Lithium increases dynorphin A(1–8) and prodynorphin mRNA levels in the basal ganglia of rats

Sivam, Subbiah P.; Takeuchi, Koji; Li, S.; Douglass, James; Civelli, Olivier; Calvetta, L.; Herbert, Edward; McGinty, Jacqueline F.; Hong, Jau–Shyong

doi:10.1016/0169-328x(88)90061-7

Cited by 33 publications

(14 citation statements)

References 35 publications

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“…Although it remains to be established whether the reported changes of LDCV protein expression contribute mechanistically to this change in the regulated secretory behavior of these cells, there is ample evidence from other groups that lithium alters the content and secretion of monoamines and selected neuropeptides, which are stored in and released from LDCV (Hesketh et al, 1978;Treiser et al, 1981;Staunton et al, 1982;Ebstein et al, 1983;Hong et al, 1983;Mitsushio et al, 1988;Sivam et al, 1988Sivam et al, , 1989Mathé et al, 1990;Husum et al, 2000;Shiah and Yatham, 2000). And, as observed in the current experiments, in the majority of these cited examples, the effect of lithium was to increase the content or secretion of the neurotransmitter or neuromodulator.…”

Section: Discussionmentioning

confidence: 99%

Convergent Effects of Lithium and Valproate on the Expression of Proteins Associated with Large Dense Core Vesicles in NGF-differentiated PC12 Cells

Cordeiro

Gundersen

Umbach

2003

Neuropsychopharmacol

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Lithium and valproate are chemically unrelated compounds that are used to treat manic-depressive illness. Previously, we reported that lithium ions upregulate genes encoding proteins primarily associated with large dense core vesicles (LDCV) in nerve growth factor (NGF)-differentiated PC12 cells, but not in undifferentiated PC12 cells. Moreover, lithium did not alter the expression of proteins associated with small-clear, synaptic-like vesicles (SSV) in these cells. Based on these observations, we investigated whether valproate had actions similar to those of lithium in PC12 cells. Thus, undifferentiated or NGF-differentiated PC12 cells were exposed to lithium (1 mM) or valproate (1 mM) for 48 h. Extracts from these cells were submitted to semiquantitative Northern and Western analyses. In NGFdifferentiated cells, both agents increased the expression of proteins associated with LDCV, the vesicular monoamine transporter 1 (VMAT1), and cysteine string protein (CSP). These same treatments did not alter the expression of proteins primarily associated with SSV, the vesicular acetylcholine transporter (VAChT), and synaptophysin (SY). Furthermore, neither drug affected the expression of these proteins in undifferentiated cells. Interestingly, secretion of 3 H-dopamine was increased in cells exhibiting the increase of VMAT1 and csp. Taken together, the convergent effects of these chemically diverse compounds suggest that altered dynamics of LDCV may play a vital role in the biochemical pathway, leading to the relief of the symptoms of manic depression.

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Section: Discussionmentioning

confidence: 99%

Convergent Effects of Lithium and Valproate on the Expression of Proteins Associated with Large Dense Core Vesicles in NGF-differentiated PC12 Cells

Cordeiro

Gundersen

Umbach

2003

Neuropsychopharmacol

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“…Similar mechanisms may also be involved in the effect of lithium to prevent the development of dependence to clonidine. First, lithium is reported to enhance the biosynthesis (Sivam et al 1986(Sivam et al & 1988Dziedzicka et al 1990) or release (Stauntun et al 1982;Sivam et al 1987) of endogenous opioids in the brain tissues although some studies are not in agreement (Stengaard-Pedersen & Schou 1982). Our observation that naloxone produced withdrawal signs in clonidine-treated mice, and the report that naloxone reversed the clonidine-induced hypotension (Farsang & Kunos 1979) together with the clonidine-associated gastroprotection (Gyries et al 2000), suggest the possibility of the interaction between opioid receptors and a 2 -adrenoceptors, and that the clonidine withdrawal syndrome may have an opioidergic component.…”

Section: Discussionmentioning

confidence: 99%

Lithium Inhibits the Development of Physical Dependence to Clonidine in Mice

Dehpour¹,

Sadr

Roohi-Azizi

et al. 2002

Pharmacology & Toxicology

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Based on our previous finding that chronic lithium treatment reduced naloxone-precipitated withdrawal syndrome in morphine-treated mice, the effect of chronic lithium treatment was evaluated on the development of dependence to clonidine. Dependence was induced by injection of either morphine (50, 50 and 75 mg/kg, intraperitoneally with 3 hr interval for 3 consecutive days), or clonidine (2 mg/kg/day, intraperitoneally for 10 days). Naloxone (4 mg/kg, intraperitoneally) precipitated withdrawal signs in both morphine-and clonidine-treated mice. Yohimbine (5 mg/kg, intraperitoneally) precipitated withdrawal signs in the clonidine-treated mice, similar to morphine withdrawal signs; but failed to precipitate any significant sign in the morphine-treated mice. Coadministration of lithium was carried out by adding lithium chloride to drinking water (600 mg/l for 20 days; 10 days before the beginning of clonidine administration and 17 days before the administration of morphine to allow the lithium concentration to reach steady-state). The results indicated that chronic lithium administration significantly attenuated the withdrawal signs, precipitated either by yohimbine or naloxone, in clonidine-treated mice. As a conclusion, clonidine withdrawal signs are very similar to opioid withdrawal signs, and lithium is able to prevent the development of physical dependence to clonidine.

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“…a week or longer) has also been shown to reduce the expression of G-protein a-subunit (as and ai) but to increase expression of adenylyl cyclase types I and II [14][15][16]. It is also reported that lithium alters the mRNA levels of a number of neuropeptides [17,18]. For example, acute treatment with lithium enhances basal expression of the neuropeptide Y gene in rat hippocampus [17].…”

Section: Introductionmentioning

confidence: 99%

“…For example, acute treatment with lithium enhances basal expression of the neuropeptide Y gene in rat hippocampus [17]. Chronic administration of lithium (3 weeks) increased the prodynorphin mRNA abundance in the rat striatum [18]. Considering these findings of lithium's effect on gene expression together, nonetheless, provides an incomplete picture of the underlying mechanism of action of this drug in BD.…”

Section: Introductionmentioning

confidence: 99%

Differential display PCR reveals increased expression of 2′,3′‐cyclic nucleotide 3′‐phosphodiesterase by lithium

Wang¹,

Young²

1996

FEBS Letters

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Differential display PCR was used to study the effects of lithium on gene expression. Four candidate genes were isolated and verified by Northern hybridization after 1 week treatment of C6 glioma cells with therapeutically relevant concentrations of LiCI (1 mM). Sequencing analysis revealed three previously unidentified cDNA fragments in addition to a sequence with 99% homology with the cDNA for 2',3'-cyclic nucleotide 3'-phosphodiesterase type II (CNPasell). Since CNPaselI is important in myelinogenesis and possibly neuronal growth and repair, the present findings suggest that lithium treatment may regulate these processes.

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Lithium increases dynorphin A(1–8) and prodynorphin mRNA levels in the basal ganglia of rats

Cited by 33 publications

References 35 publications

Convergent Effects of Lithium and Valproate on the Expression of Proteins Associated with Large Dense Core Vesicles in NGF-differentiated PC12 Cells

Convergent Effects of Lithium and Valproate on the Expression of Proteins Associated with Large Dense Core Vesicles in NGF-differentiated PC12 Cells

Lithium Inhibits the Development of Physical Dependence to Clonidine in Mice

Differential display PCR reveals increased expression of 2′,3′‐cyclic nucleotide 3′‐phosphodiesterase by lithium

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