It is becoming increasingly clear that synaptic plasticity in pain-sensitive pathways has many features in common with better understood forms of synaptic plasticity, such as hippocampal long-term potentiation. Now Hartmann and colleagues have shown that AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors, which are vital mediators of hippocampal plasticity, are also important modulators of inflammatory pain and of synaptic plasticity in the spinal nociceptive system.

Most AMPA receptors in the central nervous system — those that contain the GluRB subunit together with GluRA, C or D subunits — have low permeability to Ca2+. However, receptors that lack the GluRB subunit have much higher Ca2+ permeability, and many of these receptors are found in the spinal dorsal horn. AMPA receptors in the dorsal horn are also unusual in that they are found presynaptically on the axon terminals of primary sensory afferent neurons, and activation of these receptors depolarizes the afferent neurons and thereby reduces neurotransmission from afferent fibres to second-order neurons in the spine.
(Source: Signalling Gateway Org)

I concur. Plus, it hurts like fuck.