Dorsal column nuclei neurons recorded in a brain stem-spinal cord preparation: Characteristics and their responses to dorsal root stimulation

Recordings were obtained from dorsal column nucleus (DCN) neurons in a neon atal rat brain stem-spinal cord preparation to study their basic electrophy siological properties and responses to stimulation of a dorsal root. Whole- cell patch-clamp recordings were made from 21 neurons that responded to dor sal root stimulation with a fast excitatory postsynaptic potential (EPSP). These neurons were located lateral to, but at the level of, the area postre ma at depths of 100-268 mu m below the dorsal surface of the brain. The neu rons could be divided into groups according to the shape of their action po tentials or voltage responses to hyperpolarizing current steps; however, th e response profiles of the groups of neurons to dorsal root stimulation wer e not significantly different and all neurons were considered together. Dor sal root stimulation elicited excitatory postsynaptic potentials (EPSPs) in all neurons with a very low variability in onset latency and an ability to follow 100-Hz stimulation, indicating that they were mediated by activatio n of a monosynaptic pathway. The peak amplitude of the EPSP increased with membrane hyperpolarization, and applications of the non-NMDA receptor antag onists 6-nitro-7-sulfamoylbenzo[f] quinoxaline-2,3-dione (NBQX) and 6,7-din itroquinoxaline-2,3-dione (DNQX) decreased the amplitude of the EPSP to 14. 2% of the control response (n = 6). The descending phase of the EPSP decrea sed with membrane hyperpolarization and was reduced by the N-methyl-D-aspar tate (NMDA) receptor antagonist AP-5 (n = 2). The EPSPs were also reduced i n amplitude by applications of the gamma-aminobutyric acid-B (GABA(B)) rece ptor agonist baclofen, which had no effect on membrane potential or input r esistance. These results show that fast EPSPs in DCN neurons elicited by do rsal root stimulation are mediated by an excitatory amino acid acting at bo th non-NMDA and, to a lesser extent, NMDA receptors. In addition, GABA acti ng at presynaptic GABA(B) receptors can inhibit these responses.