Abstract

Although assessing hedonic responses in nonverbal animals can be difficult, one relatively tractable approach comes from detailed analyses of rodents’ consummatory behaviour – either through licking microstructure or “taste” reactivity testing methods. My first example of applying these techniques comes from the study of taste aversion learning. This is most typically characterised as a “special” and highly selective evolved mechanism for poison avoidance. However, evidence for disgust reactions elicited by non-taste contextual stimuli, and the blocking of taste-nausea learning by contextual cues, directly questions this view. Moreover, further evidence for the unique features of conditioned disgust might explain the persistence of the received wisdom on taste aversion learning. My second example comes from the study of rodent models of human psychiatric disorders. Here, the evidence questions the completeness of some putative psychosis models, as well as providing new avenues for exploring aspects of affective disturbance linked to dementia. In short, hedonic responses are critical in many aspects of behaviour, and assessing them can provide information about the general affective state of animals and the particular learning processes they exhibit.

Since completing my PhD studies in Cambridge in 1999, and moving to Cardiff University in 2002, one major strand of my research involves the assessment of hedonic responses in rodents. Animal models are of critical importance in investigating the underlying biological contributions to many human disorders such as dementia, depression or schizophrenia. To fully understand these animal models we require ways to assess how animals feel, as well as how they think. As it happens, a detailed examination of the way in which rodents drink is particularly informative with respect to how much they like what they are drinking. My lab currently applies these techniques to investigate how animals learn to like and dislike particular foods and also how such hedonic processes are disrupted (or not) in animal models of human disorders, in particular dementia and schizophrenia.