Primary afferent depolarization in the rat spinal cord is mediated by pathways utilising NMDA and non-NMDA receptors

In the present experiments the dorsal root-evoked dorsal root potential (DR-DRP) has been measured in vitro from a mature rat sacrococcygeal preparation. The DR-DRP is an index of presynaptic inhibition since it represents the depolarization of primary afferent terminals by gamma-aminobutyric acid (GABA) released synaptically from interneurones. The present study shows that the synaptic excitation of the GABAergic interneurons contains a large component resistant to the selective N-methyl-D-aspartate (NMDA) receptor antagonists 2-amino-5-phosphonopentanoate (AP5) (100 microM) and 3((+)-2-carboxypiperazin-4-yl)propyl-1-phosphonate (CPP) 20-100 microM. This non-NMDA receptor mediated component reflected in the DR-DRP was depressed markedly by the non-selective excitatory amino acid receptor antagonists kynurenate (1-2 mM) and 6-cyano-2,3-dihydroxy-7-nitro-quinoxaline (CNQX) (10-20 microM). Because previous reports show non-cholinergic activation of Renshaw cells to be blocked by NMDA receptor antagonists the present observations suggest that pre- and postsynaptic inhibition in the spinal cord are mediated by different types of excitatory amino acid receptor.