Glutamate　is　the　primary　excitatory　transmitter　of　sensory　transmission　and　perception　in　the　central　nervous　system.　Painful　or　noxious　stimuli　from　the　periphery　＇teach＇　humans　and　animals　to　avoid　potentially　dangerous　objects　or　environments,　whereas　tissue　injury　itself　causes　unnecessary　chronic　pain　that　can　even　last　for　long　periods　of　time.　Conventional　pain　medicines　often　fail　to　control　chronic　pain.　Recent　neurobiological　studies　suggest　that　synaptic　plasticity　taking　place　in　sensory　pathways,　from　spinal　dorsal　horn　to　cortical　areas,　contributes　to　chronic　pain.　Injuries　trigger　long-term　potentiation　of　synaptic　transmission　in　the　spinal　cord　dorsal　horn　and　anterior　cingulate　cortex,　and　such　persistent　potentiation　does　not　require　continuous　neuronal　activity　from　the　periphery.　At　the　synaptic　level,　potentiation　of　excitatory　transmission　caused　by　injuries　may　be　mediated　by　the　enhancement　of　glutamate　release　from　presynaptic　terminals　and　potentiated　postsynaptic　responses　of　AMPA　receptors.　Preventing,　＇erasing＇　or　reducing　such　potentiation　may　serve　as　a　new　mechanism　to　inhibit　chronic　pain　in　patients　in　the　future.