Dose Of LiCl Research Articles

Intraperitoneally injected cholecystokinin-octapeptide activates pica in rats

Cholecystokinin-octapeptide (CCK-8) was injected intraperitoneally into rats to see if it could cause them to eat kaolin (clay)—a pica behavior which has been shown to indicate gastric distress. In the first study, a single large dose of CCK-8 (20 μg/kg) failed to produce pica. In the second study, 4 smaller doses of CCK-8 (8 μg/kg), 30 min apart, produced significant ingestion of kaolin compared to the baseline condition of vehicle injections. The pica was comparable to that observed in another group of rats given a toxic dose of LiCl (127 mg/kg, IP). It is concluded that interperitoneal injections of CCK-8 can induce a state of gastric distress in the rat.

Ability of lambs to learn with a delay between food ingestion and consequences given meals containing novel and familiar foods

We studied: (1) whether lambs could learn to avoid a novel food given delays of up to 8 h between food ingestion and gastrointestinal illness (long-delay study); (2) how gastrointestinal illness affected the selection of several foods differing in familiarity to lambs (mixed-meal study). Gastrointestinal illness was induced by administering encapsulated lithium chloride (LiCl; 160 mg kg −1 body weight) to lambs using a balling gun. In the long-delay study, lambs were offered a novel food for 5 min. If they consumed 10 g or more of the food, LiCl was administered 0,2,4,6, or 8 h later. Intake of the novel food was measured in 5 min trials for the next 3 days. When the delay between food ingestion and the administration of LiCl was 2 or 4 h, the lambs reduced their intake of the novel food after a single dose of LiCl. The lambs also reduced their intake of the novel food when the delay between food ingestion and the administration of LiCl was 6 or 8 h. However, LiCl was administered twice before the lambs reduced their intake of the novel food; they were also given a stronger dose (320 mg kg −1 body weight) of LiCl on Day 2 than on Day 1. Thus, repeated exposures, greater gastrointestinal distress, or both may be required before lambs reduce their intake of a novel food given delays of 6 h or more. For the mixed-meal study, we used five foods; lambs had eaten two of the foods since weaning, two of the foods for 25 days prior to the onset of the trials, and one food was novel. When lambs were offered the novel food for 5 min followed by the four familiar foods for 20 min, and then given LiCl, they refused to eat the novel food for the next 3 days. Some of the lambs also reduced their intake of the foods they had eaten for 25 days. The lambs did not decrease their intake of the foods they had eaten since weaning.

Lithium-induced decrease of brain inositol and increase of brain inositol-1-phosphate is transient.

The effects of a single dose of LiCl (2.5 or 10 mEq/kg) on brain inositol and inositol-1-phosphate (Ins1P), intermediates of brain phosphoinositide (PI) turnover, were determined in male Han: Wistar rats. There was a remarkable, 36-58 fold elevation of brain Li+ as the single dose of LiCl was increased 4-fold. Moreover, the accumulation of brain lithium was slow during repeated administration of LiCl. Brain lithium did not correlate with changes in brain PI turnover either after a single or repeated doses. Thus, after a single dose of LiCl the increases in brain Ins1P were much less than the decreases in brain inositol. Also, brain inositol was significantly decreased only with the high dose of LiCl whereas brain Ins1P accumulation was more prominent with the lower dose. Moreover, repeated daily doses of LiCl only transiently increased brain Ins1P at 1 and 7 d whereas inositol remained at control levels throughout the 14 d observation period. Lithium probably caused the transient decrease in brain inositol by inhibiting several enzymes, in addition to the inhibition of myo-inositol mono-phosphates, in the PI cycle. Moreover, a slow dampening down of PI turnover by lithium, possible via an inhibitory action on G-protein-coupling, may also explain the present findings.

Cerebral lithium, inositol and inositol monophosphates.

Cerebral regional inositol, inositol-1-phosphate (Ins1P), and inositol-4-phosphate (Ins4P), intermediates in phosphoinositide (PI) cycle, and brain lithium levels were studied in male Han:Wistar rats 24 hr after an intraperitoneal injection of a single dose (2.5-18 mEq./kg) of LiCl. A dose of LiCl higher than 5 mEq/kg caused a remarkable accumulation of Li+ in the brain. Basal brain regional inositol levels (17-22 mmol/kg) were reduced by 6-8 mmol/kg dry brain tissue at doses exceeding 5 mEq/kg of LiCl in all brain regions except the piriform cortex. However, higher doses of LiCl did not cause any further decrease in brain inositol. LiCl increased basal brain regional Ins1P levels (170-240 mumol/kg) by 0.8 mmol/kg dry brain tissue at most, and there were no consistent additional increases of Ins1P at LiCl doses exceeding 5 mEq./kg. Moreover, lithium slightly decreased regional cerebral concentrations of Ins4P. Thus, lithium-induced accumulation of Ins1P or changes of Ins4P levels do not explain lithium-induced decrease in cerebral inositol. Effects of lithium on brain P1 turnover are likely to be multifocal and to differ markedly at different concentrations of Li+ in the brain.

