Postdoc, University of California San Diego
Anhedonia is the inability to experience pleasure and is a core symptom in neuropsychiatric disorders, such as major depressive disorder (MDD) and schizophrenia (SCZ). The prefrontal cortex (PFC) is implicated in anhedonia due to imbalances in dopamine (DA) concentrations. Dopamine in the PFC has been implicated in processing negatively valence stimuli (Vander Weele et al., 2018), and can produce avoidance (Gunaydin et al., 2014), but is suggested to be a major component in reward prediction (Schultz et al., 1997), indicating that DA modulates mPFC encoding of both positive and negative valence in behavior. However, it remains unknown how DA modulates mPFC valence-specific neurons during anhedonia. We hypothesize that mPFC valence-specific neuronal populations are differentially regulated via DA transmission and are altered during stress-induced anhedonia. To study this, we implemented the learned helplessness (LH) protocol to induce anhedonia within mice. Using in vivo 2-photon Ca2+ imaging techniques, we examined mPFC-valence specific neuronal population activity within anhedonic mice. These findings will provide a greater understanding of the activity and dynamics in mPFC valence-specific neuronal populations during anhedonia.