Published online by Cambridge University Press: 08 August 2009
The synaptic efficacy of the afferent volleys entering the spinal cord can be modulated by presynaptic inhibition. As a result, the information flowing through sensory terminals can be modified before it reaches the target neurones through a process that can be controlled selectively by supraspinal centres to optimise motor performance and sensory discrimination. All afferents are subject to presynaptic inhibition controlled by descending tracts (cf. Rudomin & Schmidt 1999) but, so far, methods have been developed for human subjects to estimate only presynaptic inhibition of Ia terminals. This is because it is easy to stimulate Ia afferents selectively, and they are the only afferents to have significant monosynaptic projections onto motoneurones.
Background from animal experiments
Initial findings
In the cat, Frank and Fuortes (1957) described a depression of monosynaptic Ia EPSPs in motoneurones occurring without a detectable change in motoneurone membrane potential or conductance. This presynaptic inhibition was extensively investigated by Eccles and colleagues. They described its main features and showed that the inhibition is associated with primary afferent depolarisation (PAD), both phenomena most probably mediated by the same interneurones acting on Ia terminals through axo-axonic synapses (see Eccles, 1964). These interneurones are referred to as PAD interneurones in the following, even though there is so far no record of PAD in human subjects.
General features
Location
Although PAD interneurones have not yet been specifically labelled, there are strong indications that last-order PAD interneurones mediating presynaptic inhibition of Ia terminals are located within the intermediate zone.
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