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PubMed1978

Effect of lithium chloride on electrically stimulated guinea-pig longitudinal muscle-myenteric plexus.

Lithium chloride, in the concentration range of 10(-4)M to 10(-2)M, increases the height of electrically induced contractions of guinea-pig longitudinal muscle-myenteric plexus preparation. Higher concentrations of the salt cause a progressive block of contractions. Sodium chloride shows no augmentation of contraction height, but concentrations above 10(-2)M only cause block of contractions. Inhibition of contractions by LiCl exactly parallels inhibition of responses of the tissue to exogenous acetylcholine (ACh); thus, the site of action is considered to be directly on the muscle. Sodium chloride causes insignificant inhibition of responses to exogenous ACh. Guinea-pigs injected chronically with high doses of LiCl (2 months, 5 mEq/kg show no stimulatory effect on LiCl in vitro, only inhibition. This finding suggests that tolerance to at least some of the actions of LiCl may occur upon chronic administration, particularly if the dose used is very high.

Acetylcholine↗
PubMed1999

Direct effects of lithium chloride on the activities of delta 5-3 beta and 17 beta-hydroxysteroid dehydrogenase in the testis and Bidder's organ of the adult toad (Bufo melanostictus)--in vitro study.

Steroidogenic key enzymes, i.e. delta 5-3 beta and 17 beta-hydroxysteroid dehydrogenase (delta 5-3 beta and 17 beta-HSD) activities, in the testis and Bidder's organ of the toad were inhibited and ascorbic acid synthesis in these organs was decreased by a wide range of lithium concentration in in vitro study. A significant inhibition was noted at a concentration of 2.0 mM, which is easily achieved in the blood during the treatment of manic patients by lithium chloride. This experiment reflected that lithium exerts a direct inhibitory effect on hydroxysteroid dehydrogenase activities in the testis and Bidder's organ--a rudimentary ovary in Bufo.

17-Hydroxysteroid Dehydrogenases↗
PubMed2001

Chronic morphine treatment exaggerates the suppressive effects of sucrose and cocaine, but not lithium chloride, on saccharin intake in Sprague-Dawley rats.

Three experiments examined the effect of chronic morphine treatment on cocaine-, sucrose-, and lithium chloride (LiCl)-induced suppression of saccharin intake in Sprague-Dawley rats. All rats were either water- or food-deprived and then implanted subcutaneously with 1 morphine (75 mg) or vehicle pellet for 5 days. They were then given brief access to 0.15% saccharin and soon thereafter injected with either cocaine (10 mg/kg s.c.), LiCl (0.009 M, 1.33 ml/100 g body weight i.p.), or saline, or, in Experiment 2, given a 2nd access period to either a preferred 1.0 M sucrose solution or the same 0.15% saccharin solution. There was 1 taste-drug or taste-taste pairing per day for a number of days. The results showed that a history of chronic morphine treatment exaggerated the suppressive effects of a rewarding sucrose solution and cocaine but not those of the aversive agent, LiCl. These data provide further support for the reward comparison hypothesis.

Animals↗
PubMed2005

Dose response effects of lithium chloride on conditioned place aversions and locomotor activity in rats.

The present study examined the multi-variable locomotor activity effects of lithium chloride (LiCl) treatment in male rats. Of interest was a determination of which variables might show a dose-response relationship in LiCl-induced conditioned place aversions. Automated open-fields were partitioned into two chambers distinct in tactile and visual cues. A control group [n=8] received saline (NaCl; 0.15 M) paired with both chambers while three LiCl groups (0.15 M; 32 mg/kg [n=7], 95 mg/kg [n=7], 127 mg/kg [n=7]) received LiCl paired with the normally preferred chamber and saline paired with the non-preferred chamber. During extinction trials, rats were allowed to choose between the two chambers to provide an index of conditioned place aversions. Locomotor activity and its distribution within the chambers were also assessed during both conditioning and extinction trials. Dose-dependent decreases occurred in all measures of locomotor activity following LiCl administration during conditioning. During extinction trials, place aversions developed in animals conditioned with LiCl. LiCl-treated rats spent significantly less time in the LiCl-paired chamber relative to controls but not in a dose-dependent manner. Animals that had been conditioned with 95 or 127 but not 32 mg/kg LiCl, displayed significantly more vertical activity in the LiCl-paired chamber than controls during extinction trials. These findings indicate that, in addition to producing dose-dependent unconditioned effects on locomotor activity, LiCl also produces dose-dependent conditioned effects on vertical activity. These conditioned rearing response effects provide a valid measure of the conditioned avoidance response that provides evidence for dose-dependent LiCl-induced conditioned place aversions.

Animals↗
PubMed2005

Chronic lithium chloride administration to unanesthetized rats attenuates brain dopamine D2-like receptor-initiated signaling via arachidonic acid.

