The neural mechanisms by which stress prevents empathy in mice

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Empathy has deep evolutionary roots. It is a fundamental process required for social behaviour and allows the understanding of emotions by sharing sensory and affective states with other individuals. Even the most advanced forms of empathy in humans are built on more basic forms and remain connected to core mechanisms. Empathic responses comprise cognitive, affective, and emotional components, and are modulated by situational and contextual factors. From a neuroscientific perspective this suggests that distinct neural mechanisms underlie different types of empathy-related responses. Given the complexity of empathy, investigation of its neurobiological underpinnings would be meaningless without breaking it down into component processes. An increasing amount of evidence suggests that the core components of empathy are shared among rodents and non-human mammals and neurohormones such as oxytocin and cortisol regulate these behaviours. In fact, a number of studies have indicated that oxytocin and cortisol regulate each other to influence social behaviours, but the mechanism underlying this remains unknown. The current proposal will focus on the reciprocal modulation of the stress-related neuropeptide corticotrophin–releasing hormone (CRH) and oxytocin in regulating rodent empathy. To accomplish this, we will examine the stress response as a modifier of rodent empathy by using a combination of behaviour, chemoogenetics, electrophysiology, biochemical and immunohistochemical assessment. Specifically, we will use chemogenetics to selectively dissect specific populations of neurons and determine whether CRH and/or oxytocin neurons directly regulate each other to modify empathy and affective behaviours. In addition, we will identify the synaptic and receptor changes that occur in stress-related brain regions that prevent empathy; we will then reverse these changes with