KIF17 mediates the learning and memory impairment in offspring induced by maternal exposure to propofol during middle pregnancy

Abstract

Preclinical studies suggest that propofol may cause neuronal injury to the developing brain. A previous study demonstrated that, in a rat model, maternal exposure to propofol during early or late pregnancy caused learning and memory impairment in the offspring. However, whether propofol exposure during middle pregnancy can cause long‑term behavioral deficits in the offspring remains to be elucidated. N‑methyl‑D‑aspartate receptor 2B subunit (NR2B) serves a critical role in memory modulation. To exert its function, NR2B must be transported to the neuronal membrane by kinesin family member 17 (KIF17). The aim of the present study was to investigate the role of KIF17 in learning and memory impairment in rat offspring caused by propofol exposure during middle pregnancy. Pregnant rats were exposed to propofol on gestational day 14 (G14) for 4 and 8 h, with control pregnant rats receiving an equal volume of normal saline. The learning and memory of the offspring was assessed using Morris water maze tests from postnatal day 30 (P30) to P36. The levels of KIF17 protein, total NR2B (T‑NR2B) and membrane NR2B (M‑NR2B) in the hippocampus were detected using western blotting. The results demonstrated that propofol exposure caused learning and memory deficits and decreased KIF17 and M‑NR2B protein levels in the hippocampus; however, no but changes in the expression of T‑NR2B were observed. These results indicate that maternal propofol exposure during middle pregnancy impairs learning and memory in offspring rats by suppressing the expression of KIF17 and inhibiting the translocation of NR2B to the neuronal membrane.

Effects of Maternal Abdominal Surgery on Fetal Brain Development in the Rabbit Model

“…This concern was based on preclinical evidence. Both in newborn and pregnant animals, it has been shown that repeated or prolonged exposure to virtually all commonly used anesthetics causes apoptotic neurodegeneration in the developing brain, resulting in persisting neurocognitive impairments [6][7][8][9][10][11][12][13]. Several retrospective clinical studies suggest that in young children, anesthesia exposure could be associated with structural brain deficits that result in developmental disorders later in life [14][15][16][17][18][19].…”

Suberoylanilide Hydroxamic Acid Attenuates Cognitive Impairment in Offspring Caused by Maternal Surgery during Mid-pregnancy

“…Twenty mg/kg propofol (200 mg/20 ml, jc393, Diprivan, AstraZeneca UK Limited, Italy) was injected into the pregnant rats in the Propofol group or Surgery group via the IV catheter followed by 20 mg.kg-1.h-1 of continuous infusion for 4 hours after loss of right reflex. The dosage of anesthesia induction and the maintenance of propofol were selected based on our previous study [27, 28] . The pregnant rats in control group were received equal volume of 20% intralipid instead of propofol.…”

Suberoylanilide hydroxamic acid attenuates cognitive impairment in offspring caused by maternal surgery during mid-pregnancy

“…Propofol exposure was conducted as in we previous report [28]. On day E14, a 24-gauge intravenous (IV) catheter was placed into the pregnant rat's lateral tail vein.…”

“…Twenty mg/kg propofol (200 mg/20 ml, jc393, Diprivan, AstraZeneca UK Limited, Italy) was injected into the pregnant rats in the Propofol group or Surgery group via the IV catheter followed by 20 mg.kg-1.h-1 of continuous infusion for 4 hours after loss of right reflex. The dosage of anesthesia induction and the maintenance of propofol were selected based on our previous study [27,28]. The pregnant rats in the control group received an equal volume of 20% intralipid instead of propofol.…”