At onset of contraction PI to contracting muscles decreased PI to other muscles increased, leads to increased gain in stretch reflex arc focuses activity in motor nuclei
 

Differential Control of Presynaptic Inhibition
At onset of contraction, decreased PI to contracting muscles combined with increased PI to antagonist muscles leads to increased gain in stretch reflex arc.

Also serves to create more ìcontrastî in motoneural pool between agonists and antagonists.

Differential Control of Presynaptic Inhibition
How do we know presynaptic inhibtion  exists?

Vibration of Achilles leads to depression of soleus H-reflex but expression of tonic vibration reflex - that reflects increase in motoneuronal activity.  Thus the decrease in soleus H-reflex can be the result of a depressed motoneuronal pool - must be selective inhibtion

Differential Control of Presynaptic Inhibition
Another way to explore PI is by providing pulses of electricity to antagonist muscle this produces PI that is maintained for roughly 200 ms  (Fig 21.1)

Decrease in PI of IAs at onset of contraction results in facilitation of monosyaptic Ia pool.  This facilitation is not due to changes in contraction induced depolarization because facilitation is much less during tonic contraction.

Differential Control of Presynaptic Inhibition
Enhanced facilitation - (that is, decreased PI) evident at the beginning of the contraction does not last the entire contraction  (Figure 21.3).

The initial facilitation at the onset of muscle contraction increase as the force to be exerted at the end of the contraction increases.  Greater contractile force is positively correlated with initial motoneuronal pool facilitation.

Differential Control of Presynaptic Inhibition
Presynaptic inhibition of muscles not involved in a contraction is increased at the onset of an agonist muscle.

Differential Control of Presynaptic Inhibition
Decrease in PI to contracting muscles is not due to contraction-induced afferent discharge since it occurs 50 prior to contraction (e.g. inhibitory Renshaw cells, GTOís)
Plus, the PI persists when group I fibers are blocked
Interpretation is the PI must be centrally generated (e.g. motor cortex)

Differential Control of Presynaptic Inhibition
No evidence that centrally generated signals increase presynaptic inhibition in muscles not involved in the contraction.

These muscles can be inhibited by spinal mechanisms resulting from the agonist muscle contraction (reciprocal inhibtion).

A beautiful example of cortical and spinal processing working together to achieve desired outcome.