Following noxious stimulation (e.g., colitis in the present study), excitatory neurotransmitters such as BDNF, substance P, and CGRP release centrally from the primary afferent neurons into the spinal dorsal horn [46, 48–50] where they can bind to their respective receptors and facilitate signal transduction [4, 9, 35, 46], ultimately resulting in pain hypersensitivity (central sensitization) [51]. This evidence concerns the gene TAC1 and colitis.