Although iodine deficiency has primarily been implicated in the causation of goitre, the significant role played by food goitrogens in the etiology of iodine deficiency disorder (IDD) is being increasingly recognized. Impaired brain development is the major cause of concern in IDD. Detailed experimental studies were undertaken to ascertain various biochemical changes associated with developing brain in response to treatment with a goitrogens--thiocyanate. Addition of thiocyanate to food deprived of KI brought down significantly the circulating levels of thyroxine (T4) in rats. Nucleic acids and protein content in different regions of brain were significantly lowered in rat pups exposed to thiocyanate. The rate of microtubule assembly, which is detrimental for neurite growth was considerably lowered, thereby influencing both myelin deposition and synaptogenesis in developing brain. Goitrogen intake not only caused an adaptive increase in the activity of type II 5'-deiodinase, which governs availability of triiodothyronine (T3) in brain, it also increased the latter's binding to brain nuclear receptors under conditions of thiocyanate induced hypothyroid state. Addition of adequate quantities of KI mitigated thiocyanate induced alterations by restoring circulating level of thyroxine. These investigations suggest that goitrogens play a significant role in influencing biochemical events unique to developing brain.