Somatosensation and pain

神经性疼痛涉及敏感性的深刻转换，因此低强度的输入可以产生疼痛。与伤害性疼痛不同，神经性疼痛确实是对正常疼痛特异性模式的破坏。在临床上，周围神经病变疼痛广泛存在于周围神经损伤、中毒性和代谢性神经病以及带状疱疹、艾滋病等病毒性传染病患者中。不幸的是，传统的抗疼痛药物在治疗神经性疼痛时往往不能表现出令人满意的效果。

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 promote neuropathic pain: central sensitization, disinhibition, and central afferent terminal sprouting. However, how and whether spino-brain communication is involved in 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 top-down and bottom-up circuits involved in bi-directional mind-body communication and are trying to decipher their roles in regulating tactile and neuropathic pain sensitivity. By further dissection of neural circuits involved in somatosensation and pain control, our studies shed light on the underlying mechanisms of pain hypersensitivity and design of novel therapeutic interventions to treat pain.