Three techniques, namely, midbrain lesions, fluorescence histochemistry, and brain cannulation, were used in combination to analyze noradrenergic projections to the paraventricular nucleus of the hypothalamus (PVN) and their function in stimulating feeding behavior. The convergence of evidence indicates that the dorsal component of the central tegmental tract (CTT), which ascends through the dorsal pons and then projects through the medial tegmental radiations (TR) into the ventral tegmentum just dorsal to the media lemniscus, contains the crucial noradrenergic axons which innervate the PVN and mediate noradrenergic stimulation of feeding behavior. The primary evidence for this conclusion is that dorsal tegmental electrolytic or 6-OHDA lesions which damaged specifically these fibers invariably caused: (1) a reduction of catecholamine varicosities within the PVN (most notably, fine and moderate-size, rounded varicosities within the parvocellular area); (2) a strong reduction or loss of the feeding response elicited by PVN injection of the presynaptically-acting drugs tranylcypromine and desipramine; and (3) a potentiation of the same response produced by injected norepinephrine. These pharmacological and neurochemical changes in the PVN were reduced in magnitude if the dorsal CTT and medial TR fibers received only partial damage, and these changes did not occur at all if the lesion fell immediately dorsal to these fibers without damaging them. Specific lesions in the ventral tegmentum, which also failed to damage the dorsal CTT and TR axons but instead damaged the ventral component of the CTT, not only failed to disrupt the action of the antidepressant agents but actually potentiated their effectiveness in the PVN. Ventromedial lesions, however, which severed the rostroventral extension of the dorsal CTT and medial TR fibers, had the same behavioral consequences as had the dorsal lesions which damaged this projection at a more dorsocaudal level. Finally, damage to other catecholamine projections had little effect on PVN function in stimulating eating.