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PubMed2000

The role of CNS glucagon-like peptide-1 (7-36) amide receptors in mediating the visceral illness effects of lithium chloride.

Peripheral administration of large doses of lithium chloride (LiCl) to rats causes a spectrum of effects that are consistent with visceral illness. LiCl reduces food intake, decreases salt ingestion after sodium depletion, induces pica, and produces robust conditioned taste aversions. Because some of the effects of peripheral LiCl are mimicked by centrally administered glucagon-like peptide-1 (7-36) amide (GLP-1), we hypothesized that this peptide is involved in the neural pathways by which LiCl causes visceral illness. To test this hypothesis, we pretreated rats with a selective and potent GLP-1 receptor antagonist given directly into the third ventricle via an indwelling cannula before administration of peripheral LiCl. The GLP-1 receptor antagonist completely blocked the effect of LiCl to reduce food intake, induce pica, and produce a conditioned taste aversion. The same dose of GLP-1 receptor antagonist did not reverse the LiCl-induced reduction in NaCl intake. The data indicate a role for GLP-1 receptors in the CNS pathway that mediates some of the effects of visceral illness.

Angiotensins↗
PubMed1986

Differential Effects of Lithium Chloride on In Vitro Growth of Clavibacter michiganense subsp. nebraskense Depending upon Inoculum Source.

The bacterium Clavibacter michiganense subsp. nebraskense (Corynebacterium michiganense subsp. nebraskense) was grown in broth cultures and inoculated into corn plants. The plating efficiency of cells from broth cultures was essentially the same on nutrient broth-yeast extract and the semiselective medium for this bacterium, CNS. However, when cells were isolated from Goss bacterial wilt- and blight-infected corn, very few were recovered on CNS compared with the amount recovered on nutrient broth-yeast extract agar. When lithium chloride was omitted from the CNS, recoveries from infected corn were nearly the same as on nutrient broth-yeast extract agar. No other ingredient of CNS was inhibitory, nor did substitution of other salts for lithium chloride cause equal inhibition. The amount of inhibition was proportional to lithium chloride concentration. The inhibition by lithium chloride occurred with several strains of the bacterium isolated from one corn cultivar and with one of the strains recovered from three different cultivars of infected corn.

Journal Article↗
PubMed2006

The effect of lithium chloride on morphine-induced tolerance and dependence in isolated guinea pig ileum.

The chronic use of opioids is often accompanied by the development of tolerance and/or dependence upon these agents due to the adaptive changes in the response of the subject to the agent. On cellular level, these phases of altered responsiveness have been shown to be the sequelae of a combination of multiple independent components acting in concert. Changes in the number, affinity, or membrane trafficking of opioids receptors, the coupling of receptors to G-proteins or in associated second messenger systems have been implicated in underlying the aforementioned phenomena. Several observations have been shown that lithium is able to contradict the expected response in animals pre-treated with morphine. These facts clearly manifest the involvement of lithium in at least one of the diverse pathways that lead to morphine dependence and/or tolerance. The aim of the present study was to investigate the effect of lithium on acute morphine-induced tolerance and dependence in an in vitro model of isolated guinea pig ileum which has been extensively used for the assessment of these effects of opioids. Morphine inhibited electrically stimulated twitch of ileum in a concentration-dependent manner (pD(2)=7.27+/-0.16). Tolerance to this effect was induced by the incubation of ileum with 2xIC(50) of morphine for 2 h that induced a degree of tolerance of 14.7. The co-incubation of ileum with morphine along lithium chloride (1 mM) reduced the degree of tolerance significantly (P<0.001) and restored the sensitivity of ileum to the morphine inhibitory effect. Lithium chloride can also reduce the expression of tolerance to morphine significantly (P<0.01). Dependence was induced by incubation with 4xIC(50) of morphine for 2 h and was assessed based on naloxone-induced contractions (10(-5 )M). Lithium chloride (1 mM) can attenuate the development but not the expression of dependence to morphine as shown by the significant decrease in naloxone-induced contractions (P<0.05). These results suggest that lithium chloride can reduce the development and expression of acute tolerance to and development of dependence on morphine in the myenteric plexus of guinea pig ileum.

