Inflammatory-induced changes in synaptic drive and postsynaptic AMPARs in lamina II dorsal horn neurons are cell-type specific.

Persistent peripheral inflammation alters trafficking of AMPA receptors (AMPARs) at the synapses between primary afferents and dorsal horn (DH) neurons that contribute to the maintenance of inflammatory pain. However, whether peripheral inflammation changes the synaptic activity within the DH circuitry and how it modulates synaptic AMPARs in different neuronal types still remain unknown. We find that complete Freund adjuvant (CFA)-induced peripheral inflammation prominently augments excitatory neurotransmission in rat lamina II neurons characterized by intrinsic adapting firing properties and apparently decreases it in the tonic firing lamina II neurons, suggesting different roles of these types of interneurons in pain processing. Peripheral inflammation also differentially changes inhibitory neurotransmission in these neuronal types, shifting the balance between neuronal excitation and inhibition toward excitation of the adapting firing, but toward inhibition of the tonic firing lamina II neurons. Synaptic AMPARs were differentially changed in the adapting firing and the tonic firing neurons, implying different mechanisms of AMPAR adjustment at the synapses in these types of interneurons during persistent inflammation. The inflammatory-induced, neuron-type specific changes in synaptic drive within the DH circuitry and synaptic AMPAR functioning in lamina II neurons may contribute to the persistent pain maintenance.