toxic lithium chloride (LiCl) injections, 3. after conditioning with 3 contingent pairings of quinine and LiCl, and 4. after extinction with repeated unpaired infusions of quinine. Intraoral infusions of quinine induced c-FLI in the iNTS only after acquisition of a CTA against quinine; quinine failed to induce c-FLI in the iNTS of unconditioned, noncontingently treated, or extinguished rats. The pattern of c-FLI in the iNTS induced by expression of a CTA against quinine was quantitatively and anatomically similar to that elicited by sucrose in rats expressing a CTA against sucrose. We conclude that aversive responses per se are not sufficient to induce c-FLI in the iNTS. Furthermore, contingent pairing of quinine and LiCl does not cause a shift in behavioral response from palatable, ingestive behaviors to aversive behaviors as in acquisition of a CTA against sucrose. Thus, we also conclude that a shift in behavior from ingestive to aversive responses is not required for increased c-FLI expression in the iNTS during CTA expression. Therefore, the induction of c-FLI in the iNTS during expression of a CTA may be correlated with neuronal processes specific to acquisition and expression of a CTA.

Animals↗
PubMed1981

Lithium chloride and delta-9-THC lead to conditioned aversions in the pigeon.

Conditioned aversive effects of delta 9-tetrahydrocannabinol (THC) and lithium chloride (LiCl) were demonstrated in pigeons. Pigeons injected with 0.15 M LiCl showed a reduction in preference for red water compared to pigeons injected with NaCl (P less than 0.001). Pigeons injected with saline or vehicle showed the same preference for red water while the pigeons injected with 2.0 mg/kg of THC showed a decreased preference (P less than 0.05).

Animals↗
PubMed1995

Systemic administration of lithium chloride and tacrine but not kainic acid augments citrulline content of rat brain.

The effects of tacrine (5 mg/kg i.p.) in lithium chloride (LiCl; 12 mEq/kg i.p.)-pretreated (24 h beforehand) animals and of kainate (10 mg/kg i.p.) on brain citrulline, the co-product of nitric oxide (NO) synthesis, were studied in rats. High performance liquid chromatography analysis of whole brain tissue homogenates from rats treated with LiCl and tacrine revealed a significant increase in citrulline content before the onset of seizures. This effect was prevented in a stereoselective manner by N omega-nitro-L-arginine methyl ester (10 mg/kg i.p., given 20 min before tacrine), an inhibitor of NO synthase. By contrast, kainic acid (10 mg/kg i.p.) did not affect significantly brain citrulline during the pre-convulsive period. In conclusion, our data indicate that in rats seizures induced by LiCl and tacrine but not kainic acid are triggered by excessive NO production in the brain.

Animals↗
PubMedDate not supplied

Effect of lithium chloride on the neurosecretory system of the rat hypothalamus.

The response of the hypothalamic-pituitary neurosecretory system (HPNS) of rats to a single and repeated injection (200 mg/kg each time) of lithium chloride was studied by quantitative cytochemical analysis. The response of the HPNS was found to depend directly on the dose of lithium given and to consist of activation of synthesis and liberation of neurosecretion after a single dose of LiCl or inhibition of hormone formation in the hypothalamus and exhaustion of the reserves of neurosecretion in the neurohypophysis after a course of injections. In the recovery period (7--30 days after stopping the course of injections of LiCl) the previous state of the HPNS was gradually restored.

Animals↗
PubMed2003

The use of lithium chloride to study human milk micelles.

Various methods have been used to study the dissociation of milk micelles in attempts to determine their structure and the interactions that stabilize them. These include the addition of urea, cooling to alter hydrophobic bonding, the addition of EDTA to sequester calcium, and changes in pH to alter molecular charge. For this study, the mild chaotropic agent LiCl was added to human milk micelles, and measurements were made on the relative percentages of the six different phosphorylation levels of beta-casein (CN) at various LiCl concentrations for different lengths of time and at different temperatures. Added LiCl had little effect at 37 degrees C but caused maximal dissociation, mainly of the beta-CN species with higher phosphorylation levels, at 23 degrees C and 4 degrees C between 1 and 2 M concentration. Comparison was made with 2-M additions of NaCl, MgCl2, and KCl at 4 degrees C, with LiCl showing the only appreciable change. The results suggest that Li+ may displace Ca2+ in protein-Ca2+-protein or protein-colloidal calcium phos+ phate-protein salt bridges and that the nonphosphorylated form of human beta-CN may change its conformation and mode of interaction upon phosphorylation. Lithium chloride may be useful to study the dissociation of the different CN in bovine milk micelles.

Calcium↗
PubMed2002

The effects of lithium chloride and other substances on levels of brain N-acetyl-L-aspartic acid in Canavan disease-like rats.

