An in vivo pharmacological study of single group Ia fibre contacts with motoneurones in the cat spinal cord.

1. Direct experimental evidence was obtained on the spatial distribution of active synaptic contacts from single Ia muscle afferents on the dendrites of lumbosacral motoneurones in anaesthetized cats. 2. An extracellular micropipette was used to pressure eject the AMPA/kainate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline (NBQX) in close proximity to the intracellular recording site, in order to create an extracellular concentration gradient of the antagonist. The effect of antagonist ejection on the time course and amplitude of excitatory postsynaptic potentials (EPSPs) evoked in motoneurones by impulses in single group Ia fibres was examined. 3. Pressure ejection of NBQX resulted in a complete block of the monosynaptic group Ia EPSP in two cells, and a significant reduction to 23-57% of control EPSP peak amplitudes in a further six cells (mean, 27%; n = 8). These effects were not associated with changes in membrane potential or membrane time constant. 4. The reduction in amplitude of these single group Ia fibre EPSPs following ejection of NBQX was usually accompanied by a pronounced slowing in the time course of the EPSPs. On average, the EPSP rise times and half-widths were increased by 269 and 37%, respectively. This is most probably due to a considerable spatial spread of the synaptic contacts along the dendrites of motoneurones, with the most proximal synaptic contacts (producing the briefest synaptic potentials) subjected to a greater reduction in amplitude due to a higher local antagonist concentration. 5. An equivalent dendritic cable model of the motoneurone was used to interpret the observed changes in the time course of single fibre EPSPs. The time course of control single fibre EPSPs examined in the present study could be well matched using the cable model and assuming a single location for synaptic input. The observation of a slowed EPSP time course following antagonist ejection indicated that this assumption was not correct and that there was in fact considerable spatial spread in the synaptic contacts arising from these single afferent fibres. These results provide direct evidence that spatial spread of synaptic input may not be detected using the time course of a synaptic potential in conjunction with a neuronal cable model of the postsynaptic cell.