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Results for “Lithium Chloride”

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PubMed1976

[Effects of lithium chloride on norepinephrine and dopamine metabolism in the rat brain].

Lithium chloride (LiCl) was injected acutely (2.4 mEq/kg and 1.2mEq/kg X 2 for 3 hr, i.p.) or subacutely (2.5 mEq/kg X 2/day for 4.5 days, i.p.) in rats, and behavioral effects, steady state levels of norepinephrine (NE), dopamine (DA) and serotonin (5HT) and the metabolism of intraventricularly administered 14C-NE and 14C-DA in the brain were investigated. Acute and subacute administratin of LiCl suppressed the spontaneous motor activity, but had no effect on the levels of NE, DA and 5HT in the brain. Acute administration of LiCl did not influence the total radioactivity and the levels of NE and its metabolites in NE metabolism, while subacute administration of LiCl increased the deaminated metabolites. In DA metabolism, the deaminated metabolites were decreased by acute administration of LiCl and the O-methylated deaminated metabolites were increased by subacute administration. From these results, it is suggested that LiCl stimulates the monoamine oxidase pathway in NE and DA metabolism and the behavioral sedative effects of LiCl are attributed to the reduced functional activity of brain NE and DA neurons.

Animals↗

PubMed2003

Lithium chloride, administered chronically to rats, does not affect the fractional phosphorylation of brain cytosolic phospholipase A2, while reducing its net protein level.

Lithium, used to treat bipolar disorder, has been reported to decrease rat brain mRNA and protein levels of cytosolic phospholipase A(2) (cPLA(2)), an enzyme that selectively hydrolyzes arachidonic acid from the stereospecifically numbered (sn)-2 position of membrane phospholipids, and to decrease PLA(2) activity. cPLA(2) can be activated by being phosphorylated at its Ser-228, Ser-505, and Ser-727 sites. In this study, we show that the percent phosphorylated cPLA(2) protein in rat brain is unaffected by lithium. Male Fischer-344 rats were fed lithium chloride for 6 weeks, so as to produce a therapeutically equivalent brain lithium concentration; control rats were fed lithium-free chow under parallel conditions. cPLA(2) was immunoprecipitated from brain homogenate and phosphorylated cPLA(2) protein was quantified using an anti-phosphoserine antibody, and compared to net cPLA(2) protein. The mean ratio of phosphorylated/total cPLA(2) was not changed significantly in the lithium-treated compared to the control group. Thus, decreased brain PLA(2) enzyme activity caused by chronic lithium is likely a consequence only of lithium's downregulation of cPLA(2) transcription.

Animals↗

PubMed2004

Rapid toxin-induced gustatory conditioning in rats: separate and combined effects of systemic injection or intraoral infusion of lithium chloride.

The present experiment examined the individual and combined effects of systemic injection and oral ingestion of lithium chloride (LiCl) on both within and across session shifts in palatability. Male rats fitted with intraoral cannulae received two conditioning days in which they were injected with either LiCl or sodium chloride (NaCl) and were then presented with brief intraoral infusions of a sucrose plus LiCl or NaCl solution. The individual taste reactivity responses during the intraoral infusions were videotaped and later analyzed for response frequency. Forty-eight hours after the second conditioning day the same sucrose plus salt solution was presented again in the absence of any injection. The present results demonstrate that systemic injections of LiCl result in profound within session and across session decreases in ingestive responding accompanied by increased active and passive aversive responses. Animals receiving LiCl by injection as well as ingestion demonstrated an exaggerated response. Rats which received LiCl only through intraoral infusions produced the same pattern of decreased ingestive responding to the sucrose plus salt flavored tastant on each test trial suggesting little or no across session conditioning effects. A two process model by which animals may regulate toxicosis is discussed.

Animals↗

PubMed2005

Lrp5-independent activation of Wnt signaling by lithium chloride increases bone formation and bone mass in mice.