Conditioned taste aversions: how sick must a ruminant get before it learns about toxicity in foods?

Relatively little attention has been paid to the behavioural mechanisms that large herbivores may use to avoid being poisoned by toxins in plants. To determine if the food-avoidance learning abilities of large herbivores are as poorly developed as has previously been assumed, we investigated the relationship between the acquisition of a conditioned taste aversion (CTA) by sheep and the dose of gastrointestinal poison (LiCl) administered with a particular food. We also investigated feeding neophobia as a function of the LiCl dose associated with the previous novel food encountered. We found that the degree of CTA varied closely with the LiCl dose administered. A strong CTA was induced with 150 mg LiCl kg −1 body mass, which is similar to the dose required for a strong CTA in rats. We also found that feeding neophobia among sheep increased as a function of the LiCl dose associated with the last novel food encountered. When sheep and goats were offered food containing 2% LiCl, their daily intake after the third day fluctuated about a level that resulted in a LiCl dose of 39 mg kg −1 for sheep and 27 mg kg −1 for goats. These dosages are not much higher than that which causes mild discomfort in humans. We conclude that the food-avoidance learning abilities of ruminants are better developed than was previously assumed, and that CTA behaviour could be an important means by which large herbivores reduce the risk of being poisoned while foraging.

Influence of repeated administration of lithium on urinary excretion of prostaglandins in rats.

The present study was undertaken to examine whether urinary excretions of prostaglandins increase by repeated administration of a non-toxic dose of lithium. Our previous study demonstrated that 2 mEq/kg/day of lithium chloride (LiCl) is not a toxic dose; and therefore, this dose of LiCl in 1 ml vehicle (5% glucose solution) or 1 ml of vehicle alone was injected intraperitoneally for 7 days into Wistar rats. On day 7, 3% body weight of 1% NaCl solution was given orally; and urine for the determination of PGE2 and 6-keto-PGF1 alpha, a metabolite of PGI2, was collected for 6 hr after dosage. Thereafter, blood samples for measuring plasma renin activity (PRA) were obtained. The urinary amounts of PGE2 and 6-keto-PGF1 alpha in the Li-treated rats were significantly greater than those in the control animals. The values of PRA did not significantly differ between the two groups of rats. These findings indicate that the production of prostaglandins, including those of PGE2 and PGI2, are enhanced during repeated administration of a non-toxic dose of lithium. The enhanced production of prostaglandins might not be mediated through the activated renin-angiotensin system.

Food aversion learning in sheep: persistence of conditioned taste aversions to palatable shrubs (Cercocarpus montanus and Amelanchier alnifolia)

We studied the persistence of conditioned taste aversions in sheep and whether or not sheep averted to one shrub species would avoid another shrub species. Three-month-old lambs were averted to the shrub Cercocarpus montanus by pairing its ingestion with lithium chloride (LiCl), a nonlethal gastrointestinal poison. When lambs were yearlings, they were offered C. montanus plants growing in 8-liter pots. During the persistence trial, averted sheep took fewer (P less than .05) bites of C. montanus than controls did (19 vs 64 bites/sheep, respectively). Following the persistence trial, sheep that had been previously averted to C. montanus and consumed C. montanus received LiCl. Complete aversion to C. montanus was re-established in previously averted sheep with a single dose of LiCl. When sheep previously averted to C. montanus were offered potted Amelanchier alnifolia shrubs, averted sheep consumed 21 bites of A. alnifolia but controls consumed 58 bites (P less than .05). This result suggests that previously averted sheep were either more food neophobic than controls or generalized their aversion from C. montanus to A. alnifolia. As with C. montanus, a single dose of LiCl completely averted sheep to A. alnifolia. When sheep grazed a pasture containing C. montanus and A. alnifolia averted sheep took fewer (P less than .05) bites of the two shrubs than controls did (.2% vs 18%). Sheep showed no signs of extinguishing the aversion to either shrub during the grazing season (May-Sept.). Aversive conditioning may be useful to manipulate diet selection of free-ranging livestock.