Canavan disease (CD) is a human early-onset leukodystrophy, genetic in nature and resulting from an autosomally inherited recessive trait. CD is characterized by loss of the axon's myelin sheath, while leaving the axons intact, and spongiform degeneration, especially in white matter. It is an osmotic disease that affects both gray and white matter and is caused by the inability of oligodendrocytes to hydrolyze N-acetyl-L-aspartate (NAA) because of a lack of aspartoacylase activity. As a result, there is a build-up of NAA in brain with both cellular and extracellular edema, as well as NAA acidemia and NAA aciduria. Recent studies have indicated that several compounds have the ability to reduce brain levels of NAA in normal mice and rats. In this investigation, these compounds have been tested, using a CD-like rat model of the human disease to evaluate their potential for use in the treatment of the disease. Of seven substances tested in an acute 5-day study, only lithium chloride treatment resulted in a significant reduction of about 13% in whole-brain NAA levels in the CD-like rat model. This is the first pharmacological investigation of the effect of drugs on the level of brain NAA in an animal model of CD, and the first report of a substance that can reduce the brain NAA level in this model.

Animals↗
PubMed2006

Adolescent rats are protected from the conditioned aversive properties of cocaine and lithium chloride.

In humans, most drug use is initiated during adolescence and adolescent users are more likely to become drug-dependent than adult users. Repeated, high levels of use are required for the transition from use to addiction. Individual levels of drug use are thought to result from a balance between the pleasant or rewarding and the unpleasant or aversive properties of the drug. Repeated high levels of drug use are required for the transition from drug use to dependence. We hypothesized that diminished aversive effects of drugs of abuse during adolescence might be one reason for higher rates of use and addiction during this phase. We therefore tested adolescent and adult CD rats in single-dose cocaine conditioned taste aversion (CTA) at a range of doses (10-40 mg/kg), and examined whether various behavioral markers of addiction vulnerability were correlated to outcome in cocaine CTA. We found that adolescents are indeed less susceptible to cocaine CTA. In fact, age was the predominant predictor of CTA outcome, predominating over measures of novelty-seeking, anxiety, and stress hormone levels, which are all known to be related to drug intake in other models. Furthermore, we found that adolescent rats are also less susceptible to conditioned taste aversion to a low dose of a non-addictive substance, lithium chloride. These results suggest that one explanation for elevated drug use and addiction among adolescents is reduced aversive or use-limiting effects of the drugs. This contributes to our understanding of why adolescence is a particularly vulnerable period for development of drug abuse.

Aging↗
PubMed1984

Ingestion of a novel flavor before exposure to pups injected with lithium chloride produces a taste aversion in mother rats (Rattus norvegicus).

In a series of experiments, the ability of a mother rat to learn aversions to novel flavors ingested prior to the illness of her pups was investigated. In Experiment 1, mother rats learned to avoid a novel flavored solution ingested prior to the illness of their nursing litters. Experiment 2 was designed to investigate the extent to which any adult rat is capable of such learning: Nonlactating multiparous female rats learned aversions to novel flavors ingested prior to exposure to pups injected with lithium chloride, whereas nonlactating nulliparous female and male rats did not learn these aversions. Several possible reasons for differences in this learning ability are discussed. In Experiments 3 and 4, the nature of the unconditioned stimulus for these aversions was investigated. Visual, auditory, and taste cues associated with the lithium-injected pups did not mediate the aversions (Experiments 3A-C). The evidence suggests that olfactory characteristics of the lithium-injected pups mediate the flavor aversions in the present experiments (Experiment 3D). Finally, these olfactory cues did not appear to be general stress signals but instead were likely specific cues for gastrointestinal discomfort (Experiment 4). The results of the experiments are discussed in terms of classical conditioning and also of their adaptive significance for both mother and offspring.

Animals↗
PubMed1979

Effects of lithium chloride injections on rank-related fighting, maternal aggression and locust-killing responses in naive and experienced 'TO' strain mice.

Three experiments investigated lithium chloride's (LiCl) effects on three forms of aggression in male 'TO' strain mice. Models of aggression investigated, included attack by preisolated males on male conspecifics (rank-related or intermale fighting), attack by lactating females on male intruders (maternal aggression) and the locust-killing response (a form of predatory aggression?) In the first study, injections of naive male mice with 0.2 and 0.4 mEq of LiCl resulted in marked declines in rank-related fighting. The effects of this treatment on locust killing could not be assessed, as this activity was already at a low incidennce in controls. In a second experiment, LiCl injection had little influence on the locust-killing response in selected, experienced male killer mice. As in Experiment 1, rank-related fighting was suppressed by this treatment. The third experiment revealed that LiCl injections did not influence either maternal aggression or locust killing in naive females and predatory aggression in experienced-killer females. These results provide further support for the contention that these three behaviors have very different physiological bases. The data suggests that one should be cautious when extrapolating between different models of aggression even within the same species.

