Effects of Physiological Need States on Affect and Reward Sensitivity
thesisposted on 08.02.2018 by Jillian Leigh Seiler
In order to distinguish essays and pre-prints from academic theses, we have a separate category. These are often much longer text based documents than a paper.
It is well known that hunger alters reward sensitivity for food, which then enhances goal-directed, motivated behavior to find food. However, the mechanisms by which hunger, and other physiological need states, such as thirst, act to motivate behavior remain incompletely understood, specifically when it comes to rewards that do not act to fill the need state. The present study sought to determine the manner in which physiological signals of hunger and thirst alter reward sensitivity and motivated behavior. We attempted to capture reward sensitivity using a well-validated (Carlezon Jr & Chartoff, 2007) intracranial self-stimulation (ICSS) paradigm to determine the theoretical threshold for ICSS. We then determined how specific ‘hunger’ or ‘thirst’ mimetics altered ICSS threshold using a within-subjects design. We first attempted to confirm that our ‘hunger’ and ‘thirst’ mimetics induced feeding or drinking. We administered intracerebroventricular (ICV) infusions of ghrelin, neuropeptide Y (NPY), 5-thio-d-glucose (5TG), Angiotensin II, and vehicle (saline) and measured chow and water intake. We found that, while only NPY administration caused a significant increase in food intake, ghrelin and NPY also showed a trend toward an increase in feeding compared to saline. Next, we used threshold for brain stimulation reward (BSR) during ICSS to examine reward sensitivity before and after administration of these same compounds. We found that infusions of ghrelin, NPY, and 5TG all increased threshold for brain stimulation reward when compared to both vehicle infusions and the animals threshold values from the day preceding infusions. Finally, in order to compare these manipulations to natural hunger and thirst, we deprived animals of food or water for a 24-hour period and compared their thresholds for BSR. We found that neither 24-hour food nor water restriction had a significant effect on threshold BSR. While others have shown a decrease in threshold for BSR following food and water restriction (see Table 3), their parameters for stimulation differed greatly and most targeted the medial forebrain bundle (MFB) or lateral hypothalamus (LH) as their stimulation site, whereas this study stimulated the ventral tegmental area (VTA). It is therefore possible that stimulation to the VTA is less sensitive to natural hunger than the MFB and LH. It has been demonstrated by others that manipulations associated with negative affective states, such as withdrawal from drugs of abuse, cause an increase in threshold for BSR and those associated with positive affective states, such as cocaine use, cause a decrease in threshold for BSR (Barr, Markou, & Phillips, 2002; Carlezon Jr & Wise, 1996). Thus, the increase in BSR threshold following infusions of ‘hunger’ mimetics suggests that activation of these specific neural pathways may be aversive and generate a negative affective state. Further, artificial stimulation of these physiological pathways may not mirror natural hunger and thirst states. Future work will aim to identify the specific neural substrates that underlie changes in reward sensitivity and affective state during physiological need states.