A taste aversion model of drug discrimination learning: training drug and condition influence rate of learning, sensitivity and drug specificity

A model of drug discrimination based on a lithium chloride (LiCl) flavour aversion was described and examined. Mildly thirsty rats were presented daily with 4 ml of a distinctly flavoured solution which was followed on 50% of the days by an IP injection of LiCl. Prior to the flavour presentation, the rats were injection SC with saline or a training drug (0.04 mg/kg fentanyl or 20 mg/kg pentobarbital) to signal whether LiCl would follow. Almost all rats eventually exhibited stable behaviour that involved drinking most or all of the fluid when it was not to be followed by LiCl and little or no drinking when it was. Such discrimination occurred regardless of whether drug predicted LiCl (learned-discomfort) or predicted no LiCl (learned-safety). However, with fentanyl there were clear differences between rats trained with drug under learned-safety and under learned-discomfort conditions for 1) the rate of acquisition of stable performance as a function of LiCl dose, 2) generalization of the training dose to a test dose that was lower, and 3) elicitation of fentanyl responses by pentobarbital. These findings, together with indications that such effects did not always occur with pentobarbital as the training drug, were discussed from theoretical and practical perspectives.

Effects of lithium on an amphetamine animal model of bipolar disorder

1. This study examines the effects of chronic lithium administration on changes induced by amphetamine administration and withdrawal on open field locomotor activity of rats, and considered as an animal model of behaviors displayed in bipolar disorders. 2. For 21 days, rats were administered either single daily intraperitoneal injections (IP) of 0.9% saline, 0.15 mEq/kg, or 1.5 mEq/kg lithium chloride (LiCl). From day 7 to day 16, half of the animals in each group consisting of 12 rats were administered twice daily IP injections of either 1.5 mg/kg d-amphetamine or 0.9% saline. From day 17 to 21, d-amphetamine was withdrawn. 3. Neither dose of LiCl significantly altered the increases in activity levels produced by amphetamine. The withdrawal of amphetamine lead to an immediate return to baseline activity levels which neither dose of LiCl significantly affected. 4. The absence of interactive effects suggests that the influence of lithium and amphetamine on activity are mediated by different neurotransmitter systems.

Administration of activated charcoal or sodium polystyrene sulfonate (Kayexalate) as gastric decontamination for lithium intoxication: an animal model.

To determine whether sodium polystyrene sulfonate (SPS; Kayexalate) is effective in decreasing the absorption of lithium (Li) and to test the assumption that Li is poorly adsorbed by activated charcoal, 130 mice were administered an orogastric dose of LiCl (250 mg/kg) followed immediately by orogastric SPS (10 g/kg, SPS Group), activated charcoal (6.7 g/kg, AC Group), or water in an equivalent volume (Control Group). Subgroups of each of the 3 groups were sacrificed at 1, 2, 4 and 8 hr after treatment and serum analyzed for Li concentration. Statistical analyses revealed no overall difference between the AC Group and the Control Group. However, the SPS Group differed from both the Control and the AC Group at each time interval, with Li concentrations significantly lower in the SPS Group. These results demonstrate that: 1) SPS, in this study, effectively reduced serum Li concentrations in an in vivo model, and 2) activated charcoal did not.

Enhancement of flavor aversion conditioning in weanling but not adult rats by prior conditioning to an odor

In four experiments, we tested the effect of signaled and unsignaled preexposure to the US on conditioning of a taste aversion to saccharin, which was induced by pairing the saccharin (CS) with lithium chloride (US). Rats of two ages were tested, weanlings 21 days old at the time of conditioning and adults 60–80 days old at the time of conditioning. The procedures generally were designed to minimize the deleterious effects of US preexposure on conditioning in adults. In Experiment 1, preexposure to a US signaled by a novel odor (banana) facilitated conditioning in the weanlings but not in the adults. In Experiments 2A and 2B, these results were completely replicated. Only the weanlings were tested in the final experiment, in which it was determined that saccharin-LiCl conditioning was again facilitated by a prior pairing of the banana odor and LiCl, but only if the LiCl doses (.15M or.30 M) were the same for the signaled US preexposure and for the taste-aversion conditioning itself. In all of these experiments, a conditioned aversion to saccharin paired with LiCl was enhanced by prior pairing of an unrelated odor with LiCl, in the weanlings but not the adults. These results agree with others in suggesting that during the first three postnatal weeks rats may have a special disposition for cross-modal transfer.

