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Chronic pain is not only a sensory experience; it also affects overall quality of life by profoundly increasing fatigue, depression and anxiety. A common feature of these symptoms is a lack of enjoyment of spending time with others and participating in social activities. Under normal circumstances social encounters are naturally rewarding(9) and these interactions activate the same neural regions as those required for drug rewards. It is well known that chronic pain changes the brain circuits involved in reward processing, however, whether these changes alter social reward, decrease social motivation or result in depression/anxiety remains largely unexplored. One aspect of our current research offers the perspective of bridging two very important fields of neuroscience – pain and emotions – in order to determine how chronic pain rewires the brain to profoundly alter sensory and emotional experiences.
Empathy has deep evolutionary roots. It is a fundamental process 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. We are currently interested in the synaptic, protein and genetic level modifications that underlie empathy and the affective communication of pain and we use behaviour, molecular biology, immunohistochemistry and electrophysiology in all of our experiments.
It has been suggested that one of the greatest risk factors for the development of chronic pain may be concurrent or past pain. However, the anxiety of impending pain, and not the pain itself, may be more crucial in determining whether pain sensitivity is altered. Behaviours associated with pain may not be intrinsic to the stimulus of pain, but may be a response to environmental reinforcers. This is in line with learning processes such as conditioning whereby a previously experienced stimulus (i.e. acute pain) reliably predicts future behaviours (i.e. fear responses). In humans, psychological factors such as stress, anxiety and expectation play an important role in shaping pain perception, and in the clinic, when pain is anticipated, patients often report heightened pain sensations. We are currently developing a mouse model of pain memory that can be used to assess altered pain responses when pain is anticipated. In this model we use the experience of prior pain to alter nociceptive sensitivity and examine the influence of environmental variables. This paradigm is quite different from commonly used conditioned fear paradigms in that it doesn’t measure behavioral fear responses (i.e. freezing), but rather a conditioned change in pain sensitivity itself.