Nomenclature of eukaryotic DNA polymerases

vious experiment (Table 1). It could be argued that after a nearly complete depletion of norepinephrine an additional small and undetectable decrease in norepinephrine might surpass some critical threshold and lead to the release of eating. However, if this were true we would also expect this threshold would have been surpassed in at least some of the more than 150 rats in our laboratory which have undergone VNAB destruction via 6-OH-DA injection or electrolytic lesions in previous experiments. In actuality, seven of the eight animals in the combined lesion group ate more food per day than any of the previous VNAB animals studied in this laboratory. Our results would explain why Gold's (5) most effective hypothalamic lesions coincided with the distribution of the ventral bundle. Lesions in the medial hypothalamus that destroy portions of the diffuse projections of the VNAB should lead to exceptional hyperphagia such as that observed with dual lesions in the present study. Thus, medial hypothalamic hyperphagia and ventral bundle hyperphagia are separable phenomena; the evidence is: (i) norepinephrine loss caused hyperphagia only at night and less hyperphagia overall, (ii) hypothalamic lesions caused overeating without norepinephrine depletion, and (iii) the two forms of destruction combined produced a level of hyperphagia equal to