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118. Regulation of Hypocretin by Metabolic Signals.

Author

Lecea, Luis, Sutcliffe, J. Gregor, Wortley, Katherine E., and Leibowitz, Sarah F.

Abstract

These results indicate that hypocretin/orexin neurons in the PFH are highly responsive to changes in circulating and dietary nutrients. They have similar properties to NPY/AgRP-expressing neurons in the ARC, in being stimulated by negative energy balance, such as after food deprivation, when glucose levels are declining and corticosterone and ghrelin levels are elevated. They are also similar to galanin-expressing neurons in the PVN, in being stimulated by dietary fat and circulating lipids and in exhibiting a natural rise during the first half of the circadian feeding cycle when fat ingestion normally increases. In states of both energy deficiency and elevated fat consumption, the hypocretin/orexin peptides may provide an important link between energy homeostasis and brain mechanisms coordinating sleep/wakefulness and motivated behaviors. Specifically, they may function to increase arousal and locomotor activity that facilitate food-seeking behavior under conditions of food deprivation, and they may also facilitate activity-based energy expenditure and hyperphagia under conditions of excess dietary fat intake. [ABSTRACT FROM AUTHOR]

Published
2005
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133. Prenatal Exposure to Nicotine Stimulates Neurogenesis of Orexigenic Peptide-Expressing Neurons in Hypothalamus and Amygdala.

Author

Guo-Qing Chang, Karatayev, Olga, and Leibowitz, Sarah F.

Subjects
APPETITE stimulants, PHYSIOLOGICAL effects of nicotine, DEVELOPMENTAL neurobiology, NEURONS, HYPOTHALAMUS, AMYGDALOID body, CELL proliferation
Abstract

Animal and clinical studies show that gestational exposure to nicotine increases the propensity of offspring to consume nicotine, but the precise mechanism mediating this behavioral phenomenon is unclear. The present study in Sprague Dawley rats examined the possibility that the orexigenic peptide systems, enkephalin (ENK) and orexin (OX), which are stimulated by nicotine in adult animals and promote consummatory behavior, may be similarly responsive to nicotine's stimulatory effect in utero while having long-term behavioral consequences. The results demonstrated that nicotine exposure during gestation at low doses (0.75 or 1.5 mg/kg/d) significantly increased mRNAlevels and density of neurons that express ENK in the hypothalamic paraventricular nucleus and central nucleus of the amygdala, OX, and another orexigenic peptide, melanin-concentrating hormone, in the perifornical lateral hypothalamus in preweanling offspring. These effects persisted in the absence of nicotine, at least until puberty. Colabeling of the cell proliferation marker BrdU with the neuronal marker NeuN and peptides revealed a marked stimulatory effect of prenatal nicotine on neurogenesis, but not gliogenesis, and also on the number of newly generated neurons expressing ENK, OX, or melanin-concentrating hormone. During adolescence, offspring also exhibited significant behavioral changes, increased consumption of nicotine and other substances of abuse, ethanol and a fat-rich diet, with no changes in chow and water intake or body weight. These findings reveal a marked sensitivity during gestation of the orexigenic peptide neurons to low nicotine doses that may increase the offspring's propensity to overconsume substances of abuse during adolescence. [ABSTRACT FROM AUTHOR]

Published
2013
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