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To investigate the mechanism of dexmedetomidine in alleviating the propofol induced hippocampal neurons destruction in developing rats. 189 healthy specific pathogen-free rats of 10 d old were divided into 9 groups by random number table method, namely, group N, group F, group D, group P, PD25 group, PD50 group, PD75 group, LYPD group and TDPD group, each with 21 cases. Then various indexes were observed, including general conditions, blood gas analysis, the messenger ribonucleic acid expression levels of phosphoinositide 3-kinase, protein kinase B and glycogen synthase kinase 3 beta, the protein expression levels of protein kinase B, glycogen synthase kinase 3 beta, phospho protein kinase B (ser473) and phospho glycogen synthase kinase 3 beta (ser9) in hippocampus, as well as ultrastructure of hippocampal neurons. 1 h after the consciousness recovery, the body weight, pH value, pressure of inhaled oxygen, partial pressure carbon dioxide, arterial oxygen saturation, bicarbonate and base excess had no difference among these groups (p<0.05). The phospho protein kinase B (ser473)/protein kinase B of PD75 group and TDPD group as well as the p glycogen synthase kinase 3 beta (ser9)/glycogen synthase kinase 3 beta in PD25 group, PD50 group, PD75 group, LYPD group and TDPD group were higher than those of group P (p<0.05). The phospho protein kinase B (ser473)/protein kinase B and phospho glycogen synthase kinase 3 beta (ser9)/glycogen synthase kinase 3 beta in LYPD group were lower than those of the PD75 group (p<0.05), while the p protein kinase B (ser473)/protein kinase B and p glycogen synthase kinase 3 beta (ser9)/glycogen synthase kinase 3 beta in TDPD group were higher than those of the PD75 group (p<0.05). Propofol anesthesia can cause damage to hippocampal neurons in developing rats; neuroprotection effect of dexmedetomidine may be related to activation of phosphoinositide 3-kinase/protein kinase B/glycogen synthase kinase 3 beta signal pathway. [ABSTRACT FROM AUTHOR]