the neuroprotective effect of lithium in cannabinoid dependence is mediated through modulation of cyclic amp, erk1/2 and gsk-3β phosphorylation in cerebellar granular neurons of rat
نویسندگان
چکیده
lithium (li), a glycogen synthase kinase-3β (gsk-3β) inhibitor, has used to attenuate thecannabinoid-induced dependence/withdrawal signs, but molecular mechanisms related to this areunclear. recent studies indicate the involvement of upstream extracellular signal kinase1/2 (erk1/2)and downstream gsk-3β pathways in the development of cannabinoid-induced dependence. thisis mediated through cannabinoid receptor 1 (cb1) enriched in cerebellar granular neurons (cgns).accordingly, the present study aimed to investigate the mechanism of modulatory/neuroprotectiveeffects of li on a cannabinoid agonist (win 55,212-2 (win))-induced dependence, throughquantitative analysis of some involved proteins such as erk1/2, gsk-3β and related signalingpathways including their phosphorylated forms; and camp level as the other molecular mechanismsleading to dependence, in cgns model. the cgns were prepared from 7-day-old wistar rat pup in a12-well plate, pretreated with li (1mm) and an erk1/2 inhibitor sl327 (sl, 10 μm). the win (1μm) was added 30 minutes prior to treatment and am251 (am, 1 μm), as a cannabinoid antagonistwas co-treated with win. the camp level, as an indicator of cannabinoid-induced dependence, wasmeasured by elisa following forskolin (fsk) stimulation. western blot analyses determined thephosphorylated forms of erk1/2 (p-erk1/2), gsk-3β (p-gsk-3β) as well as their total expressionsin various treatment times and doses in cgns. win alone could down regulate the camp/p-erk1/2cascade compared to am treatment. however, p-gsk-3β was up-regulated with li and win orwith sl and li pretreatment to am-induced cellular response, which was the highest 60 minutesafter cgns exposure. results further suggested the potential role of li pretreatment to diminishthe development of cannabinoid-induced dependence/neuronal injury through possible mechanismsof modulating the camp/p-erk1/2 cascade independent of p-gsk-3β signaling pathway in-vitro.
منابع مشابه
The neuroprotective effect of lithium in cannabinoid dependence is mediated through modulation of cyclic AMP, ERK1/2 and GSK-3β phosphorylation in cerebellar granular neurons of rat
Lithium (Li), a glycogen synthase kinase-3β (GSK-3β) inhibitor, has used to attenuate thecannabinoid-induced dependence/withdrawal signs, but molecular mechanisms related to this areunclear. Recent studies indicate the involvement of upstream extracellular signal kinase1/2 (ERK1/2)and downstream GSK-3β pathways in the development of cannabinoid-induced dependence. Thisis mediated through cannab...
متن کاملThe neuroprotective effect of lithium in cannabinoid dependence is mediated through modulation of cyclic AMP, ERK1/2 and GSK-3β phosphorylation in cerebellar granular neurons of rat
Lithium (Li), a glycogen synthase kinase-3β (GSK-3β) inhibitor, has used to attenuate thecannabinoid-induced dependence/withdrawal signs, but molecular mechanisms related to this areunclear. Recent studies indicate the involvement of upstream extracellular signal kinase1/2 (ERK1/2)and downstream GSK-3β pathways in the development of cannabinoid-induced dependence. Thisis mediated through cannab...
متن کاملThe Neuroprotective Effect of Lithium in cannabinoid Dependence is Mediated through Modulation of Cyclic AMP, ERK1/2 and GSK-3β Phosphorylation in Cerebellar Granular Neurons of Rat
Lithium (Li), a glycogen synthase kinase-3β (GSK-3β) inhibitor, has used to attenuate the cannabinoid-induced dependence/withdrawal signs, but molecular mechanisms related to this are unclear. Recent studies indicate the involvement of upstream extracellular signal kinase1/2 (ERK1/2) and downstream GSK-3β pathways in the development of cannabinoid-induced dependence. This is mediated through ca...
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عنوان ژورنال:
iranian journal of pharmaceutical researchجلد ۱۴، شماره ۴، صفحات ۱۱۲۳-۱۱۳۵
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