Results of Animal Model Studies

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It may be that any peripherally adversive stimulus — especially one that stimulates sympathetic activity — thus has the potential to activate brain areas of prime importance in the formation of anxiety symptoms. As a result of pharmacological challenge studies, biochemical assays, neuroimaging and studies of animal models, a number of centrally acting neurotransmitters, and their relevant neural circuits, are implicated in anxiety. These neurotransmitters include norepinephrine, serotonin, GABA, neuropeptide Y, cholecystokin and substance P. 

For most chemical substances, useful and relevant human data are not available. The risk assessment is therefore most often based on studies in experimental animals. The results of animal studies are used to predict the possible effect in humans, i.e., effects in animals are used to model corresponding effects in humans. Animal data are also used as a supplement to human data, which are equivocal, or to identify the active substances in a mixture to which humans have been exposed. 

The use of animal models for breast cancer allows control of single dietary variables. In such studies, diets high in fat have increased the incidence of spontaneous (19-22), chemically induced (23-26), and radiation-induced mammary tumors (27), and enhanced the growth of transplantable breast tumors (28-31). The effects of protein on breast cancer have not been studied as extensively, and the results have been less consistent. Several investigators have found no effect from increasing dietary protein (32,33), whereas others have noted a stimulation (34,35) or an inhibition of mammary tumori-genesis (36,37). 

The aim of this study was to determine, as a proof of concept, if DMXB-A significantly improves neurocognition and to assess, by effects on P50 inhibition, whether its actions are consistent with activation of oc7-nicotinic receptors. Because the proposed effect is agonism at a ligand-gated ion channel, biological effects were expected immediately, consistent with the results from animal models (Stevens et al., 1998). Twelve persons with schizophrenia consented to the study. They were concurrently treated with neuroleptic medications. Subjects who had not used nicotine or tobacco within the last month were selected to avoid possible interaction with chronic nicotine exposure. DMXB-A was administered orally (150 or 75 mg) followed 2 h later by a half dose (75 or 37.5 mg). The half dose, administered at the predicted half-life of the... 

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