Foldi Lab research
About Dr Claire Foldi
Dr Claire Foldi completed her PhD in Behavioural Neuroscience at the Queensland Brain Institute in 2012 under the supervision of Associate Professor Thomas Burne and Professor Darryl Eyles. Her doctoral thesis was focused on determining the biological plausibility of advanced paternal age as a risk factor for neurodevelopmental disorders, particularly schizophrenia and autistic spectrum disorders. Following Postdoctoral training in electrophysiology at the Karolinska Institutet in Stockholm, Sweden, she was recruited to the laboratory of Professor Brian Oldfield at Monash University in 2015. Dr Foldi now leads a program of research on anorexia and feeding disorders within the Metabolic Neurosciences Laboratory in the Department of Physiology.
Dr Foldi’s research priority is to understand the neurobiological mechanisms that underlie serious psychiatric disease. She is particularly interested in the often-unreported response heterogeneity that occurs in single neurons, animal models and patients in the clinic. She believes that interrogating the mechanisms underpinning this variability will inform the development of more effective treatment strategies.
- The roles of reward and cognitive control in susceptibility to anorexia nervosa
- The impact of a single nucleotide polymorphism in the BDNF gene on body weight maintenance and metabolic control
- Determining behavioural and immune mediators of vulnerability to pathological body weight loss
- Investigating the influence of serotonergic 2A receptor (5-HT2AR) signalling on pathological body weight loss and behaviour
Visit Dr Claire Foldi's Monash research profile to see a full listing of current projects.
1. Pathway-specific chemogenetics
In the lab, we utilise “pathway-specific chemogenetics” to selectively manipulate the activity of neural circuits and investigate how they impact on behaviour. This technique relies on the coincident injection of two constructs – a retrogradely transporting Cre vector (infused into a projection field) and Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) that are modified G-protein coupled receptors (infused into target region). We can then turn this pathway on or off in a behaving animal by administering a designer ligand, clozapine-n-oxide (CNO).
2. Validating DREADD receptor activity
We always validate DREADD receptor activity to determine the extent by which CNO changes the activity of brain circuits. We can do this at a “population level” by examining the proportion of DREADD labelled cells that also express Fos (an early marker of neuronal activation) using immunohistochemistry. We can also do this at the single-cell level, using patch-clamp electrophysiology to record the electrical activity of DREADD-expressing neurons in real time, and see how activity changes in response to CNO application.
3. In pursuit of predisposing factors
We have recently uncovered that not all “normal” (wildtype) animals are susceptible to pathological body weight loss in the activity-based anorexia (ABA) model, and see a proportion of animals that are resistant to the paradigm. We know that these resistant animals eat more food when food is available and don’t engage in excessive running on the wheel. We are now focused on identifying what causes animals to be susceptible or resistant to ABA, which could shed light on why, even in the same environment of societal pressures to be thin, only some people are vulnerable to developing anorexia nervosa.
The most well-accepted animal model of anorexia nervosa, known as activity-based anorexia (ABA), exploits the innate motivation of laboratory rats to run in wheels. When rats with access to running wheels are placed on a restricted feeding schedule, there is a paradoxical increase in running activity despite substantially decreased caloric intake, causing a profound reduction in body weight. It is important to recognise that food is only limited in terms of time and not quantity, and that animals quickly learn to increase their food intake to maintain body weight if this is the only parameter that is changed. Similarly, given access to running wheels and free access to food, they maintain their body weight well. It is only the combination of timed availability of food and access to running wheels that initiates the precipitous reduction in body weight that typifies the ABA model.
In the lab, we use the ABA model as a means to study factors that influence reward-based feeding, compulsive exercise behaviour and body weight maintenance.
Dr Foldi collaborates nationally with Professor Maarten van den Buuse (LaTrobe University) and internationally with Professor York Winter (Humboldt University, Berlin) and his R&D company PhenoSys, which provides innovative solutions for animal behaviour research. Together with Professor Brian Oldfield, Dr Foldi has also established a collaboration with Dr Paul Liknaitsky (Mind Medicine Australia) and Dr Martin Williams (PRISM). Dr Foldi's other Monash collaborators are Professor Jakob Hohwy (Head of Department, Philosophy) and Dr Adeel Razi (Turner Institute).
Click on the map to see the details for each of these collaborators (dive into specific publications and outputs by clicking on the dots).
Student research projects
The Foldi Lab offers a variety of Honours, Masters and PhD projects for students interested in joining our group. There are also a number of short term research opportunities available.
Please visit Supervisor Connect to explore the projects currently available in our Lab.