Disease relevance of LITHIUM CHLORIDE

• Neither hyperalgesia nor its blockade by naloxone were due to variations in tail-skin temperature induced by LiCl [1].
• Five minutes after the beginning of the exposure, half of the litters were injected ip with the illness-inducing agent lithium chloride (LiCl; 0.20 M, 2% of body weight); the other half was treated with saline solution (8% NaCl) [2].

Psychiatry related information on LITHIUM CHLORIDE

• Acute amphetamine (3 mg/kg) increased locomotor activity in C57BL/6nCrlBR mice and LiCl (1-4 mEq/kg) blocked this effect [3].
• In 4 experiments, the authors (a) confirmed their initial observation, (b) showed that the effect is not due to retrograde amnesia produced by LiCl, and (c) confirmed that memories less than 15 min old are available for other types of learning [4].
• In Experiment 1, the rats were tested under 24-hr food deprivation after injections of CCK, LiCl, and saline (in counterbalanced order) [5].
• After adaption to a water-deprivation schedule which permitted 10-min access to water each day, the rats were given 10-min access to 0.1% saccharin solution which was followed by intraperitoneal injections of either H2O, DMSO, LiCl, or AF of varying doses according to group assignment [6].

High impact information on LITHIUM CHLORIDE

• Embryos cultured in medium containing WNT3A or the WNT pathway activator lithium chloride (LiCl) display accelerated formation of expanded placodes, and LiCl induces the formation of ectopic placode-like structures that show elevated expression of the placode marker Wnt10b [7].
• Exposure to a saccharin solution (CS) which had previously been paired with lithium chloride (LiCl; US) induced significant c-Fos-like immunoreactivity (c-FLI) in the intermediate zone of the nucleus of the solitary tract (NTS), a response that was quite similar to that displayed following administration of LiCl alone [8].
• These findings strongly implicate forebrain input in this cellular correlate of CTA learning and also indicate that the pathways mediating the response to the US (LiCl) and the CS (saccharin) differ [8].
• Phenobarbital in doses ranging from 20 to 80 mg/kg significantly attenuated taste aversion induced by lithium chloride (LiCl) and x-radiation, the maximal effect occurred with the 60 mg/kg dose [9].
• Furthermore, the same GLP-1R antagonist that can block the aversive effects of LiCl in the rat failed to do so in the mouse [10].

Biological context of LITHIUM CHLORIDE

• Immunohistochemical analysis of the protein product of the c-fos gene, showed that central administration of PrRP activated some areas of the brain in common with both CCK and LiCl administered peripherally [11].
• To elucidate the role of PrRP, its actions were compared with those of a homeostatic regulator of food intake, the satiety factor, cholecystokinin (CCK), and a nonhomeostatic regulator, lithium chloride (LiCl), which reduces food intake due to visceral illness [11].
• We assessed whether pharmacological inhibition of GSK-3beta with lithium chloride (LiCl) was sufficient to stimulate myogenesis [12].
• Activation of the pathway by lithium chloride (LiCl) had no effect on cell number but inhibited alkaline phosphate activity (ALP), a marker of APC differentiation, whereas EGCG increased ALP activity [13].
• Addition of IGF-I or LiCl stimulated myogenesis, evidenced by increased myotube formation, muscle creatine kinase (MCK) activity, and troponin I (TnI) promoter transactivation during differentiation [12].

Anatomical context of LITHIUM CHLORIDE

• In rats, central administration of glucagon-like peptide-1 (GLP-1) elicits symptoms of visceral illness like those caused by the toxin lithium chloride (LiCl), including anorexia, conditioned taste aversion (CTA) formation, and neural activation in the hypothalamus and hindbrain including activation of brainstem preproglucagon cells [10].
• The major goal of these experiments was to further test the hypothesis that the central nervous system GLP-1 system is critical to the visceral illness actions of LiCl by using mice with a targeted disruption of the only described GLP-1R [10].
• However, the mechanism of action of these drugs is quite different with the area postrema and related emetic circuitry critical to the response to LiCl but not amphetamine. c-Fos immunohistochemistry was used to define brain regions activated during drug administration and during expression of a CTA using either amphetamine or LiCl as the US drug [14].
• LiCl inhibition of mouse oocyte GSK-3 modified organization of microtubules and/or function of meiotic spindles thus compromising segregation of condensed bivalent chromosomes [15].
• Similar to immunoneutralization, significantly fewer zygotes cultured with either LiCl or alsterpaullone developed past the two-cell stage compared to controls and this mitotic block was not reversible [16].

Associations of LITHIUM CHLORIDE with other chemical compounds

• Additionally, CTA produced by administration of MTII was found to be more resistant to extinction than that produced by LiCl [17].
• Each of the opioids decreased LiCl-induced activation of NTS neurons as well as OT and VP cells in the PVN and SON [18].
• Aversive properties of lithium chloride (LiCl) are mediated via pathways comprising neurons of the nucleus of the solitary tract (NTS) and oxytocin (OT) and vasopressin (VP) cells in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei [18].
• OBJECTIVE: To evaluate possible reabsorption and systemic effects of lithium released by lithium-chloride-coated heat and moisture exchangers (HMEs) during prolonged mechanical ventilation [19].
• Rats whose body temperatures were not reduced (0 min immersion) showed no saccharin aversion when the LiCl was delayed 90 min [20].

Gene context of LITHIUM CHLORIDE

• Rats with AP lesions exhibited a similar OT and AVP response to LiCl and APO but the OT response to CCK-8s was significantly diminished [21].
• Furthermore, the lack of Lef-1 mRNA in treated and untreated embryos indicates the LiCl induced axial defects in the mouse are not mediated by the beta-catenin/Lef-1 pathway [22].
• However, LiCl activated more neurons in the area postrema and fewer neurons in the nucleus of the solitary tract compared with CCK [23].
• In contrast, chronic administration of lithium-chloride (40 mg/kg) did not affect the amount of the two AP-2 isoforms [24].
• Most compellingly, pharmacological antagonists of the GLP-1 receptor (GLP-1R) block several effects of LiCl in rat [10].

Analytical, diagnostic and therapeutic context of LITHIUM CHLORIDE

• This was accomplished by associating ES with intraperitoneal (i.p.) injection of lithium chloride (LiCl), following the session with electrical stimulation [25].
• LiCl, at a concentration of 2 mmol of Li per liter, has no negative effect on the survival of common respiratory pathogens or on the results of immunoassays [26].
• Following each test, males were made ill with lithium chloride (LiCl) by intragastric intubation or intraperitoneal injection [27].
• In addition, morphine analgesia was reduced in the hot plate test 40 min and 24 h following LiCl [28].
• An intraperitoneal injection of lithium chloride (LiCl) produced hyperalgesia that was blocked in a dose-dependent manner by subcutaneous injection of the opioid antagonist naloxone [1].

References