Congenital iodine deficiency and hypothyroidism impair LTP and decrease c-fos and c-jun expression in rat hippocampus

NeuroToxicology

Volumn 26, Issue 3, 2005, Pages 417-426

  Dong, Jing ^a   Yin, Hongbo ^b   Liu, Wanyang ^a   Wang, Ping ^b   Jiang, Ying ^a   Chen, Jie ^a  

^a CHINA MEDICAL UNIVERSITY   (China)

^b Shenyang Center for Disease Control and Prevention   (China)

Author keywords

Brain development; Cognitive function; Hypothyroidism; IEG; Iodine deficiency; Synaptic plasticity

Indexed keywords

IODINE; PROTEIN C FOS; PROTEIN C JUN; THIAMAZOLE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BRAIN DEPTH STIMULATION; BRAIN DEVELOPMENT; CONTROLLED STUDY; EXPOSURE; HIPPOCAMPUS; HYPOTHYROIDISM; IODINE DEFICIENCY; LACTATION; NERVE CELL PLASTICITY; NEWBORN; NONHUMAN; PERINATAL PERIOD; POSTSYNAPTIC POTENTIAL; PREGNANCY; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; SPIKE WAVE;

AGING; ANIMALS; ANIMALS, NEWBORN; BODY WEIGHT; DEFICIENCY DISEASES; ELECTROPHYSIOLOGY; GENE EXPRESSION; GENES, FOS; GENES, JUN; HIPPOCAMPUS; HYPOTHYROIDISM; IMMUNOHISTOCHEMISTRY; IODINE; LONG-TERM POTENTIATION; RADIOIMMUNOASSAY; RATS; RATS, WISTAR;

EID: 20344369755     PISSN: 0161813X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neuro.2005.03.003     Document Type: Article

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