Subacute and Chronic In Vivo Lithium Treatment Inhibits Agonist‐ and Sodium Fluoride‐Stimulated Inositol Phosphate Production in Rat Cortex

We have investigated the effects of in vivo lithium treatment on cerebral inositol phospholipid metabolism. Twice-daily treatment of rats with LiCl (3 mEq/kg) for 3 or 16 days resulted in a 25-40% reduction in agonist-stimulated inositol phosphate production, compared with NaCl-treated controls, in cortical slices prelabelled with [3H]inositol. A small effect was also seen with 5-hydroxytryptamine (5-HT) 24 h after a single dose of LiCl (10 mEq/kg). Dose-response curves to carbachol and 5-HT showed that lithium treatment reduced the maximal agonist response without altering the EC50 value. This inhibition was not affected by the concentration of LiCl in the assay buffer. Stimulation of inositol phosphate formation by 10 mM NaF in membranes prepared from cortex of 3-day lithium-treated rats was also inhibited, by 35% compared with NaCl-treated controls. Lithium treatment did not alter the kinetic profile of inositol polyphosphate formation in cortical slices stimulated with carbachol. Muscarinic cholinergic and 5-HT2 bindings were unaltered by lithium, as was cortical phospholipase C activity and isoproterenol-stimulated cyclic AMP formation. [3H]Inositol labelling of phosphatidylinositol 4,5-bisphosphate was significantly enhanced by 3-day lithium treatment. The results, therefore, indicate that subacute or chronic in vivo lithium treatment reduces agonist-stimulated inositol phospholipid metabolism in cerebral cortex; this persistent inhibition appears to be at the level of G-protein-phospholipase C coupling.

Copulationllness associations in male rats: Lithium chloride dose and delay manipulations.

Male rats that receive an injection of lithium chloride (LiCl) after each pairing with an estrous female gradually decrease their copulatory behaviors. In the present experiments we demonstrated that a 6.0 mEq/kg (0.3 M, 20 ml/kg) dose of LiCl injected after trials spaced twice weekly at 3-4-day intervals induced more rapid acquisition of copulation-illness associations than a 3.0 mEq/kg (0.15 M, 20 ml/kg) dose. Contingent 0.3 M saline or noncontingent 0.3 M LiCl injections did not affect copulatory behaviors. The location of the male rat (home cage or test chamber) during a portion of the aversive state induced by LiCl did not influence rate of acquisition. Copulation-illness associations, once established, were retained over a 60-day interval. Comparable decrements in copulatory behaviors were evident when LiCl was injected at 1-, 5-, or 15-min intervals after pairings with estrous females when the males were detained in the test chambers during the delay intervals; decrements were not observed when the interval was increased to 30 or 60 min. An electric shock analog to the aversive state induced by LiCl did not induce decrements in copulatory behaviors. It was suggested that odor-illness associations may, in part, account for the decrements in copulatory behaviors in this paradigm.

The influence of context and UCS intensity on the UCS preexposure effect in a flavor aversion paradigm

Three studies were conducted to evaluate the influence of environmental context and UCS preexposure intensity on the acquisition of a flavor aversion. In the first study, rats were exposed to two UCS-alone presentations at one of three dose levels of LiCl. The rats were given the two UCS preexposures in one of two contexts (familiar or novel). Following the UCS-alone treatment, all of the subjects received two pairings of sucrose and LiCl (1.25 meq) in the familiar context. Animals receiving UCS preexposures in the same context as used during conditioning consumed significantly more sucrose than did saline control animals. In contrast, the influence of prior UCS preexposure was not evident when UCS preexposure was experienced in a context different from that experienced during conditioning. In Experiment 2, all animal received UCS preexposure and conditioning in the novel room. Animals received either two or four preexposures at 0, 1.25, or 3.75 meq dose of LiCl. Two UCS preexposures at 3.75 meq dose produced a stronger UCS preexposure effect than did the 1.25 meq dose. Animals in Experiment 3 received two exposures to either 0-, 1.25-, or 3.75-meq LiCl in one of two contexts, followed by conditioning with the 1.25-meq LiCl dose in the same context as preexposure. Greater UCS interference occurred in animals preexposed to LiCl in the novel rather than familiar environment, with no specific dose effects in either context. These observations are discussed in terms of context blocking and generalization decrement models of the UCS preexposure effect.