One of the well characterized cell biologic actions of lithium is the inhibition of glycogen synthase kinase-3beta and the consequent activation of canonical Wnt signaling. Because deficient Wnt signaling has been implicated in disorders of reduced bone mass, we tested whether lithium could improve bone mass in mice. We gavage-fed lithium chloride to 8-week-old mice from three different strains (Lrp5(-/-), SAMP6, and C57BL/6) and assessed the effect on bone metabolism after 4 weeks of therapy. Lrp5(-/-) mice lack the Wnt coreceptor low-density lipoprotein receptor-related protein 5 and have markedly reduced bone mass. Lithium, which is predicted to act downstream of this receptor, restored bone metabolism and bone mass to near wild-type levels in these mice. SAMP6 mice have accelerated osteoporosis due to inadequate osteoblast renewal. Lithium significantly improved bone mass in these mice and in wild-type C57BL/6 mice. We found that lithium activated canonical Wnt signaling in cultured calvarial osteoblasts from Lrp5(-/-) mice ex vivo and that lithium-treated mice had increased expression of Wnt-responsive genes in their bone marrow cells in vivo. These data lead us to conclude that lithium enhances bone formation and improves bone mass in mice and that it may do so via activation of the canonical Wnt pathway. Lithium has been used safely and effectively for over half a century in the treatment of bipolar illness. Prospective studies in patients receiving lithium should determine whether it also improves bone mass in humans.

Analysis of Variance↗

PubMed1991

Chronic treatment of guinea pigs with lithium chloride: effects on myenteric plexus preparations and on cyclic AMP levels.

We studied the effects of lithium chloride, given i.p. in doses of 0.05, 1, 2, 4 and 8 mEq/kg twice daily for 14 days, on preparations of guinea pig myenteric plexus. The effects of lithium added to isolated myenteric plexus preparations derived from chronically treated animals showed that relatively low lithium concentrations produced a statistically significant decrease in the force of contraction, this effect being concentration-dependent. 3-Isobutyl-1-methylxanthine (IBMX) induced a statistically significant inhibition, between 30 and 50%, of the lithium effects. cAMP levels in animals treated chronically with lithium were studied, using an isotopic displacement technique. Our results show that only the highest dose of lithium (8 mEq/kg per day) significantly decreased basal levels of cAMP. In the presence of IBMX, low doses of lithium (1 mEq/kg per day) induced a very significant decrease in cAMP levels, but the inhibition remained constant, approximately 30-35%, at doses from 2 mEq/kg per day. In guinea pig myenteric plexus preparations from acutely treated animals, our results show a direct relationship between lithium concentration and inhibition of the cAMP accumulation induced by IBMX.

Animals↗

PubMed1990

Discriminative properties of morphine that modulate associations between tastes and lithium chloride.

Wistar rats learned to withhold consumption of a target solution when morphine preceded presentation of the target solution and lithium chloride (LiCl) and to consume the same target solution when saline preceded the presentation of the solution. After this serial feature discrimination training, morphine did not block the formation of a Pavlovian association between saccharin and LiCl but did suppress consumption of familiar tap water. After Pavlovian conditioning, morphine blocked the formation of an association between saccharin and LiCl but did not suppress consumption of a familiar tap water solution. The roles of morphine and saline can be interchanged. It appears that the morphine discriminative stimulus is calling up a representation of neither the conditioned stimulus nor the unconditional stimulus alone, but rather a modified representation of some aspect of their association.

Animals↗

PubMed1995

The chemotherapeutic efficacy of diminazene aceturate and lithium chloride against relapse infection of Trypanosoma brucei brucei in rats.

