Effect of perinatal thyroid hormone deficiency on expression of rat hippocampal conventional protein kinase C isozymes.

Thyroid hormone (TH) is essential for the proper development of mammalian central nervous system. TH deficiency during critical period of brain development results in permanent cognitive and neurological impairments. Hippocampus is a structure involved in various memory processes that are essential for creating new memories, and lesions to hippocampus result in impaired learning and memory. Protein kinase C (PKC) isoforms play an important role in many types of learning and memory, and deletion of specific PKC genes results in deficits in learning. In the present study, we used real-time PCR and Western blot to investigate the conventional PKC expression in developing rat hippocampus with different thyroid status, trying to establish a correlation between TH deficiency and conventional PKC expression in developing rat hippocampus. We found that PKCβI and PKCγ expression decreased significantly both in mRNA and protein levels in hypothyroid group compared with the normal controls, and thyroxine replacement could restore it. As for PKCα, we did not find any difference between different thyroid status. Though the expression of PKCβII also decreased in the TH deficiency group, the change was not significant. Taken together, our data indicate TH deficiency can cause hippocampal PKCβ1 and PKCγ downregulation during rat brain development. Since there are other PKC isoforms in the rat brain, whether these change is related to impaired learning and memory of perinatal hypothyroid rats requires further researches.