Objective To evaluate the effects of isoflurane anesthesia on NR1 expression and neuronal apoptosis in the hippocampus and cortex of adult rats .Methods Thirty-six adult male Sprague-Dawley rats , weighing 250-280 g ,were randomly assigned into 3 groups using a random number table :control group (group C , n=6 ) ,O2 inhalation group (group O , n=6 ) and isoflurane anesthesia group (group I , n=24 ) .The rats were exposed to 2% isoflurane (group I) ,to pure oxygen (group O) ,or to air (group C) for 2 h .At 2 h ,and 1 ,7 and 14 days after the rats were awake (T1-4 ) ,Morris water maze test was performed .The rats were then sacrificed and brains were removed for isolation of the hippocampus and cortex .NR1 expression was detected using SABC immuno-histochemical technique and neuronal apoptosis was determined using TUNEL .Results Compared with group C , the escape latency at T2 and total swimming distance at T1 ,2 were significantly prolonged , and the expression of NR1 in hippocampi was down-regulated at T1 ,2 in group I ,and the expression of NR1 in the cortex was down-regulated in O and I groups ( P<0.05) .There was no significant difference in the apoptosis index between the three groups ( P> 0.05 ) .Conclusion Isoflurane anesthesia can decrease the cognitive function transiently ,which is related to inhibition of up-regulation of NR1 expression in the hippocampi ,but not related to neuronal apoptosis in adult rats .

Objective To evaluate the effect of emulsified isoflurane on cognitive function in rats.Methods Seventy-two adult male SD rats,aged 8 weeks,weighing 250-300 g,were randomly divided into 3 groups:normal control group (group C,n =12),intralipid group(group E,n =12),and 8％ emulsified isoflurane group ( group EI,n =48).Morris water maze test was performed at 2 h after administration in group E and at 2 h,1,7,14 d after administration in 12 rats at each time point in group EI.The escape latency,staying time at the original platform quadrant,frequency of crossing the original platform and swimming speed were recorded.Orbital blood samples were taken from 6 rats in each group after water maze test for determination of the plasma corticosterone concentration,and then the animals were sacrificed and their hippocampi were removed for determination of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) contents.Brains were removed from another 6 rats in each group after water maze test for determination of the expression of BDNF and NGF in DG,CA3,CA2,CA1 of hippocampus.Results Compared with group C,in group EI the escape latency at 2 h after administration was prolonged,staying time at the original platform quadrant was shortened,the expression of BDNF in DG and CA3 of hippocampus was down-regulated and the BDNF content in hippocampus was decreased at 2 h and 1 d after administration( P ＜ 0.05 or 0.01).The escape latency was shortened and staying time at the original platform quadrant was prolonged at 7 and 14 d after administration,the content of NGF in hippocampus was increased at 1,7 and 14 d after administration and the expression of BDNF in DG and CA3 of hippocampus was up-regulated at 1d after administration as compared with those at 2 h after administration in group E1( P ＜ 0.05 or 0.01).There was no significant difference in the variables mentioned above between groups E and C( P ＞ 0.05 ).There was no significant difference in plasma corticosterone concentration among the 3 groups ( P ＞ 0.01 ).Conclusion The mechanism by which emulsified isoflurane results in transient cognitive impairment in rats is related to down-regulating the expression of BDNF in hippocampus,but not related to corticosterone and NGF.