Lithium in opiate abuse: A theoretical approach

Flemenbaum, Abraham; Cronson, Alvin J.; Weddige, Richard L.

doi:10.1016/0010-440x(79)90063-4

Cited by 8 publications

(5 citation statements)

References 42 publications

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“…These results are consistent with and extend previous studies, in which LiCl significantly reduced self-stimulation facilitated by morphine (Liebman and Segal 1976), reduced voluntary morphine ingestion in addicted rats (Tomkiewicz and Steinberg 1974), decreased amphetamine-and cocaine-induced hyperactivity (Beaulieu et al 2004;Xu et al 2009), attenuated the morphine withdrawal syndrome (Dehpour et al 1995), and had anti-euphoric effects in drug-free opiate addicts (Jasinski et al 1977). Our study also demonstrated that GSK-3b may be a possible molecular mechanism of the effect of LiCl on addiction-associated behavior, and LiCl, a GSK-3b inhibitor, may be useful in the treatment of drug addiction (Flemenbaum et al 1979;Abrahamson 1983).…”

Section: Role Of Gsk-3b In Addiction-associated Behaviorssupporting

confidence: 54%

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Glycogen synthase kinase 3β in the basolateral amygdala is critical for the reconsolidation of cocaine reward memory

Xue

Ding

et al. 2011

Journal of Neurochemistry

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J. Neurochem. (2011) 10.1111/j.1471‐4159.2011.07277.x Abstract Exposure to cocaine‐associated conditioned stimuli elicits craving and increases the probability of cocaine relapse in cocaine users even after extended periods of abstinence. Recent evidence indicates that cocaine seeking can be inhibited by disrupting the reconsolidation of the cocaine cue memories and that basolateral amygdala (BLA) neuronal activity plays a role in this effect. Previous studies demonstrated that glycogen synthase kinase 3β (GSK‐3β) plays a role in the reconsolidation of fear memory. Here, we used a conditioned place preference procedure to examine the role of GSK‐3β in the BLA in the reconsolidation of cocaine cue memories. GSK‐3β activity in the BLA, but not central amygdala (CeA), in rats that acquired cocaine (10 mg/kg)‐induced conditioned place preference increased after re‐exposure to a previously cocaine‐paired chamber (i.e., a memory reactivation procedure). Systemic injections of the GSK‐3β inhibitor lithium chloride after memory reactivation impaired the reconsolidation of cocaine cue memories and inhibited subsequent cue‐induced GSK‐3β activity in the BLA. Basolateral amygdala, but not central amygdala, injections of SB216763, a selective inhibitor of GSK‐3β, immediately after the reactivation of cocaine cue memories also disrupted cocaine cue memory reconsolidation and prevented cue‐induced increases in GSK‐3β activity in the BLA. The effect of SB216763 on the reconsolidation of cocaine cue memories lasted at least 2 weeks and was not recovered by a cocaine priming injection. These results indicate that GSK‐3β activity in the BLA mediates the reconsolidation of cocaine cue memories.

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Section: Role Of Gsk-3b In Addiction-associated Behaviorssupporting

confidence: 54%

“…1977). Our study also demonstrated that GSK‐3β may be a possible molecular mechanism of the effect of LiCl on addiction‐associated behavior, and LiCl, a GSK‐3β inhibitor, may be useful in the treatment of drug addiction (Flemenbaum et al. 1979; Abrahamson 1983).…”

Section: Discussionmentioning

confidence: 61%

Glycogen synthase kinase 3β in the basolateral amygdala is critical for the reconsolidation of cocaine reward memory

Xue

Ding

et al. 2011

Journal of Neurochemistry

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“…Our previous study (Xu et al 2009) and current findings confirmed that GSK-3b may be a possible molecular mechanism of the therapeutic effect of LiCl, and indicate that GSK-3b is involved in neuroadaptation and behavioral adaptation after repeated psychostimulant exposure. Previous study also demonstrated that LiCl, a GSK-3b inhibitor, may be useful in the treatment of drug addiction (Flemenbaum et al 1979;Abrahamson 1983).…”

Section: Discussionmentioning

confidence: 97%

Glycogen synthase kinase 3β in the nucleus accumbens core is critical for methamphetamine‐induced behavioral sensitization

Xu¹,

Wang²,

et al. 2011

Journal of Neurochemistry

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J. Neurochem. (2011) 10.1111/j.1471‐4159.2011.07281.x Abstract As a ubiquitous serine/threonine protein kinase, glycogen synthase kinase 3β (GSK‐3β) has been considered to be important in the synaptic plasticity that underlies dopamine‐related behaviors and diseases. We recently found that GSK‐3β activity in the nucleus accumbens (NAc) core is critically involved in cocaine‐induced behavioral sensitization. The present study further explored the association between the changes in GSK‐3β activity in the NAc and the chronic administration of methamphetamine. We also examined whether blocking GSK‐3β activity in the NAc could alter the initiation and expression of methamphetamine (1 mg/kg, i.p.)‐induced locomotor sensitization in rats using systemic administration of lithium chloride (LiCl, 100 mg/kg, i.p) and brain region‐specific administration of the GSK‐3β inhibitor SB216763 (1 ng/side). We found that GSK‐3β activity increased in the NAc core, but not NAc shell, after chronic methamphetamine administration. The initiation and expression of methamphetamine‐induced locomotor sensitization was attenuated by systemic administration of LiCl and direct infusion of SB216763 into the NAc core, but not NAc shell. These results indicate that GSK‐3β activity in the NAc core mediates the initiation and expression of methamphetamine‐induced locomotor sensitization, suggesting that GSK‐3β may be a potential target for the treatment of psychostimulant addiction.

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“…Although not seeming to be of direct clinical importance, lithium is reported to significantly reduce the self-stimulation facilitated by morphine (Luebman & Segal 1976), and the amount of voluntary ingestion of morphine by addicted rats (Tomkiewitcz & Steinberg 1974). Some clinical studies also suggested the use of lithium for the treatment of drug addiction (Jasinski et al 1977;Flemenbaum et al 1979;Abrahamson 1983). We have previously reported that lithium inhibits naloxone-precipitated withdrawal syndrome in the morphine-dependent mice (Dehpour et al 1995(Dehpour et al & 2000 and the naloxone-precipitated withdrawal syndrome of cholestatic mice (Dehpour et al 1998).…”

mentioning

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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Lithium in opiate abuse: A theoretical approach

Cited by 8 publications

References 42 publications

Glycogen synthase kinase 3β in the basolateral amygdala is critical for the reconsolidation of cocaine reward memory

Glycogen synthase kinase 3β in the basolateral amygdala is critical for the reconsolidation of cocaine reward memory

Glycogen synthase kinase 3β in the nucleus accumbens core is critical for methamphetamine‐induced behavioral sensitization

Lithium Inhibits the Development of Physical Dependence to Clonidine in Mice

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