Effects of anterior basolateral amygdala lesions on taste aversions produced by high and low oral doses of LiCl and lactose in the rat

Adult male hooded rats ( n = 12) with bilateral electrolytic lesions centred on the anterior basolateral amygdala (BLA) were given training using procedures meant to produce two different types of conditioned taste aversions (CTAs) to test whether the disruptive effects of such lesions on this form of learning were dependent upon the dosages of the illness-inducing agents used as unconditioned stimuli (UCSs). The CTAs were produced by either LiCl-induced toxicosis or lactose malabsorption. Comparison with sham-operated control subjects ( n = 8) indicated that the disruptive effects of the lesions were inversely related to the dosage level of LiCl but not lactose: whilst the lesions disrupted CTAs produced by a low i.p. dose of LiCl and by a low, but not a high, oral dose of LiCl, they did not alter CTA learning produced by either high or low oral doses of lactose. These results were interpreted as providing further evidence that BLA mediates only certain types of CTA learning.

Evidence that inositol 1-phosphate in brain of lithium-treated rats results mainly from phosphatidylinositol metabolism

In cerebral cortex of rats treated with increasing doses of LiCl, the relative concentrations of Ins(1)P, Ins(4)P and Ins(5)P (when InsP is a myo-inositol phosphate) are approx. 10:1:0.2 at all doses. In rats treated with LiCl followed by increasing doses of pilocarpine a similar relationship occurs. myo-Inositol-1-phosphatase (InsP1ase) from bovine brain hydrolyses Ins(1)P, Ins(4)P and Ins(5)P at comparable rates, and these substrates have similar Km values. The hydrolysis of Ins(4)P is inhibited by Li+ to a greater degree than is hydrolysis of Ins(1)P and Ins(5)P. D-Ins(1,4,5)P3 and D-Ins(1,4)P2 are neither substrates nor inhibitors of InsP1ase. A dialysed high-speed supernatant of rat brain showed a greater rate of hydrolysis of Ins(1)P than of D-Ins(1,4)P2 and a lower sensitivity of the bisphosphate hydrolysis to LiCl, as compared with the monophosphate. That enzyme preparation produced Ins(4)P at a greater rate than Ins(1)P when D-Ins(1,4)P2 was the substrate. The amount of D-Ins(3)P [i.e. L-Ins(1)P, possibly from D-Ins(1,3,4)P3] is only 11% of that of D-Ins(1)P on stimulation with pilocarpine in the presence of Li+. DL-Ins(1,4)P2 was hydrolysed by InsP1ase to the extent of about 50%; both Ins(4)P and Ins(1)P are products, the former being produced more rapidly than the latter; apparently L-Ins(1,4)P2 is a substrate for InsP1ase. Li+, but not Ins(2)P, inhibited the hydrolysis of L-Ins(1,4)P2. The following were neither substrates nor inhibitors of InsP1ase; Ins(1,6)P2, Ins(1,2)P2, Ins(1,2,5,6)P4, Ins(1,2,4,5,6)P5, Ins(1,3,4,5,6)P5 and phytic acid. myo-Inositol 1,2-cyclic phosphate was neither substrate nor inhibitor of InsP1ase. We conclude that the 10-fold greater tissue contents of Ins(1)P relative to Ins(4)P in both stimulated and non-stimulated rat brain in vivo are the consequence of a much larger amount of PtdIns metabolism than polyphosphoinositide metabolism under these conditions.

Cholecystokinin octapeptide and lithium produce different effects on feeding and taste aversion learning

The strengths of taste aversion induced by sulphated cholecystokinin 26–33 (CCK-8; 1,2,4 and 8 μg/kg IP) and lithium chloride (LiCl; 7.5, 15, 30 and 60 mg/kg IP) were determined in order to assess the relative aversiveness of the two compounds. All doses of LiCl induced strong aversion, but only the highest dose of CCK-8 induced aversion, which was mild. Effects of CCK-8 and LiCl on food intake were then compared in the hour (hr) following 8 hr of food deprivation; rats were on this food deprivation schedule for a relatively long time (78 days) throughout testing. All doses of CCK-8 reduced food intake significantly. Most doses of LiCl either did not affect or significantly increased food intake. Although 60 mg/kg LiCl did not affect food intake when administered 15 or 30 min before food presentation, it significantly increased food intake when administered 1, 2 or 3 hr before food presentation. Overeating of solid food may be an illness-induced behavior. Although a very high dose of LiCl (120 mg/kg) decreased food intake markedly, the rats were obviously distressed, not satiated. Failure of CCK-8 to affect feeding behavior like LiCl is indirect evidence that the reduction of food intake by CCK-8 is not merely the result of aversiveness, but is an extremely potent and specific behavioral effect.

