Properties and plasticity of synaptic inputs to rat dorsal column neurones recorded in vitro

1. The mechanisms regulating the flow of sensory signals and their modification by synaptic interactions in the dorsal column nuclei are incompletely understood. Therefore, we examined the interactions between EPSPs evoked by stimulation of dorsal column and corticofugal fibres in the dorsal column nuclei cells using an in vitro slice technique. 2. Dorsal column EPSPs had briefer durations at depolarised membrane potentials than corticofugal EPSPs. Superfusion of the NMDA receptor antagonist 2D(-)-2-amino-5-phosphonovaleric acid (AP5) did not modify dorsal column EPSPs but reduced corticofugal EPSPs. Application of the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) abolished both dorsal column and corticofugal EPSPs in cells held at the resting potential. Therefore, dorsal column EPSPs were mediated by non-NMDA receptors but corticofugal EPSPs revealed both non-NMDA- and NMDA-dependent components. 3. Paired-pulse stimulation of dorsal column fibres elicited a depression of the second EPSP at pulse intervals of < 50 ms; however, paired-pulse stimulation of corticofugal fibres evoked facilitation of the second EPSP at pulse intervals of < 30 ms. When stimulation of the corticofugal fibres preceded stimulation of the dorsal column fibres, facilitation of the dorsal column EPSP was observed at pulse intervals of < 100 ms. This facilitation was blocked at hyperpolarised membrane potentials or in the presence of AP5, suggesting activation of NMDA receptors. There was a depression of corticofugal EPSPs by previous dorsal column stimulation. 4. Dorsal column EPSPs were gradually depressed during stimulation with barrages at frequencies of > 10 Hz, while corticofugal EPSPs were facilitated and summated at frequencies > 30 Hz. Hyperpolarisation and application of AP5 prevented the facilitation of corticofugal EPSPs. High frequency stimulation of the corticofugal input elicited a short-lasting AP5-sensitive facilitation of both corticofugal and dorsal column EPSPs. Depolarising current facilitated dorsal column EPSPs but not corticofugal EPSPs. 5. These results indicate that synaptic interactions include different forms of activity-dependent synaptic plasticity, with the participation of NMDA receptors and probably Ca(2+) inflow through voltage-gated channels. These complex synaptic interactions may represent the cellular substrate of the integrative function of the dorsal column nuclei observed in vivo.