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Removal of norepinephrine and/or epinephrine signaling in the perifornical hypothalamus attenuates nicotine's hypophagic action

Previously we reported (Guan et al., Life Sci. 74:2725–2737, 2004) that intermittent nicotine (NIC) in the dark phase altered meal patterns, attenuated food intake and suppressed body weight. Infusion of the NIC receptor antagonist, mecamylamine (MEC), into the fourth ventricle attenuates the hypophagic action of i.p. administered NIC. One potential action of MEC is blocking NIC receptors on norepinephrine (NE)/epinephrine (EPI) producing C2/C3 neurons adjacent to the fourth ventricle. C2/C3 neurons project axons to the perifornical hypothalamus (PFH) region. We hypothesize that EPI released from C2/C3 neuronal axons binds adrenergic receptors in the PFH modulating neuronal activity that subsequently affects feeding. To test this hypothesis, bilateral PFH lesions were made using 4 μg of 6‐OHDA hydrobromide (free base) in a volume of 0.3 μl. The animals were pretreated by injecting i.p. pargyline to enhance the lesion effect and bupropion HCl to protect dopamine neurons 30 minutes prior to 6‐OHDA infusion. Controls received sham operations. Cannula placement and infusion was verified histochemically. After recovery of the pre‐surgery body weights the animal's food intake was recorded before and after NIC injection. NIC injection altered meal patterns and attenuated body weight, but after lesioning the PFH NIC did not alter meal patterns or attenuate body weight. This suggests that the PFH is necessary, in part, for NIC to alter meal patterns and body weight.