The chemotherapeutic efficacy of diminazene aceturate (Berenil) and lithium chloride (LiCl) in relapse infection of trypanosomiasis was investigated in rats experimentally infected with Trypanosoma brucei brucei. The study showed that the combination of diminazene aceturate at (7 mg/kg) and LiCl (10 micrograms/kg) appeared more effective therapeutically than diminazene aceturate, or diminazene aceturate and LiCl and dexamethasone group, as more of the rats in the diminazene aceturate and LiCl treated-group remained aparasitaemic for longer days (60 days). Relapse parasitaemia occurred on days 10 and 12 in diminazene aceturate (7 mg/kg); diminazene aceturate (7 mg/kg) and LiCl (10 micrograms/kg) plus dexamethasone (1 mg/kg) treated group respectively, while relapse parasitaemia did not occur in the diminazene aceturate and LiCl treated group until day 20. Histopathological examination of the brain did not show any signs of inflammatory reaction in the diminazene aceturate and LiCl and dexamethasone treated group. However lesions associated with meningoencephalitis, such as cellular infiltration of mononuclear cells, perivascular cuffings and perivascular congestion and oedema were observed in the diminazene aceturate; diminazene aceturate and LiCl treated groups.

Animals↗

PubMed1978

Electrophysiological changes induced by paradoxical sleep deprivation and lithium chloride poisoning in rats.

In an attempt to analyze the disruption of conditioned taste aversion (CTA) caused by pre-acquisition paradoxical sleep deprivation (PSD), the effect of poisoning (0.15 M LiCl, 4% body weight) on the sleep--wakefulness pattern was studied in 12 rats with chronically implanted electrodes. The polygraphic recording showed that poisoning reduced the total sleep time in the subsequent 3 h from 57 to 42% and REM sleep from 6 to 2%. The lithium chloride effect was still more pronounced after 24-h REM sleep deprivation: the total sleep time decreased from 67 to 46% and REM sleep from 13 to 2%. The change of sleep--wakefulness pattern, most pronounced during the first hour of poisoning, gradually returned to normal but REM sleep was significantly reduced even 3 h after poisoning. It is concluded that 24-h PSD does not alleviate the subsequent poisoning. On the other hand, the lithium chloride induced reduction of post-acquisition REM sleep many enhance the learning impairment caused by pre-acquisition PSD.

Activity Cycles↗

PubMed1994

Chronic administration of lithium chloride increases immunodetectable glial fibrillary acidic protein in the rat hippocampus.

We studied the effect of treating rats with lithium salts on the content and in vitro phosphorylation rate of the astrocyte cell marker, glial fibrillary acidic protein (GFAP), in brain slices. Rats were fed a diet incorporating lithium chloride until the concentration of Li+ in serum reached 0.6-1.2 mM, a range similar to that achieved in clinical practice. Hippocampal tissue was analyzed for immunoreactive GFAP by a dot assay, and slices of hippocampus and caudate nucleus were labeled with [32P]phosphate to determine the in vitro rate of phosphorylation of GFAP. Compared with controls, the level of immunoreactive GFAP in the hippocampus from lithium-treated rats was increased 34%, and GFAP in hippocampal slices incorporated 39% more 32P. This effect of lithium was apparently not confined to the hippocampus because the in vitro rate of phosphorylation of GFAP in caudate slices was also increased in the treated rats.

Animals↗

PubMed2001

Pharmacokinetics and toxic effects of lithium chloride after intravenous adminstration in conscious horses.

OBJECTIVE: To determine the pharmacokinetics and toxic effects associated with IV administration of lithium chloride (LiCl) to conscious healthy horses. ANIMALS: 6 healthy Standardbred horses. PROCEDURE: Twenty 3-mmol boluses of LiCl (0.15 mmol/L) were injected IV at 3-minute intervals (total dose, 60 mmol) during a 1-hour period. Blood samples for measurement of serum lithium concentrations were collected before injection and up to 24 hours after injection. Behavioral and systemic toxic effects of LiCl were also assessed. RESULTS: Lithium elimination could best be described by a 3-compartment model for 5 of the 6 horses. Mean peak serum concentration was 0.561 mmol/L (range, 0.529 to 0.613 mmol/L), with actual measured mean serum value of 0.575 mmol/L (range, 0.52 to 0.67 mmol/L) at 2.5 minutes after administration of the last bolus. Half-life was 43.5 hours (range, 32 to 84 hours), and after 24 hours, mean serum lithium concentration was 0.13+/-0.05 mmol/L (range, 0.07 to 0.21 mmol/L). The 60-mmol dose of LiCl did not produce significant differences in any measured hematologic or biochemical variables, gastrointestinal motility, or ECG variables evaluated during the study period. CONCLUSIONS AND CLINICAL RELEVANCE: Distribution of lithium best fit a 3-compartment model, and clearance of the electrolyte was slow. Healthy horses remained unaffected by LiCl at doses that exceeded those required for determination of cardiac output. Peak serum concentrations were less than steady-state serum concentrations that reportedly cause toxic effects in other species.

