Gate control of mechanical itch by a subpopulation of spinal cord interneurons.

Light mechanical stimulation of the hairy skin can induce a form of itch known as mechanical itch. This itch sensation is normally suppressed by inputs from mechanoreceptors, however, in many forms of chronic itch, including alloknesis, this gating mechanism is lost. Here we demonstrate that a population of spinal inhibitory interneurons (INs) that are defined by the expression of neuropeptide Y::Cre (NPY::Cre) act to gate mechanical itch. Mice in which dorsal NPY::Cre-derived neurons are selectively ablated or silenced develop mechanical itch without an increase in sensitivity to chemical itch or pain. This chronic itch state is histamine-independent and is transmitted independently of the GRP-GRPR signaling pathway. Our studies thereby reveal a dedicated spinal cord inhibitory pathway that gates the transmission of mechanical itch

对有毛皮肤进行轻微的机械刺激可诱发一种被称为机械性瘙痒的瘙痒形式。这种瘙痒感觉通常受到机械感受器输入的抑制，然而，在许多形式的慢性瘙痒中，包括异常性瘙痒，这种门控机制丧失。在此我们证明，由神经肽Y::Cre（NPY::Cre）表达所定义的一群脊髓抑制性中间神经元（INs）起到对机械性瘙痒进行门控的作用。选择性消融或沉默背侧NPY::Cre衍生神经元的小鼠会出现机械性瘙痒，但对化学性瘙痒或疼痛的敏感性并未增加。这种慢性瘙痒状态不依赖组胺，且独立于胃泌素释放肽 - 胃泌素释放肽受体（GRP - GRPR）信号通路进行传递。因此，我们的研究揭示了一种专门的脊髓抑制通路，它控制着机械性瘙痒的传递。