Animals↗
PubMed1994

Catalase, superoxide dismutase and glutathione peroxidase activity in neutrophils of sham-operated and olfactory-bulbectomised rats following chronic treatment with desipramine and lithium chloride.

In the olfactory-bulbectomised rat model of depression, neutrophil phagocytosis was significantly decreased and phagocytosis started later in comparison to sham-operated animals. Both desipramine and lithium chloride treatment significantly reversed the depressed neutrophil phagocytosis and shortened the time to commencement of phagocytosis in drug-treated bulbectomised rats. The catalase and glutathione peroxidase (GSH-PX) activities in bulbectomised rats were decreased, while superoxide dismutase (SOD) was significantly increased. Chronic desipramine and lithium chloride treatment slightly improved catalase activity in the bulbectomised rats. Desipramine significantly reversed the reduction in activity of GSH-PX, but failed to reverse the increased activity of SOD. In contrast, lithium chloride significantly reversed SOD activity to normal values, without affecting GSH-PX activity in the bulbectomised rats.

Animals↗
PubMed1989

Effect of lithium chloride on the neurotransmitter release from adrenergic nerve terminals of guinea-pig atria.

Lithium chloride at 1 and 10 mM produced a dose-dependent inhibition of the cardiac response to field stimulation of the adrenergic nerve terminals, without affecting myocardial contractility in electrically stimulated guinea-pig atria. This effect was calcium-independent and was also present in preparations superfused with 10 mM myoinositol. Moreover, 10 mM lithium chloride reduced the positive inotropic effect of tyramine. These results indicate that lithium reduces the evoked release of noradrenaline from the adrenergic nerve endings, probably lowering the content of releasable neurotransmitter.

Animals↗
PubMed1993

Influence of cattle age, lithium chloride dose level, and food type in the retention of food aversions.

The influences of animal age and lithium chloride (LiCl) dose levels were evaluated in forming and retaining food aversions to licorice-flavored alfalfa pellets and beet pulp. Lithium chloride (100, 200, 300 mg/kg BW) was given to yearling and mature cattle by gavage (four animals per age-dose treatment group) after meals of the test food. Cattle dosed with the higher levels of LiCl formed aversions more rapidly in both trials than those dosed at lower levels. Both age classes extinguished aversions to licorice-flavored alfalfa pellets, but aversions to beet pulp persisted. Mature cattle retained aversions to beet pulp to a greater extent than did young cattle in social facilitation and single-choice persistence trials. Of dosages studied, the optimum for retaining aversions to beet pulp was 200 mg/kg BW for mature cows. Yearling cattle required 300 mg/kg for complete abstinence.

Aging↗
PubMed1988

Effects and mechanism of action of lithium chloride on gastric acid secretion in rats.

Lithium chloride reduce the measured parameters of gastric secretion (gastric volume, hydrogen ion concentration, and gastric acid output) 2 h after intracerebroventricular, intravenous, or subcutaneous administration in pylorus-ligated rats, in a dose-dependent manner. Intracerebroventricular administration of lithium was approximately five times and 10 times more potent than intravenous and subcutaneous injection, respectively. Time-course study demonstrated that the action of lithium (400 micrograms) on gastric secretion reached a peak at 1 h after intracerebroventricular administration; however, the effects on volume and output were still significant after 8 h. Prior intracerebroventricular injection of indomethacin (400 micrograms) reversed the action of centrally administered lithium on gastric secretion. However, central administration of the opiate receptor blocker naltrexone (100 micrograms), as well as subcutaneous administration of indomethacin (5 mg/kg), failed to modify the effect of lithium on gastric acid secretion. Our data suggest that lithium appears to act centrally to modulate gastric acid secretion in rats through a mechanism involving the synthesis of prostaglandinlike material(s) in the brain. Furthermore, the effect of centrally administered lithium is independent of stimulation of opiate receptor(s) in the brain.

Animals↗
PubMed2000

A low dose of lithium chloride selectively induces Fos protein in the central nucleus of the amygdala of rat brain.

