Neuroprotective effect and cognitive outcome of chronic lithium on traumatic brain injury in mice

Zhu, Zhihua; Wang, Qingguang; Han, Bo; William, Callie P.

doi:10.1016/j.brainresbull.2010.07.008

Cited by 71 publications

(56 citation statements)

References 56 publications

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“…Mood stabilizers, such as lithium have been demonstrated to attenuate IL1b production in the brain in animal studies and this may contribute to their neuroprotective effects within the brain (Zhu et al, 2010). Therefore, an IL-1b reducing property of mood stabilizers and AEDs might contribute to their therapeutic action.…”

Section: Discussionmentioning

confidence: 99%

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Himmerich¹,

Bartsch²,

Hamer³

et al. 2013

Journal of Psychiatric Research

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Section: Discussionmentioning

confidence: 99%

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Himmerich¹,

Bartsch²,

Hamer³

et al. 2013

Journal of Psychiatric Research

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“…In a mouse model of moderate TBI produced by controlled cortical impact, a method widely used for the accurate control of mechanical input, chronic lithium pretreatment for 14 days attenuated the loss of hemispheric tissue, brain edema, IL-1b expression, and hippocampal neuronal degeneration. In addition, these effects of lithium pretreatment in moderate TBI mice were associated with improved spatial learning and memory (Zhu et al, 2010).…”

Section: B Tbimentioning

confidence: 91%

“…The neural stem cells in the SVZ migrate into the olfactory bulb and then differentiate into interneurons, and new neurons in the subgranular zone migrate into the adjacent DG granule cell layer. It is known that cerebral ischemia enhances neurogenesis in regions that are traditionally neurogenic and nonneurogenic, perhaps as part of the self-repair system of ischemic Nonaka and Chuang, 1998;Cimarosti et al, 2001;Ma and Zhang, 2003;Ren et al, 2003;Xu et al, 2003;Roh et al, 2005;Bian et al, 2007;Yan et al, 2007;Kim et al, 2008;Li et al, 2010aTsai et al, 2011;Hemorrhagic stroke Rat intracerebral hemorrhagic model Kang et al, 2012 TBI Rat and mouse models of controlled cortical impact Shapira et al, 2007;Zhu et al, 2010;Dash et al, 2011;Yu et al, 2012a,b HD Rat excitotoxic model; rat corticostriatal slices; transgenic mice; neuroblastoma cells Wei et al, 2001;Carmichael et al, 2002;Wood and Morton, 2003;Senatorov et al, 2004;Berger et al, 2005;Senatorov and Chuang, 2007;Sarkar et al, 2008;Crespo-Biel et al, 2009;Chiu et al, 2011 AD Cultured cells and hippocampal slices; rabbits and rats; transgenic mice; Drosophila Hong et al, 1997;Munoz-Montano et al, 1997;Alvarez et al, 1999Alvarez et al, , 2002Inestrosa et al, 2000;Wei et al, 2000;Sang et al, 2001;Sun et al, 2002;…”

Section: A Strokementioning

confidence: 99%

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder

et al. 2013

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“…Previous studies have reported that lithium has neuroprotective effects. The neuroprotective mechanism contains interaction of N-Methyl-D-aspartic acid or N-Methyl-D-aspartate (NMDA) receptors, reduction in pro-apoptotic proteins, p53 and bax, increased number of Bcl2, cytoprotective proteins and cell survival kinase activation [11,12]. It has previously been shown that lithium at therapeutic dose is able to ameliorate vincristine-induced neuropathy [13].…”

mentioning

confidence: 99%

Lithium Attenuates Peripheral Neuropathy Induced by Paclitaxel in Rats

Pourmohammadi

Alimoradi

Mehr

et al. 2011

Basic Clin Pharma Tox

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As a cancer chemotherapeutic agent, paclitaxel (Taxol Ò ) causes dose-related peripheral neuropathy in human beings. The mechanisms underlying this toxicity are currently unknown, and there are no validated treatments for its prevention or control. To assess whether lithium as a pre-treatment and at subtherapeutic dose could prevent the peripheral neuropathy produced by it, rats were treated with paclitaxel (2 mg ⁄ kg i.p. every other day for a total of 16 times) and ⁄ or lithium chloride (300 mg ⁄ l) via water supply. General toxicity and body-weight were measured regularly during the experiment. To evaluate the sensory and motor neuropathy hot-plate, open-field test and nerve conduction velocity were used. In rats treated with only paclitaxel, there was behavioural, electrophysiological and histological evidence of a mixed sensorimotor neuropathy after 16 injections. Lithium robustly reduced the rate of mortality and general toxicity. Paclitaxel-induced sensorimotor neuropathy was significantly improved as indicated by changes in hotplate latency, total distance moved and a significant increase in sciatic, sural and tail sensory or motor nerve conduction velocity. The same results were observed in histopathological examinations; however, dorsal root ganglion neurons did not significantly change in the paclitaxel-treated groups. These results suggest that lithium, at subtherapeutic doses, can prevent both motor and sensory components of paclitaxel neuropathy in rats. Thus, lithium at these doses, as an inexpensive and relatively safe salt, may be useful clinically in preventing the neuropathy induced by paclitaxel treatment.Paclitaxel is an effective anti-tumour agent initially isolated from the bark of the pacific yew tree, Taxus brevifolia, and is regularly used to treat long, ovarian cancer either by itself or in combination with other anti-tumour agents [1][2][3]. Paclitaxel causes excessive tubulin polymerization leading to mitotic arrest and thus inducing apoptosis in dividing cells [4].Microtubules play an important role in cellular functions such as membrane and cellular scaffolding, intracellular transport of organelles or proteins and transmission of signals initiated at cell surface receptors. Thus, microtubules interfering agents like vincristine or paclitaxel may disturb non-neoplastic cells such as nerves and finally cause apoptosis. Hence, peripheral neuropathy is one of the most frequent side effects of these two drugs that usually result in dose modification and changes in the treatment plan [5][6][7][8].As a mood stabilizer, lithium is commonly prescribed for bipolar disorders, and although its mechanism of action remains unknown, it is well established that lithium exerts some of its therapeutic effects through G-protein-coupled pathway, glycogen synthase kinase-3 (GSK3b), inositol monophopsphate and nitric oxide-dependent pathways and augmentation of serotonin function in the central nervous system [9,10]. Previous studies have reported that lithium has neuroprotective effects. The...

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Neuroprotective effect and cognitive outcome of chronic lithium on traumatic brain injury in mice

Cited by 71 publications

References 56 publications

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder

Lithium Attenuates Peripheral Neuropathy Induced by Paclitaxel in Rats

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