Fig. 1. Western blot evaluation of changes in phosphorylated levels of extracellular signal-regulated kinase 1/2 (pERK-1, pERK-2) and serine/threonine-specific protein kinase (pAkt) 120 min after administration of saline (Sal) or intralipid (IL) control, lithium (Li, 6 mEq/kg), ketamine (Keta, 40 mg/kg), propofol (Prop, 50 mg/kg), or lithium in combination with ketamine (Keta + Li) or propofol (Prop + Li). (  A ) Representative blots for protein under each treatment condition. (  B ) Values for pups treated with lithium alone (n = 13) are compared to values for littermate saline controls (n = 13). Lithium induced a significant increase in pERK-1 (  P = 0.0064) and pERK-2 (  P = 0.0020), but it had no effect on pAkt. (  C ) Values for pups treated with vehicle (n = 21), ketamine (n = 6), ketamine plus lithium (n = 6), propofol (n = 8), or propofol plus lithium (n = 8). The vehicle control group consists of pups treated with saline (control for ketamine) or intralipid (control for propofol). These groups were combined into a single vehicle control group because their mean values were not significantly different. Compared to the vehicle controls, both ketamine and propofol produced a significant suppression of pERK-1, pERK-2, and pAkt (  P < 0.01 for pAkt, vehicle  vs. ketamine;  P < 0.001 for all other comparisons). Administration of lithium in combination with ketamine or propofol prevented the suppressant effects of ketamine and propofol on pERK-1 and pERK-2, leaving these values unchanged from vehicle control. Lithium counteracted the suppressant effect of ketamine on pAkt, but only to a marginally nonsignificant degree (  P = 0.0503).