We studied the effect of lithium chloride on dopaminergic neurotransmission via D2-like receptors coupled to phospholipase A2 (PLA2). In unanesthetized rats injected i.v. with radiolabeled arachidonic acid (AA, 20:4 n-6), regional PLA2 activation was imaged by measuring regional incorporation coefficients k* of AA (brain radioactivity divided by integrated plasma radioactivity) using quantitative autoradiography, following administration of the D2-like receptor agonist, quinpirole. In rats fed a control diet, quinpirole at 1 mg/kg i.v. increased k* for AA significantly in 17 regions with high densities of D2-like receptors, of 61 regions examined. Increases in k* were found in the prefrontal cortex, frontal cortex, accumbens nucleus, caudate-putamen, substantia nigra, and ventral tegmental area. Quinpirole, 0.25 mg/kg i.v. enhanced k* significantly only in the caudate-putamen. In rats fed LiCl for 6 weeks to produce a therapeutically relevant brain lithium concentration, neither 0.25 mg/kg nor 1 mg/kg quinpirole increased k* significantly in any region. Orofacial movements following quinpirole were modified but not abolished by LiCl feeding. The results suggest that downregulation by lithium of D2-like receptor signaling involving PLA2 and AA may contribute to lithium's therapeutic efficacy in bipolar disorder.

Animals↗
PubMed2000

Lithium chloride inhibits thrombin-induced intracellular calcium mobilization in C6 rat glioma cells.

In this study, the authors have demonstrated the effect of lithium, a typical mood stabilizer, on thrombin-evoked Ca2+ mobilization in C6 cells to elucidate the action mechanisms of the drug. Thrombin-induced Ca2 mobilization was reduced 24 hr after 1 or 10 mM lithium chloride (LiCl) pretreatment. The Ca2+ rise was reduced in a time-dependent manner, and the significant inhibition was observed 9 hr pretreatment with 10 mM LiCl. On the other hand, pretreatment of the cells with 10 mM LiCl for 24 hr did not alter the amount of Galphaq/11 significantly. Pretreatment with 10 mM LiCl for 24 hr failed to reduce the 5-HT-induced Ca2+ mobilization or to affect the desensitization of the 5-HT signal. Finally, thrombin-elicited Ca2+ rise was markedly inhibited in the presence of 0.05 U/ml plasmin, however, the Ca2+ rise was not further attenuated in the presence of plasmin in C6 cells pretreated with LiCl for 24 hr. These results indicate that pretreatment with LiCl attenuated thrombin-evoked intracellular Ca2+ mobilization in plasmin sensitive manner in C6 rat glioma cells. Thus, it is important to investigate the effect of lithium on thrombin-induced cellular responses to clarify the action mechanism of lithium in relation to some abnormality in thrombin-evoked Ca2+ rise observed in bipolar disorders.

Animals↗
PubMed2003

In situ complexation of lithium chloride by amphiprotic cyclophosphazenes.

The amphiprotic cyclophosphazene [CH3O(CH2)3NH]6P3N3 (1) incorporates lithium chloride via successive protonation with HCl and deprotonation with Bu(n)Li (or vice versa) to generate the coordination polymer 1.2LiCl, a molecular model compound for lithium ion containing solid polymer electrolytes.

Journal Article↗
PubMed1986

Lithium chloride as an enhancing agent for metaphase preparations from rodent lymphocytes.

Circulating lymphocytes of many mammals, especially rodents, have proven refractory to PHA stimulation of mitotic activity. Addition of small amounts of lithium chloride to the culture medium removes the refractoriness and increases the yield of metaphase cells 7 fold. This simple procedure makes possible the routine use of circulating lymphocytes in rodent karyology.

Animals↗
PubMed1991

Lithium chloride potentiates tumor necrosis factor-induced and interleukin 1-induced cytokine and cytokine receptor expression.

The antimalignant cell activity of tumor necrosis factor (TNF) in many cell types can be enhanced by lithium chloride (LiCl). This study shows the in vitro effect of LiCl on the TNF-induced or interleukin 1 (IL-1)-induced expression of IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3, IL-2, and the IL-2 receptor-alpha (IL-2R alpha). The levels of IL-6 and GM-CSF in the medium of TNF-treated L929 fibrosarcoma cells were increased by cotreatment with LiCl. In contrast, enhancement of IL-6 production by dibutyryl cyclic AMP or cycloheximide was not affected by LiCl. The production of IL-6 and GM-CSF was not correlated with sensitivity to TNF-mediated cell killing. IL-1 by itself had no measurable effects on L929 cells. However, LiCl potentiated the IL-1-induced synthesis of IL-6, GM-CSF, IL-3, and IL-2 in PC60 murine T-cell hybridoma cells. TNF alone induced only GM-CSF production in these cells, but in the presence of LiCl, increased amounts of GM-CSF as well as small amounts of IL-2 and IL-6 could be detected. It is also shown that in these PC60 cells the expression of the IL-2R alpha was induced by TNF + LiCl treatment but not by TNF alone. IL-2R alpha expression was likewise considerably enhanced by IL-1 + LiCl treatment, as compared with treatment with IL-1 alone. The effects of LiCl on the TNF-induced and the IL-1-induced gene expression seem to be independent of the protein kinase A and C pathways. These results show that LiCl can modulate both TNF-mediated cytotoxicity and TNF-induced and IL-1-induced cytokine expression, suggesting that Li+ acts early in the TNF-signaling pathway, but at a step shared with the IL-1-signaling pathway.

