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EN
We have recently shown that synaptic Ca2+-impearmable AMPA receptors (AMPARs) internalization in dorsal horn neurons underlies the maintenance of nociceptive hypersensitivity in infl ammatory pain. Here we have analyzed if traffi cking of extrasynaptic AMPARs is also changed during development and maintenance of persistent pain. We report that Complete Freund’s Adjuvant (CFA)-induced infl ammation causes an increase in functional expression of extrasynaptic AMPARs in rat substantia gelatinosa (SG) neurons during the maintenance rather than development of persistent pain. This increase, revealed as a signifi cant enhancement of AMPA-induced membrane currents and [Ca2+]i transients, was observed only in neurons characterized by an intrinsic tonic fi ring properties whereas no changes were observed in neurons exhibiting a strong adaptation. The increase was also accompanied by an enhancement of surface GluR1 expression and of the total amount of cobalt-positive neurons indicating an increase in a pool of GluR2-lacking AMPARs in extrasynaptic plasma membrane. These results suggest that functional changes in extrasynaptic AMPARs of tonic SG neurons that are associated with the maintenance of nociceptive hypersensitivity may also contribute to infl ammatory pain. We also suppose that there is a different contribution of tonic and transient neurons to the detection of peripheral painful stimuli and to maintenance of nociceptive hypersensitivity.
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