Aggression↗
PubMed1976

The effect of lithium chloride on one-trial passive avoidance learning in rats.

1 Expression of a one-trial passive avoidance learning response in rats was examined following injections of lithium chloride or sodium chloride before and after initial training and before the first day of testing. Five tests were given at daily intervals, 24 h after training being the time of the first test. 2. Lithium given before the first day of testing impaired response expression on the first and all subsequent days of testing; the rate of extinction was unaffected. 3. Given both before and immediately after initial training, lithium impaired response expression on the first day of testing but slowed down the subsequent rate of extinction, leading eventually to improved performance on the fifth day, as compared with placebo-treated control subjects. 4. The results are interpreted in the light of the hypothesis that lithium impaired the central processing of sensory information.

Animals↗
PubMed1998

Potentiation of astroglial nitric oxide synthase type-2 expression by lithium chloride.

The mechanisms underlying the antimanic effects of lithium are largely unknown but may involve long-term changes in brain gene expression. To determine if lithium could modify gene expression in astrocytes, the predominant cell type in brain, we tested the effects of LiCl on expression of nitric oxide synthase type 2 (NOS-2) in cultured glial cells. Incubation of primary rat astrocytes with endotoxin [lipopolysaccharide (LPS)] and proinflammatory cytokines induced NOS-2 gene and protein expression, as assessed by nitrite production and measurement of L-citrulline synthesis in whole cell lysates. Incubation with LiCl, but not KCl, increased NOS-2 activity up to 1.6-fold. LiCl also potentiated (up to 2.7-fold) the induction of NOS-2 expression by LPS plus interferon-gamma in C6 glioma cells but had little effect on LPS-induced nitrite accumulation from mouse RAW 264.7 macrophages. LiCl increased NOS-2 mRNA steady-state levels, suggesting an effect on mRNA stability and/or NOS-2 gene transcription. These results demonstrate that LiCl can modify astroglial gene expression and suggest that chronic treatment with lithium could exacerbate inflammatory responses in brain glial cells.

Animals↗
PubMed1977

[Effect of lithium chloride on ethanol uptake by rats].

A selective uptake of ethanol by presenting its 5% solution as the only source of fluid was elaborated in rats for 2 months. It was found that lithium chloride injected intravenously in a dose of 35 mg/kg twice per 24 hours for 14 days depressed the ethanol preference causing a motivation inversion whose mechanism was associated with the changes in the activity of the hypothalamic centres of the neuroendocrine regulation. A possibility of lithium salts in the therapy of chronic alcoholism is discussed.

Alcoholism↗
PubMed1988

Lithium chloride stabilizes systolic blood pressure and increases adrenal catecholamines in the spontaneously hypertensive rat.

The effects of daily, intraperitoneal injections of LiCl (3 mEq/kg) on systolic blood pressure (SBP) and adrenal catecholamine levels were measured in spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto rats (WKY). Control animals from each strain were injected with equivalent volumes (0.1 ml/100 g b.wt.) of 0.9% saline (0.15 mEq/kg). SBP in LiCl-treated SHR was significantly lower (p less than 0.05) than that of saline-treated SHR (177 +/- 7 vs. 196 +/- 4 mm Hg, respectively) after one week. After two weeks SBP was lower in LiCl SHR than in saline controls, but this difference was not significant. While SBP of both LiCl and saline treated WKY was not significantly different (146 +/- 4 vs. 147 +/- 8 mm Hg, respectively), SBP in both WKY groups remained lower than the SBP for either group of SHR. LiCl induced a significant weight loss in the SHR, but not in the WKY. Adrenal norepinephrine and epinephrine were significantly (p less than 0.05) higher in LiCl-treated rats of both strains; dopamine was also higher in LiCl-treated rats of both strains, but significant only between SHR-LiCl and SHR controls. It appears that LiCl's effect in slowing the development of hypertension is independent of its action on adrenal catecholamines. The SHR's increased sensitivity to LiCl, relative to weight loss and SBP, may reflect differences in genetic or physiological status of the animal compared to WKY. These differences may be associated with alterations in membrane ion transport systems.

Adrenal Medulla↗
PubMed1981

Unit activity changes elicited in amygdala and neocortex of anaesthetized rats by intraperitoneal injection of lithium chloride.

Intraperitoneal injection of 0.15 M LiCl (2% body weight) to anaesthetized rats elicited, after a 6 min latency, discharge of about 50% units i basolateral amygdala (n = 27). The activation lasted for 15 min on the average. Cortical neurones were not affected by the LiCl injection. It is suggested that the amygdalar reaction to LiCl administration may account for the association of the gustatory trace with the visceral signals of poisoning which mediates acquisition of conditioned taste aversion under anaesthesia.

Amygdala↗