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The effect of short-term lithium treatment on head twitches induced by 5-hydroxytryptophan in mice

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Szymczyk H., Danilczuk Z., Wielosz M.
Current Issues in Pharmacy and Medical Sciences
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2015
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vol. 28
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issue 4
264-268
EN
The effectiveness of lithium in the treatment of affective disorders is well documented. However, the mechanism of this effect is still unknown. The purpose of this study was to investigate the effect of lithium on serotonergic neurons. The evaluation of the serotoninergic system activity was performed on the basis of an experimental model of head twitch response triggered by direct or indirect stimulation of serotonin 5-HT2 receptors in the brain. The obtained results indicated that the lithium chloride co-applied with a direct precursor of serotonin - 5-hydroxytryptophan used in a threshold dose and with carbidopa, generated head twitch response in mice. What is more, an enhancement of head twitch response in mice was observed after repeated 5-hydroxytryptophan application in head twitch-evoking doses. Moreover, inhibition of the serotonine storage in nerve endings in mice was evoked by reserpine administration. Furthermore, lithium increased the effect of 5-hydroxytryptophan given in a threshold dose and a head twitchevoking dose, respectively. In addition, when P-chlorphenylalanine (pCPA), an inhibitor of the serotonin synthesis within the serotonergic neurons, was given simultaneously with the lithium chloride, carbidopa and 5-hydroxytryptophan in the threshold dose, as well as with the lithium chloride and 5-hydroxytryptophan given at head twitchevoking dosage, pCPA administration decreased the number of head twitches responses in both experimental models, as well as in the reserpinized mice subjected to the lithium chloride and 5-hydroxytryptophan application. Finally, 5,7-dihydroxytryptamineevoked serotoninergic nerve endings destruction led to absolute inhibition of headtwitch response when observed after the lithium and 5-hydroxytryptophan application. Moreover, the increase by lithium 5-hydroxytryptophan-evoke head twitch response was inhibited by administration of the ritanserine - a 5-HT2 serotonin receptor blocking agent. In summary, our data show that lithium induced an enhancement of serotonergic neurotransmission due to its action on presynaptic serotonergic terminals.
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Mechanizm działania jonów litu w ośrodkowym układzie nerwowym

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Gawlik O., Rabe-Jabłońska J.
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issue 4
211-217
EN
The aim of this paper is to present current views on proved and possible mechanisms of action of lithium ion in the central nervous system. In spite of the long history of lithium usage in medicine, its mechanism of therapeutic action still has not been fully understood and is being under intensive researches. There have been proposed many hypotheses for this mechanism. They include: the ions (mainly sodium) transport modulation and neurotransmitters, especially monoamines, signalling modulation (regulation of dopaminergic and noradrenergic neurotransmission and stimulation of serotonin secretion); the interference with the secondary messenger systems: mainly phosphatydyloinositol (PI) signalling pathway (inositol mono- and polyphosphatase inhibition) and also cyclic adenosine monophosphate (cAMP) system; other intracellular messengers (like G proteins, protein kinase C or calcium ion); many neuroprotection effects: increasing expression of neuroprotective factors (bcl-2, BAG-1, BDNF and others), the caspases cascade leading to apoptosis inhibition, glycogen synthase kinase 3 subunit (GSK-3b inhibition – this is one of the most important targets for lithium ion in the cell), influence on neurogenesis, reduction of glutaminergic neurotransmission or possible lithium ion action as an antioxidant factor; long-term treatment with lithium salts regulates genes expression in neurons. Understanding the mechanism of lithium action would help researchers to advance not only in finding better drugs for the disease treatment by also in understanding the disease itself.
PL
Celem niniejszego opracowania jest przedstawienie obecnej wiedzy na temat udowodnionych i możliwych mechanizmów działania jonów litu w ośrodkowym układzie nerwowym. Pomimo długiej historii stosowania litu w medycynie ów mechanizm jego działań terapeutycznych wciąż nie został w pełni zrozumiany i podlega intensywnym badaniom. Zaproponowano wiele hipotez odnoszących się do tego działania, wśród których znajdują się: modulacja transportu jonów (głównie sodu) i modulacja neuroprzekaźnictwa, szczególnie w obrębie monoamin (regulacja przekaźnictwa dopaminergicznego i noradrenergicznego oraz stymulacja wydzielania serotoniny); oddziaływanie na układy wtórnych przekaźników: głównie ścieżkę fosfatydyloinozytolu (PI) (hamowanie aktywności mono- i polifosfatazy inozytolu), a także układ cyklicznego adenozynomonofosforanu (cAMP); wpływ na inne systemy przekaźnictwa wewnątrzkomórkowego (takie jak białka G, kinaza białkowa C czy jony wapnia); wiele efektów neuroprotekcyjnych: nasilenie ekspresji czynników neuroprotekcyjnych (bcl-2, BAG-1, BDNF i in.), hamowanie szlaku kaspaz prowadzącego do apoptozy, hamowanie aktywności podjednostki kinazy fosfatazy glikogenu (GSK-3b – jest to jeden z głównych punktów uchwytu dla jonów litu w komórce), wpływ na neurogenezę, redukcja przekaźnictwa glutaminianergicznego oraz możliwa rola jonów litu jako czynnika antyoksydacyjnego; długoterminowe leczenie solami litu reguluje z kolei ekspresję genów w komórkach nerwowych. Zrozumienie mechanizmów działania jonów litu może pomóc nie tylko w opracowaniu nowych lepszych leków, lecz także w dokładniejszym zrozumieniu istoty chorób układu nerwowego, w których terapii stosujemy lit.
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