Animals↗

PubMed1997

In vitro effects of lithium chloride on TNF alpha and IL-6 production by monocytes from breast cancer patients.

It is well known that lithium chloride (LiCl) is able to trigger human monocytes to release tumor necrosis factor alpha (TNF alpha). In this study we have evaluated the in vitro effect of LiCl on TNF alpha and interleukin-6 (IL-6) release by monocytes from patients affected by non-metastatic (BCa/M0) and metastatic breast cancer (BCa/M1), preincubated with autologous serum (sPt). Our data demonstrate that monocytes from cancer patients (BCa) treated with LiCl released lower amounts of TNF alpha compared to those from healthy donors (HD). Preincubation in autologous serum (sPt) impaired TNF alpha production by monocytes from BCa with LiCl. On the contrary, our data indicate that IL-6 production by monocytes treated was not impaired. Moreover, the results obtained from the same cells, preincubated in sPt and treated with LiCl, indicate that serum factors may synergize with LiCl treatment in releasing IL-6.

Aged↗

PubMed1992

Effects of i.c.v. lithium chloride administration on monoamine concentration in rat mediobasal hypothalamus.

We investigated the acute effects of a single i.c.v. injection of lithium chloride (LiCl) the neuroamine content of the rat mediobasal hypothalamus (MBH). The effects of lithium on amine synthesis and degradation enzymes were also studied in vitro. Noradrenaline (NA), dopamine (DA), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were reduced 10 min after i.c.v. injection of 24 nmol of LiCl and returned to control values 30 min after the injection. Two nmol of LiCl reduced the concentration of DA (10 and 30 min after injection) and 5-HIAA (30 min after injection). LiCl (0.5-10 mM) inhibited tyrosine hydroxylase activity (catecholamine synthesis) in vitro in a concentration dependent manner. The i.c.v. administration of a high dose of LiCl reduced the content of neuroamines in the MBH. This might result from and inhibition of synthesis. A possible link between the observed changes and some reported side effects of lithium therapy is discussed.

Animals↗

PubMedDate not supplied

[Effect of lithium hydroxybutyrate and lithium chloride on heart rhythm disorders of various origins].

It has been shown in experiments on anesthetized cats and dogs that lithium hydroxybutyrate produces antiarrhythmic action in central aconitic and strophanthine arrhythmias, prevents the development of ventricular fibrillation, and shows antiarrhythmic activity in strong occlusion on the coronary artery. The drug does not remove the atrial and aconitic patterns of arrhythmia. Lithium chloride also exhibits antiarrhythmic action in central aconitic arrhythmia, being inferior to lithium hydroxybutyrate. The drug does not influence central strophanthine arrhythmia and does not show antifibrillation activity.

Animals↗

PubMed1993

Novel diet consumption and body weight gain are reduced in rats chronically infused with lithium chloride: mediation by the chemosensitive area postrema.

The effects of chronic lithium chloride infusions on consumption of, and subsequent preferences for, a novel diet were examined in rats with ablations of the area postrema (AP) and sham-lesioned control rats. Osmotic minipumps (Alza), filled with a saturated aqueous solution of LiCl (63 g/100 ml), were implanted in the peritoneal cavity of half of the lesioned rats (n = 9) and half of the control rats (n = 8). The remaining rats received empty pumps (n = 9 and n = 7 for lesioned and controls, respectively). The LiCl or sham drug phase was paired with free access to a highly palatable novel diet (AIN diet) during a 7-day conditioning period. Subsequent preferences for the novel diet relative to a familiar diet (ground Purina lab pellets) were determined using a two-food choice procedure. The only group to show a persistent and significant reduction in novel food consumption during the conditioning phase was the sham-lesioned group infused with LiCl (p < 0.01). This group also exhibited a marked aversion for the novel diet, indicative of a conditioned food aversion (CFA), during the preference tests. No significant differences in novel diet consumption or in novel diet preference were found between the two AP-lesioned groups. This study provides evidence that anorexia and CFAs to a novel diet, induced with chronic infusions of lithium, are abolished by destruction of the chemosensitive area postrema.

