The levels of 4-hydroxy-3-methoxyphenylglycol (HMPG) and homovanillic acid (HVA), the major metabolites of, and reflecting the turnover of, noradrenaline and dopamine respectively, were estimated in the frontal cortex and striatum of cobalt-implanted rats. Previous reports showed dramatic reduction of tyrosine hydroxylase activity and compensatory reduction in catecholamine catabolising enzymes in cortical foci and striatum of this model. No significant change was found in the concentration of either metabolite in the brain regions studied. It was suggested that impairment of the saturable transport mechanism and possibly of the enzymatic conjugation of these metabolites prevented the expected reduction in their levels in those brain regions. The normal concentration of noradrenaline in cortica foci, paralleled by similar findings in the striatum could have contributed to the neuronal hyper excitability in this model. Post-mortem studies on brain tissue showed that HVA is more stable than HMPG under different conditions. These factors might have contributed to the higher HMPG levels previously reported in the cobalt model. Elaborating on the role of the dopamine system in the cobalt model of epilepsy, it was found that lysuride, apomorphine, bromocryptine and CF 25-397, that order of potency, suppressed epileptic activity in a dose-dependent manner. The chronic administration of bromocryptine attenuated the development of epileptic changes, particularly in the secondary focus. These effects were blocked by the dopamine antagonist pimozide, which itself potentiated the epileptic cortical change. This finding contrasted to the lack of effect of the anti-cholinergic.