Somatosensation and pain

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Neuropathic pain involves a profound switch in sensitivity such that low-intensity input can generate pain. Different from nociceptive pain, neuropathic pain is indeed a disruption of the normal pattern of pain specificity. Clinically, peripheral neuropathic pain is widely present in patients suffering from peripheral nerve trauma, toxic and metabolic neuropathies, and viral infectious diseases such as Herpes zoster and AIDS. Unfortunately, traditional anti-pain medicines often fail to show satisfactory effects in treating neuropathic pain. Currently, a number of mechanisms have been postulated, either independently or together, to cause neuropathic pain: central sensitization, disinhibition, and central afferent terminal sprouting. However, how do mind(brain)-body(spinal cord) communications affect neuropathic pain remains poorly understood. In our previous studies, we showed that the corticospinal neurons are required for controlling both tactile and mechanical allodynia sensitivity and thereby demonstrated a first case of a direct top-down control from the cortex (Liu et al., Nature, 2018). This project is a natural extension of previous studies. With electrophysiology, single cell sequencing and imaging techniques, we explored both descending and ascending pathways that transmit and modulate somatosensory information between our mind and body. By continuous dissection of neural circuits involved in somatosensation and pain control, our studies will shed light onto the underlying mechanisms of pain hypersensitivity and the design of novel therapeutic interventions to treat pain.