Animals↗

PubMed1993

Systemic administration of lithium chloride and tacrine increases nitric oxide synthase activity in the hippocampus of rats.

We planned to ascertain whether the administration of the anticholinesterase, tacrine (5 mg/kg i.p.), to rats pretreated 24 h before with lithium chloride (LiCl; 12 mEq/kg i.p.) produced any change in nitric oxide (NO) synthase activity in the hippocampus. A significant increase in hippocampal Ca(2+)-calmodulin-dependent NO synthase activity occurred 15 min after tacrine injection and was blocked by atropine (5 mg/kg i.p. given 15 min before tacrine) and by N omega-nitro-L-arginine methyl ester (300 micrograms given into one lateral cerebral ventricle 10 min before tacrine), a NO synthase inhibitor. A consistent cyclic guanosine 3',5'-monophosphate (cGMP) accumulation was also seen. In conclusion, the present results show that tacrine given to LiCl-pretreated rats produces a significant increase in NO synthase activity in the hippocampus and this may be responsible, at least in part, for seizures and related brain damage elicited by these drugs.

Amino Acid Oxidoreductases↗

PubMedDate not supplied

[Effect of lithium chloride on several indices of cardiac function].

Used in a dose of 100 mg/kg lithium chloride modifies the ECG patterns in rats, rabbits and cats. It increases the voltage of P and R waves, the S-T interval and slows down the rhythm of cardiac contractions. In doses of 50-300 mg/kg the compound raises the coronary circulation rate in narcotized cats. The compound exerts an antiarrhythmic action in chlorocalcium arrhythmia in rats, in strophanthin-induced one in cats and frogs and the intensity of this action is not inferior to that produced by potassium chloride, quinidine, novacainamide, izoptin and even exceeds it.

Animals↗

PubMed2002

Taste aversion after ingestion of lithium chloride: an associative analysis.

In five experiments with rats we examined the aversion established by consumption of a solution of lithium chloride (LiCl). Experiment 1 showed that consumption of LiCl established an aversion to saline (NaCl). Experiment 2 showed that the size of the aversion was reduced in rats given pre-exposure to saline (a latent inhibition effect). Experiment 3 showed that experience of a sucrose-saline compound prior to consumption of LiCl generated an aversion to sucrose (a sensory preconditioning effect). Experiments 4 and 5 examined the effects produced by consumption of a sucrose-LiCl compound and demonstrated reciprocal overshadowing between the two tastes. These results confirm that consumption of LiCl establishes an aversion to the taste of this substance. Their implications for the use of orally consumed LiCl as a technique for the control of predatory behaviour are discussed.

Animals↗

PubMed1983

Effect of pairings of pentobarbital with lithium chloride on the capacity of pentobarbital to maintain a conditioned aversion.

Rats with conditioned aversions to NaCl water were exposed to either an injection of pentobarbital (Pent) followed 30 min later by an injection of lithium chloride (LiCl) on four separate occasions or to injections of LiCl alone, Pent alone, or LiCl followed by Pent. These injections were followed by pairings of NaCl consumption with injections of Pent. The Pent leads to LiCl pairings eliminated the capacity of Pent to maintain the animals' conditioned aversion to NaCl water relative to the other groups. These findings are consistent with the idea that Pent leads to LiCl pairings cause the Pent state to elicit a compensatory response. This compensatory response seems to eliminate the properties of Pent which normally produce or maintain flavor aversions.

Animals↗