Investigating the Role of LPS-Induced Neuroinflammation as a Potential Mechanism of Anhedonia
Anhedonia, a deficit in reward processing, is a characteristic of many neuropsychiatric conditions including eating disorders, schizophrenia, substance use disorder and major depressive disorder (MDD) (American Psychiatric Association, 2013). Literature suggests a relationship between inflammation and MDD, as individuals with MDD have increased levels of pro-inflammatory cytokines (Zunszain et al., 2012). The relationship between MDD and inflammation has been studied, however inflammation and anhedonia has been studied less extensively. The goal of the current study was to investigate the relationship between neuroinflammation, induced by lipopolysaccharide (LPS) administration, and anhedonia in rats using the probabilistic reward task (PRT). In this task, rats learn to discriminate between two ambiguous stimuli for a sucrose reward. During testing, one lever is rewarded three times more than the other lever. Similar to humans, rats develop a response bias for the stimuli that is rewarded more frequently regardless of the tone that was presented. Seven days following LPS administration, rats were tested in the PRT: both SAL- and LPS-treated animals developed a response bias. The results did not indicate a deficit in reward learning in LPS-treated animals, however this does not mean that a relationship between inflammation and anhedonia does not exist. Systemic LPS administration to induce neuroinflammation may not be a successful model when testing for anhedonia. Future studies investigating the relationship between inflammation and anhedonia may need to use other models of inflammation in order to examine this relationship.