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Lithium chloride administered to rats in drinking water for 30 days caused an increase of whole brain monoamine oxidase specific activity to approximately 140% of control. Carboxylesterase and formyltetrahydrofolate synthetase activities were not affected by Li+ either in vivo or in vitro.
Lithium was found to be a selective (i.e., it antagonized aggression at doses that did not produce concurrent neuromuscular impairment) antagonist of isolation-induced aggressive behavior in mice following repeated (subacute) administration for five days. Acute (single dose) administration of lithium failed to inhibit aggression. At atiaggressive doses, lithium did not produce ataxia as measured by the inclined-screen or rotarod procedures. The mechanism of this action is discussed in terms of a possible influence on serotonergic mechanisms.
Chronic treatment with lithium chloride produced significant involution of the thymus gland with histological evidence of reduced cellularity due to loss of thymic lymphocytes and a significant reduction in the weight of the gland in normal and adrenalectomized mice. Lithium also increased corticosterone levels in normal mice without changes in adrenal weights. The involution of the thymus gland is most likely due to an effect of lithium on the gland, and it is not mediated by adrenocortical mechanisms or stress.
Lithium chloride was injected subcutaneously to mice (in amounts of 500 and 300 mg/kg) once a day for 10 and 15 days, and to rabbits in single doses via a tube into the stomach (in amounts of 400 and 850 mg/kg). After different time intervals following a single or course-wise administration of the compound the level of total lipids was determined in the muscles and liver of the mice, and of the total lipids, beta-lipoproteins, phospholipids, cholesterol, fatty acids and 11-oxycorticosteroids levels in the blood serum of rabbits and of the bile acids content in the vesical bile of these animals. Hyperlipemia that developed under the effect of lithium was caused by mobilization of fat from fat depots and by deranged interstitial lipids metabolism.
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In the acute experiment six healthy volunteers were given orally two doses of lithium chloride, 16 and 32 mmol, and placebo sodium chloride 32 mmol in a double-blind standardized procedure, with a 1-week interval between treatments. Compared to sodium, lithium produced a decrease in subjective well-being, decrease of skin conductance fluctuations, and increase in plasma calcium concentrations. Dose-related effects were maximal at the first hour after ingestion, decreasing or disappearing at 3--5 h. Most effects did not correlate with plasma or erythrocyte lithium concentrations, but drug effects and feelings of nausea were highly correlated. Accordingly, most acute effects seemed due to peripheral drug effects. In the chronic experiment six healthy volunteers were given orally 16 mmol of lithium chloride or sodium chloride (placebo) twice a day for 1 week in a double-blind standardized procedure with a 2-week interval between treatment weeks. Compared to placebo, lithium produced feelings of subjective impairment, an increase in EEG slow waves and of auditory evoked response variability, a deficit in long-term memory, and an increase in plasma magnesium concentrations. Most lithium effects did not correlate with plasma or erythrocyte lithium concentrations.
The morphological and functional changes in the thyroid tissue of white rats injected lithium chloride at doses 0.5 mekv/kg and 1.0 mekv/kg (groups 1 and 2, respectively) during three weeks were studied by the radiometric, histological and biochemical methods. The radiometric, histological and biochemical methods. The inhibitory action of lithium chloride on hormonogenesis in the thyroid gland and secretion of thyroid hormones into the blood was proved to be directly related to the lithium dose and concentration in the blood. The data of intravital radiometric and morphological analysis of the organs of the 1st group animals suggest some activization of the gland function, with the secretion of the hormones into the blood being suppressed. Increased concentration of the drug inhibits hormonogenesis and secretion of thyroid hormones into the blood.
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.
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.
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.
Lithium chloride microinjections in doses of 100 mkg/mkl into the brain structures of rabbits produce a depressive effect on the subcortical formations. The drug brings down the excitability of the hippocampus, caudate nucleus, mesencephalic reticular formations, thalamus and hypothalamus, raising the excitability of the amygdalae.
Lithium chloride administered acutely or chronically to guinea-pigs had no effect on brain level of acetylcholine or on peripheral release of acetylcholine from longitudinal muscle of the ileum. The results suggest differences between in vitro and in vivo action of lithium.
The effects of intravenous or intrahippocampal injections of lithium chloride dissolved in bidistilled water were investigated on rabbits with chronically implanted canniulas and electrodes. Bioelectric activity of the limbic structures and behavior were analyzed. Electrical activity was recorded by means of bipolar electrodes implanted chronically in the dorsal hippocampus, the gyrus cinguli, the amygdaloid complex and the medial hypothalamus, LiCl inhibited electric activity of the limbic structures and caused a reduction of spontaneous motor and exploratory activity of rabbits.
The exploratory behaviour of 20 goldfish was investigated to see whether it was affected by treatment with lithium chloride. When familiar and novel stimuli were readily discriminable, lithium treatment had no effect on exploration. In a second study, using 20 fish, it was shown that when novel and familiar stimuli were less markedly different from each other, exploratory responses to the novel stimulus were reduced by lithium. The findings may be related to a general suppressant action of lithium on the extent of stimulus generalisation, or to a reduction by lithium of the animals' responsiveness to near-threshold levels of stimulation.
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
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.
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.
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.