1. Lithium is a very effective treatment for mood disorders. To elucidate the neural substrates of the mood stabilizing actions of lithium, in the present study the authors investigated the effects of a low dose of lithium on regional expression of Fos protein. 2. The administrations of a high dose of lithium chloride (100 mg/kg) induced Fos in widespread areas of the rat brain. In contrast, administration of a low dose of lithium chloride, equivalent to a therapeutic dose in humans, induced Fos only in the central nucleus of the amygdala. 3. These results demonstrate that the central nucleus of the amygdala plays important role in the neural framework that is responsible for the mood-stabilizing effect of lithium.

Amygdala↗
PubMed1992

Synergistic induction of interleukin-6 by tumor necrosis factor and lithium chloride in mice: possible role in the triggering and exacerbation of psoriasis by lithium treatment.

One of the side effects of treatment of manic depressive disease with lithium salts is the triggering or aggravation of psoriasis. In a murine model, subcutaneous (s.c.) injection of a combination of tumor necrosis factor (TNF) and lithium chloride (LiCl) induces a psoriasiform inflammatory reaction. Recent studies suggest that interleukin (IL)-6 and its inducer TNF may play an important role in the pathophysiology of psoriasis. To understand the mechanism involved in the exacerbation of psoriasis by lithium salts, the IL-1, IL-6 and granulocyte-macrophage colony-stimulating factor (GM-CSF) levels in murine skin injected with TNF in combination with LiCl were studied. IL-6 levels in skin extracts of mice treated s.c. with a combination of TNF and LiCl were considerably increased as compared to the levels found in skin extracts from mice treated with TNF or LiCl alone. In contrast, in the same skin extracts IL-1 levels were not changed and GM-CSF was even not detectable. Although less pronounced, increased IL-6 levels could also be found in the sera of mice treated s.c. with TNF and LiCl. Injection with IL-1, interferon-gamma, lipopolysaccharide, or phorbol 12-myristate 13-acetate also induced IL-6 in murine skin. However, these IL-6 levels were not enhanced by co-treatment with LiCl. Likewise, on inflammatory reaction could be seen in mice treated with these agents. These results suggest a role for endogenous TNF and IL-6 in the triggering or aggravation of psoriasis in lithium-treated patients.

Animals↗
PubMed1990

Effect of lithium chloride on spermatogenesis and testicular delta 5-3 beta, 17 beta-hydroxysteroid dehydrogenase activities in the 'antiserum to luteinizing hormone' treated toad (Bufo melanostictus).

Activities of delta 5-3 beta- and 17 beta-hydroxysteroid dehydrogenase (delta 5-3 beta-HSD and 17 beta-HSD), Leydig cell nuclear area (LCNA) and spermatogenesis in the testis were observed after injection of lithium chloride in the 'antiserum to luteinizing hormone (LH)' treated toad. A significant decrease in the activities of steroidogenic enzymes, LCNA and spermatogenesis were noticed after the injections of 'antiserum to LH' to toads. Further decrease in the activities of the above parameters was observed in the lithium chloride--'antiserum to LH' treated toad. It is suggested that lithium chloride may inhibits testicular function without modulating the pituitary activity.

17-Hydroxysteroid Dehydrogenases↗
PubMed2001

Lithium chloride inhibits the expression and secretion of insulin-like growth factor-binding protein-1.

Insulin-like growth factor-binding protein-1 (IGFBP-1) regulates IGF availability for glucose homeostasis. The IGFBP-1 promoter shares common regulatory response elements with phosphoenol pyruvate carboxykinase (PEPCK), the expression and activity of which is inhibited by lithium chloride, associated with an inhibition of glycogen synthase kinase (GSK)-3 activity, in the rat hepatoma cell line H4-II-E. We therefore determined the effect of lithium chloride on IGFBP-1 expression and secretion in H4-II-E cells. Lithium chloride inhibited IGFBP-1 secretion in a dose response and reversible manner by approx 80% during 5-h and 16-h incubations. An inhibitory effect on IGFBP-1 mRNA expression was observed at 2 h. The inhibitory effect of lithium and insulin were not additive when used alone, but inhibition by lithium occurred when insulin action was blocked by activating AMP-activated protein kinase with 5-aminoimidazole-4-carboxamide-riboside (AICAR). These findings suggest that GSK-3 inhibition, or another pathway activated by lithium, may be involved in a pathway controlling IGFBP-1, inhibiting synthesis when insulin activity is absent or impaired.

Animals↗