In New Zealand rats are predators of native and introduced flora and fauna, with anticoagulants being the most commonly used rodenticides. However, with the development of anticoagulant resistance worldwide, and the increasing requirements for more humane and effective methods to control wild rat populations, there is an incentive to identify rat-specific and humane rodenticides. Landcare Research is developing a highly specific rodenticide (rat specific toxin; RST), for use in field conditions. Norbormide, which is similar to RST, has previously been shown to have high efficacy and supposedly a humane mode of killing, but it has a low acceptance by rats. This series of studies was conducted to assess the palatability of RST, gain insights into the mechanism(s) of low palatability, increase efficacy with the use of a synergist and finally to assess histological lesions in the possible target organs. Combination of RST with Bitrex, a masking agent, did not improve palatability in wild Norway rats and hence the mortality rates (15%) were low. Adenosine monophosphate was then used in an attempt to block the bitter taste of RST in laboratory Norway rats. The results from this experiment suggested that the low acceptance of RST may be due to mechanisms other than the bitter taste. If palatability could not be improved, it was thought that the use of a synergist, p-aminopropiophenone (PAPP), a methaemoblogin (MtHb) forming drug, could be used in combination with RST to improve the efficacy of RST. PAPP did not prove to be a successful synergist. No mortality was recorded, even when the MtHb concentrations reached as high as 80%. Rats were probably capable of converting MtHb back to haemoglobin via an active MtHb reductase. The exact mode of action of RST or norbormide is unknown. The final experiment involved perfusion of the rat with neutral-buffered formalin to study the changes to vital organ tissues such as the heart, brain and liver. Gross and histopathological examination of the brain and liver tissue did not show any major lesions. Gross examination of the heart of RST-treated rats revealed that RST may act by arresting the heart in systole. A microscopic examination of the heart did not reveal any significant lesions, except for a possible constriction of arterioles. The results from this experiment suggested that the toxic effects of RST are on the cardiovascular system - with cardiac arrest, the heart loses its ability to circulate oxygen to the vital organs and the rat inevitability dies from hypoxia and lack of energy. Further work is required to elucidate the exact mode of action of RST and also reasons for its low palatability