Intermittent nicotine administration modulates food intake in rats by acting on nicotine receptors localized to the brainstem.
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abstract
Previous studies have shown nicotine (NIC) administration leads to decreased food intake, while other investigations have reported that NIC stimulates c-Fos expression in the brainstem. Whether there is a causal relationship between NIC effects on ingestion and its effect on brainstem neurons is uncertain, however we hypothesized that blocking NIC action in the brainstem would prevent, to some extent, the hypophagic effects of NIC. In the present study, cannulas were placed in the fourth ventricle of rats. A dose of NIC or saline was injected i.p. in four equal injections during the dark phase for four days. At the start of the second day of injections the NIC receptor antagonist mecamylamine (MEC) or artificial cerebrospinal fluid (a-CSF) was infused intracerebroventricularly (i.c.v.). Thus, four experimental groups were examined: a-CSF + SAL; a-CSF + NIC; MEC + SAL; MEC + NIC. Meal patterns were recorded using a computerized system and water intake and body weight were measured daily. Peripheral NIC injections suppressed food intake by decreasing meal size, whereas infusion of the NIC receptor antagonist MEC (4 microg) into the fourth ventricle blocked the NIC suppression of food intake. Moreover, the MEC effect was due primarily to an increase in dark phase meal size, which suggests neurons localized to the brainstem transmit NIC signals that regulate feeding behavior by affecting meal size.
