The word hedonism originates from the Greek word hēdonē, meaning "pleasure." Ancient Greek philosophy described theories and lifestyles centred on the pursuit of pleasure as the highest good. Today, hedonism is often equated with indulgence in wild parties, excessive drinking, and unrestrained sensuality.
However, philosophical hedonism, particularly as advocated by thinkers like Epicurus, emphasises a measured and thoughtful pursuit of pleasure, prioritising long-term happiness and peace of mind over short-term gratification.
In medical science, the connection between hedonism and rewards lies in the brain's reward system, which governs our experience of pleasure and motivation. The brain's reward system is primarily mediated by regions like the ventral striatum, amygdala, and prefrontal cortex, with neurotransmitters like dopamine playing a central role.
Medical science has already identified “anhedonia”—the diminished drive to seek, value, and learn about rewards—as a core feature of major depressive disorder. Meanwhile, the neural underpinnings of anhedonia and how this emotional state drives behaviour have remained unclear so far.
Read the study here | Understanding the neural code of stress to control anhedonia
Study on the neural basis of anhedonia
Recently, researchers from the US published a study in Nature investigating the neural basis of anhedonia. They conducted the study based on the fact that when mice are exposed to traumatic social stress, susceptible animals become socially withdrawn and anhedonic, whereas others remain resilient.
The researchers performed high-density electrophysiology to record neural activity patterns in the basolateral amygdala (BLA) and ventral CA1 (vCA1)—regions of the brain involved in processing emotions, memory, and behaviour—to identify the neural signatures of susceptibility and resilience.
In resilient mice, the BLA showed clear patterns distinguishing between reward choices. In susceptible mice, however, the BLA displayed a "rumination-like" pattern, focusing on whether to stick with or switch to a previous choice. This meant those mice susceptible to stress had impaired decision-making linked to stress.
Notably, when the researchers manipulated the vCA1 inputs to the BLA in susceptible mice, they could rescue dysfunctional neural dynamics, amplify dynamics associated with resilience, and reverse anhedonic behaviour.
At rest, the BLA of susceptible mice also showed more distinct neural states, which helped predict their stress history better than behavioural outcomes alone. The study proves that there are individual differences in responses to traumatic stress. However, the promising factor is that modulating vCA1–BLA inputs may help to enhance resilience.
