Neuroplasticity and Pain

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Acute (physiological) nociceptive pain is protective and helps us to deal with potentially threatening or damaging environmental stimuli. However, pain is not always considered adaptive and beneficial to our survival. Pain can become chronic and can also become very resistant to pain medicine in the present drug arsenal. Finding out which molecular and cellular mechanisms are involved in the transition from acute to chronic pain and/or the ability to mediate chronic pain itself is expected to result in an improved pain management as it allows for mechanism-based treatment approaches. This course covers the basic understanding of nociceptive signaling. Moreover, it will be discussed how nociception can be modulated. Conditions of pain amplification will be then be discussed with particular attention to neuropathic pain and post-surgical pain. Peripheral and central sensitization will be discussed as processes of molecular neuroplasticity, which lays the foundation for amplification of nociceptive signaling under pathological conditions. In the last decade, it has become clear that neuro-inflammation and particularly the activation of non-neuronal cells such as central glia (microglia and astrocytes) contribute largely to amplification of pain (e.g. chronic pain) during such pathological conditions. Glial activation, via release of pro-inflammatory factors and other neuroactive mediators, is an important contributor to neuroplasticity and includes central sensitization. A better understanding of processes of neuro-inflammation and neuroplasticity in conditions of chronic pain are thought to aid in development of novel, more effective pain therapies. This course is subdivided into three parts. The first part focuses on nociceptive and inflammatory pain, discussing processes of neuroplasticity and pain, with special attention paid to the cellular and molecular nature of peripheral and central sensitization. The second part covers chronic pain conditions and underlying cellular and molecular mechanisms. The third part aims to integrate the knowledge obtained in the first two parts of the course in a translational way (bench-to-bedside-and-back-to-bench approach).