Animals↗
PubMed1986

Suppression of behavior by food pellet-lithium chloride pairings in squirrel monkeys.

Responding by squirrel monkeys was maintained under a 30-response fixed-ratio schedule of food presentation; during different sessions responding produced either sucrose-flavored or banana-flavored food pellets. Pre-session administration of doses of lithium chloride (LiCl) less than 3.0 mEq/kg did not alter rates of responding whereas pairing either type of pellet with post-session injections of 1.8 mEq/kg LiCl suppressed both lever pressing and consumption during subsequent sessions in which that pellet type was available. When post-session injections of LiCl were discontinued, responding recovered within 14 sessions. The suppression of responding, but not pellet consumption, was then reliably reproduced in each monkey by pairing post-session LiCl with the previously non-paired type of pellet. Pre-session administration of chlordiazepoxide (CDAP, 3.0-17.0 mg/kg) increased rates of suppressed responding in a dose-related manner, but did not increase pellet consumption. These data indicate that different mechanisms may be involved in the suppression of responding and the suppression of consumption of food by post-session injections of drugs. The suppression of responding by post-session injections of drugs in primates appears to be qualitatively similar to the suppression of responding by other noxious stimuli such as electric shock in that it is reversible, it can be reinstated by re-exposure to post-session drug injections, and it can be attenuated by pre-session administration of CDAP.

Animals↗
PubMed1998

[The effect of lithium chloride on the rat behavior after short-term oligemic hypoxia].

The experiments were carried out on male Wistar rats. The influence of brain oligemic hypoxia and lithium chloride (LiCl) on some behavioural parameters was investigated. Reduction of brain blood supply was performed by surgical clamping of both carotid arteries for 60 min in general anaesthesia induced by brietal (Methoxitone sodium, 10 mg/kg i.p.). Control animals had their vessels separated, but not clamped (sham operated). 6 days after surgery animals received LiCl (2.5 mEq/kg i.p.). Behavioral experiments were performed 24 h and 7 days after lithium administration. Experimental groups consisted of 12 animals. It was found that oligemic hypoxia reduced inconsiderably spontaneous locomotor and exploratory activity in rats. Similar influence of LiCl was observed. But LiCl administered to animals after oligemic hypoxia prevented them against locomotor and exploratory impairment. In addition, LiCl strongly enhanced amphetamine-induced hyperactivity and diminished haloperidol-induced catalepsy in hypoxic animals. These effects were not observed in sham operated animals. The above results could be connected with antidepressive action of LiCl and the model of moderate oligemic hypoxia used in present work could be a useful model for investigation of new antidepressive compounds.

Amphetamine↗
PubMed1997

Effects of lithium chloride as a potential radioprotective agent on radiation response of DNA synthesis in mouse germinal cells.

Mouse spermatogonial germ cells are highly sensitive to ionizing radiation. Lithium salts are reported to stimulate the postirradiation recovery of hematopoietic marrow cells. We have, therefore, examined whether administered lithium chloride (LiCl) would also be able to protect the mouse germinal cells against radiation injury. Taking DNA synthesis as an endpoint, our results show that the testicular DNA-specific activity in irradiated mice was higher by 61% on average when they had been pretreated with LiCl both 24 h and 1 h prior to gamma-irradiation (2.0 Gy). It was also observed that the DNA synthetic activity in the germinal cells fully recovered after LiCl pretreatment at doses of 40 mg per kg body weight prior to total body irradiation of 0.05-0.25 Gy, whereas at doses of 0.5-6.0 Gy, following the same procedure of LiCl pretreatment, only an incomplete recovery was observed. The dose reduction factor for LiCl is 1.84. The current findings indicate that pretreatment with LiCl provides considerable protection against radiation damage in mouse spermatogonia.

Animals↗
PubMedDate not supplied

[Effect of lithium chloride on kidney function in rats].

Test staged on rats have brought evidence that lithium chloride acts damagingly on all parts of the nephron, inhibiting, first of all, the processes of filtration and then of secretion and reabsorption. Polyuria arising under the effect of lithium is caused by reduced reabsorption of water in the tubules and anuria--by depression of the glomerular filtration.

Animals↗