Making Sense of Rodent Models of Anhedonia

Abstract

A markedly reduced interest or pleasure in activities previously considered pleasurable is a main symptom in mood disorder and psychosis and is often present in other psychiatric disorders and neurodegenerative diseases. This condition can be labeled as “anhedonia,” although in its most rigorous connotation the term refers to the lost capacity to feel pleasure that is one aspect of the complex phenomenon of processing and responding to reward. The responses to rewarding stimuli are relatively easy to study in rodents, and the experimental conditions that consistently and persistently impair these responses are used to model anhedonia. To this end, long-term exposure to environmental aversive conditions is primarily used, and the resulting deficits in reward responses are often accompanied by other deficits that are mainly reminiscent of clinical depressive symptoms. The different components of impaired reward responses induced by environmental aversive events can be assessed by different tests or protocols that require different degrees of time allocation, technical resources, and equipment. Rodent models of anhedonia are valuable tools in the study of the neurobiological mechanisms underpinning impaired behavioral responses and in the screening and characterization of drugs that may reverse these behavioral deficits. In particular, the antianhedonic or promotivational effects are relevant features in the spectrum of activities of drugs used in mood disorders or psychosis. Thus, more than the model, it is the choice of tests that is crucial since it influences which facets of anhedonia will be detected and should be tuned to the purpose of the study.

Changes in brain kynurenine levels via gut microbiota and gut‐barrier disruption induced by chronic ethanol exposure in mice

“…Similarly, antibiotic treatment reverses both the plasma LPS increase and the depressive-like phenotype caused by chronic mild stress, a well-established murine model of depression (36). In line with such evidence, we observed that the CI EtOH paradigm produced anhedonia that correlates with depressive-like symptoms in rodent models (107,108) and in which the microbiota appears to play a role. This anhedonia may be related to the elevation in brain Kyn because, just as antibiotic treatment prevented the CI EtOH-induced elevation of brain Kyn, it also returned the sucrose preference to control values.…”

Targeting PPARα in the rat valproic acid model of autism: focus on social motivational impairment and sex-related differences

“…g Two-way ANOVA, VPA exposure: F 1,24 = 1.75, n.s. ; FBR administration: F 1,24 = 4.97, p = 0.0354; interaction: NAcS play a crucial role in reward processing [37,38] as well as in the modulation of social behavior [39][40][41], and repeated treatments that relieve motivational anhedonia in rat models of depression also restore the dopaminergic response to rewarding stimuli in the NAcS [5,15,31,42]. Thus, we tested whether the social deficits induced by VPA exposure were accompanied by an impaired dopaminergic response to social reward, and whether both deficits were rescued by FBR administration from weaning to young adulthood.…”

Chronic Jet Lag Simulation Decreases Hippocampal Neurogenesis and Enhances Depressive Behaviors and Cognitive Deficits in Adult Male Rats

“…The present study used multiple behavioral measures to examine the impact of chronic phase shifts on depression and anxiety. Anhedonia (i.e., diminished interest or pleasure in all or most activity most of the day) is a core diagnostic symptom of depression and can be readily modeled in rodents using the sucrose consumption test (Scheggi et al, 2018). Reduced sucrose consumption is taken as a measure of anhedonia; an interpretation validated by the demonstration that the same rats do not exhibit reduced consumption to water (Papp et al, 1991;Matthews et al, 1995).…”