Histochemical and pharmacological analysis of catecholaminergic projections to the perifornical hypothalamus in relation to feeding inhibition.

Three techniques, namely, midbrain lesions, fluorescence histochemistry and brain cannulation, were used in combination to analyze catecholamine (CA) projections to the perifornical hypothalamus and their function in suppressing feeding behavior. The convergence of evidence indicates that the ventral adrenergic component of the central tegmental tract and dopaminergic projections from midbrain A8 and possibly A9 cell groups contain the crucial fibers which innervate the perifornical hypothalamus and mediate CA suppression of feeding behavior. The primary evidence for this conclusion is that ventral tegmental electrolytic or 6-OHDA lesions which damaged specifically these fibers invariably caused: (1) a marked reduction of CA varicosities in the perifornical area; (2) a strong reduction or loss of the anorectic response produced by perifornical injection of the presynaptically acting drugs amphetamine and mazindol; and (3) a potentiation of the anorectic response produced by perifornical injection of the CA receptor agonists dopamine and epinephrine. Lesions in the dorsal midbrain tegmentum, which left intact the ventral adrenergic and dopaminergic fibers but damaged the compact dorsal tegmental bundle, the dorsal fibers of the central tegmental tract and the medial and lateral tegmental CA radiations, had no apparent effect on the responsiveness of the perifornical hypothalamus to CA drug stimulation, as well as on the CA fluorescence in that region. Lesions in the area of the dopaminergic A10 cells and the midline tegmental CA radiations actually potentiated the effectiveness of the anorexigenic drugs in the perifornical hypothalamus.