Drugs that affect peripheral adrenergic neurotransmission were injected via implanted cannulas into the perifornical region near the posterior part of the anterior hypothalamus of satiated rats, in order to test the hypothesis that in this part of the hypothalamus particularly norepinephrine (NE) functions as a modulator of the neural system involved in regulating eating behavior. The data show that a standard injection of 20 mμ moles of NE, a compound which specifically activates alpha receptors, consistently elicited eating in satiated rats, while doses from 10-150 mμ moles of isoproterenol, a specific activator of beta receptors, did not. Forty and 120 mμ moles propranolol, an adrenergic beta-receptor blocking agent, had no effect on the eating produced by NE but 40 mμ moles of phentolamine, an adrenergic alpha-blocking agent, completely prevented this eating response to NE. Twenty mμ moles of epinephrine elicited significantly more eating than did 20 mμ moles of NE. Neither serotonin (20 mμ moles) nor dopamine (20 or 100 mμ moles) elicited prompt eating, although there was a suggestion of a delayed effect to dopamine, which is a precursor of NE. Desmethylimipramine (400 mμ moles) and lidocaine, inhibitors of the reuptake of NE into the presynaptic terminal, potentiated at least 8-fold the action of 5 mμ moles of NE. The monoamine oxidase inhibitor nialamide (200 mμ moles) elicited eating behavior when followed by 100 mμ moles of tetrabenazine, a substance which blocks the incorporation of free NE in the granules. As would be expected, the reverse sequence of these drugs did not elicit eating. These results are interpreted as strong support for the hypothesis that a specifically adrenergic hypothalamic system is involved in the eating behavior of the rat. © 1969.