Disruption of conditioned taste aversion by ECS: The role of lithium chloride

Rats were taught a conditioned taste aversion (CTA) by pairing a 10% sucrose solution (CS) with lithium chloride (LiCl)-induced poisoning (UCS). The CS-UCS interval was 30 min. The LiCl dose (20 ml/kg) was either strong (0.15 M) or weaker (0.075 M). Electroconvulsive shock (ECS) (80 mA for 600 msec) was interpolated within the CS-UCS interval at either 15 or 30 min. ECS caused a significant disruption of CTA only when the aversion was-established with the weaker dose of LiCl. These was also no indication that interference with CTA was dependent upon close temporal contiguity between the ECS and LiCl. In a second experiment a CTA was established with LiCl (0.15 M) which was heated to 45°C. Under these conditions ECS produced a similar disruption of learning to that when the UCS was the weaker dose of LiCl (0.075 M). The results suggest that an apparent differential loss of learning within the CS-UCS interval described in a previous report was accidentally created when some groups of animals were poisoned with warm and others with cold LiCl.

Visceral cortex lesions block conditioned taste aversions induced by morphine

Rats with bilateral ibotenic acid or sham lesions of the visceral (agranular insular) cortex were tested for a conditioned taste aversion (CTA) to saccharin after five pairings of morphine sulphate injections (15 mg/kg IP) with consumption of a novel solution (0.1% saccharin). Lesioned animals demonstrated no evidence of the morphine-induced CTA that was seen in the sham operated animals. A third group of rats received ibotenic acid lesions but had saccharin consumption paired with saline vehicle injections. This group had the normal preference (seen in naive rats) for saccharin on testing, showing that the visceral cortex lesion had no effect on the ability of the rats to discriminate saccharin from water. In order to test if visceral cortex lesions abolish specifically the CTA induced by morphine, we ran a similar set of CTA experiments using two new novel flavours and either 15 or 75 mg/kg IP lithium chloride (LiCl) as the unconditioned stimuli. Dose dependent CTA's to the LiCl were established in all groups indicating that the visceral cortex plays no role in mediating the aversive effect of LiCl. Using the condition place preference paradigm we investigated the role of the visceral cortex in the expression of morphine's rewarding aspects. Identical place preferences were found in groups of rats with or without visceral cortex lesions suggesting that this cortical region plays no role in either the perception of morphine's rewarding effects or the association of morphine's rewarding properties with sensory stimuli. Visceral cortex lesions also had no effect on the establishment of a conditioned place aversion to a high dose of LiCl (75 mg/kg IP). Thus, visceral cortex appears critical for the establishment of a morphine-induced CTA, but is not crucial for mediating gross taste discrimination, the aversive aspects of LiCl nor the rewarding properties of morphine.

Striatal dopamine and motor activity changes observed shortly after lithium administration.

Lithium chloride was given to rats i.p. at single doses of 2 and 10 meq/kg, respectively. It produced a suppression of motor activity and an increase in the dopamine content of the striatum. The magnitude of these effects were dose- and time-dependent as well as transient in nature. After 60 min of injection, the higher dose (10 meq/kg) reduced motor activity by 67% and increased striatal dopamine content by 56% while the lower dose (2 meq/kg) reduced motor activity by 42% and elevated striatal dopamine by 36%. These effects vanished 24 h after administration regardless the dose employed. None of the two doses of LiCl altered either dopamine biosynthesis in vivo (measured as the accumulation of a precursor of synthesis after decarboxylase inhibition), or the activity of tyrosine hydroxylase ex vivo under subsaturating conditions (i.e. enzyme activity in the tissues obtained from the animals post mortem). An increased deamination of tyramine by monoamineoxidase (MAO) was found in striatal homogenates after 60 min of the injection of 2 or 10 meq/kg of LiCl. This was due to a lower Km for the substrate as revealed by kinetic studies. LiCl treatment did not change the proportion of MAO A:B. As neither dopamine synthesis was increased nor the activity of the catabolic enzyme MAO was reduced (but it was oppositely enhanced), the increment in striatal dopamine content might have likely resulted from a reduced release and/or an increased amine reuptake by the neurons. We postulate that the reduced motor activity observed shortly after injection of LiCl would be related to an interference with striatal dopaminergic neurotransmission.