A Classic Innate Behavior, Sodium Appetite, Is Driven by Hypothalamic Gene-Regulatory Programs Previously Linked to Addiction and Reward

Excerpt

Instinctive behavior is intricately linked to organismal homeostasis and species survival (Denton et al. 1996, 2009; Lehrman 1953; Richter 1956). Instincts are embodied by the brain, in particular, the hypothalamus. The classic instinct of sodium appetite is commonly evoked by depletion, that is, lack of appropriate intake in the face of sodium loss, further by adrenocorticotropic hormone (ACTH) acting on the suprarenal cortex to produce gluco- and mineralocorticoids, which act on the brain, and associated with reproduction in pregnancy and lactation (Blair-West et al. 1995; De Luca et al. 2010; Denton et al. 1999; Johnson and Thunhorst 1997; Fitzsimons 1998; Morris et al. 2008; Na et al. 2007; Roitman et al. 1997; Wolf 1964). In a recent publication (Liedtke et al. 2011), we have elucidated gene-regulatory programs in the hypothalamus as underlying sodium appetite. Furthermore, we were able to attenuate sodium intake behavior of sodium appetite by application of antagonists of dopamine receptor-1 (DRD1) both systemically as well as by microinjection into the lateral hypothalamus. This chapter will elucidate these results and discuss them in a number of contexts not covered in the original publication. In the original report, the term “gratification” is used throughout. This refers to the subjective sentiment of feeling gratified after satiation of an instinctive craving—in this context, sodium appetite and thirst for water—but in a general sense applicable to any instinct. Gratification, it can be argued, is difficult to verify in a setting of animal experimentation. However, its use to describe animal behavior by veteran researchers in the field is noteworthy and should be respected.