A number of different classes of segmental interneurones serve to control motoneurone excitability. One form of postsynaptic inhibition, recurrent inhibition, has been intensively studied over the years and is known to be mediated by Renshaw cells (Eccles et al. 1954). These interneurones use glycine andÏor GABA as their neurotransmitter Fyffe, 1991a;Schneider & Fyffe, 1992), and make contact predominantly on the dendrites of their target motoneurones (Fyffe, 1991b). Although the role of recurrent inhibition in motor control is still not well defined (see e.g. Binder et al. 1996), it remains important to understand how Renshaw cells themselves might be regulated. Recent work suggests that Renshaw cells are subject to strong glycinergic inhibitory inputs distributed over their cell bodies and proximal dendrites (Alvarez et al. 1997). In addition, a number of lines of evidence point to the presence of a powerful cholinergic input to Renshaw cells, a significant proportion of which is probably mediated by postsynaptic nicotinic acetylcholine receptors. The most prominent cholinergic input comes via the recurrent collaterals of motor axons; Renshaw cells display a characteristic high frequency burst of action potentials following antidromic stimulation of motor axons, and a single impulse in a single motor axon is sufficient to elicit action potentials in a Renshaw cell (van Kuelen, 1981) or to modulate its firing rate (Ross et al. 1975). The EPSP underlying motor axon collateral activation of Renshaw cells has a monophasic time course lasting longer than 50 ms

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