Spinal changes associated with mechanical hypersensitivity in a model of Guillain–Barré syndrome

Guillain–Barré syndrome (GBS) is an inflammatory disease of the peripheral nervous system which can cause pain via mechanisms that are poorly understood. Here, we show that in rat experimental autoimmune neuritis (EAN) mechanical allodynia developed up to 9 days before the onset of detectable neurological deficits. Allodynia was associated with an increase in the number of microglial cells in the dorsal horn of the spinal cord. The expression of the chemokine CX3CL1 (fractalkine) and its receptor CX3CR1 were also higher in EAN than in control dorsal horns suggesting spinal microglia and CX3CL1/CX3CR1 may play a role in the pain-like behaviour.