Peripheral nerve injuries produce a variety of negative structural and functional changes in the central terminal sites of damaged axons, as well as the injured primary afferents. Such changes have been shown to be involved in the development of neuropathic pain, which includes abnormal pain sensations such as allodynia and hyperalgesia. Since the spinal dorsal horn is the first central site where signals from peripheral sensory nerves are transmitted and shows a variety of changes after peripheral nerve injury or chronic inflammation of peripheral tissues, it is one of the most important sites contributing to the mechanisms underlying the development of neuropathic pain. The functional disruption of inhibitory interneurons and glial activation in the spinal dorsal horn after peripheral nerve injury cause reorganization of neuronal circuits and changes in the excitability of second-order neurons. These events are involved in the development or maintenance of neuropathic pain. Here, we describe the interactions of primary afferents, interneurons, and glial cells that may cause reorganization of synaptic inputs to spinal dorsal horn neurons after peripheral nerve injury.