AN IN-VIVO PHARMACOLOGICAL STUDY OF SINGLE GROUP-I A FIBER CONTACTS WITH MOTONEURONS IN THE CAT SPINAL-CORD

1. Direct experimental evidence was obtained on the spatial distributi on of active synaptic contacts from single Ia muscle afferents on the dendrites of lumbosacral motoneurones in anaesthetized cats. 2. An ext racellular micropipette was used to pressure eject the AMPA/kainate re ceptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or dihy droxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline (NBQX) in close proximi ty to the intracellular recording site, in order to create an extracel lular concentration gradient of the antagonist. The effect of antagoni st ejection on the time course and amplitude of excitatory postsynapti c potentials (EPSPs) evoked in motoneurones by impulses in single grou p Ia fibres was examined. 3. Pressure ejection of NBQX resulted in a c omplete block of the monosynaptic group la EPSP in two cells, and a si gnificant reduction to 23-57% of control EPSP peak amplitudes in a fur ther six cells (mean, 27%; n = 8). These effects were not associated w ith changes in membrane potential or membrane time constant. 4. The re duction in amplitude of these single group Ia fibre EPSPs following ej ection of NBQX was usually accompanied by a pronounced slowing in the time course of the EPSPs. On average, the EPSP rise times and half-wid ths were increased by 269 and 37%, respectively. This is most probably due to a considerable spatial spread of the synaptic contacts along t he dendrites of motoneurones, with the most proximal synaptic contacts (producing the briefest synaptic potentials) subjected to a greater r eduction 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 EPSP s. The time course of control single fibre EPSPs examined in the prese nt study could be well matched using the cable model and assuming a si ngle location for synaptic input. The observation of a slowed EPSP tim e 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. T hese results provide direct evidence that spatial spread of synaptic i nput may not be detected using the time course of a synaptic potential in conjunction with a neuronal cable model of the postsynaptic cell.