Dorsal horn neurons receive powerful excitatory inputs from sensory primary afferents. In chronic pain states maladaptive changes occur that lead to hypersensitivity and receptive field expansion – manifest as hyperalgesia (increased response to noxious stimuli) and allodynia (perception of previously innocuous stimuli as noxious). A key component of this functional plasticity and the focus of our work here is the reorganisation of proteins associated with excitatory glutamate receptors in the postsynaptic density of spinal sensory neurons. Behavioral reflex sensitivity was assessed in models of chronic neuropathic and inflammatory pain and spinal cord tissue analyzed by biochemical approaches to assess protein: protein interactions. We have identified changes in synaptic trafficking of AMPA receptor subunits, their association with key partner proteins and differential linkage of glutamate receptors with downstream signaling enzymes that could participate differentially in neuropathic or inflammatory pain states. The functional hypersensitivity that occurs in chronic pain states is associated with marked dynamic plasticity in the location, interactions and downstream signaling of excitatory glutamate receptors.