Abstract: Objective To study the effect of maternal iodine deficiency and hypothyroid on activity of protein kinase C (PKC) and the expression of c-fos and c-jun in hippocampus of offspring rats and to explore the mechanism of iodine deficiency in brain development.Methods The rat models of iodine deficiency and hypothyroid were established by pre-treatment with thiamazole and shortage of iodine in feed,respectively.PKC activities in the brain cytoplasm and cell membrane of iodine dificiency,hypothyroidism and control rats were measured.The expressions of c-fos and c-jun in hippocampus tissue on postnatal day 30 were detected by means of S-P immunohistochemical technique and micrograph analysis system.Results The PKC activity of cytoplasm in iodine deficiency and hypothyroidism groups was lower than that of the control group and the PKC activity of cell membrane was higher than that of the control group.As compared to age-matched controls(0.6493±0.2943),iodine deficiency and hypothyroidism led to a significantly higher ratio of membrane PKC activity to that in cytosol (1.1871±0.4325,1.4143±0.3940) (P< 0.01).The means of average gray value of c-fos and c-jun in the iodine deficiency and hypothyroid groups on postnatal day 30 were significantly higher than those in the control group (P<0.01).Conclusion Maternal shortage of iodine and hypothyroidism during development may lead to translocation of the PKC from cytoplasm to plasmalemma and impair the expression of both c-fos and c-jun of the offsprings,and may influence the developments of nerves and intelligence.It may result in some damages of hippocampus and decline of study and memory.