Presynaptic inhibition

Reflexes dependent on sensory input through Ia, Ib, and II afferents, can be customized by presynaptic inhibition from inhibitory GABAergic interneurons in the spinal cord. Such interneurons make axoaxonal synapses on the afferent terminals. GABA is secreted at these synapses acts on GABA_A receptors to bring about depolarization as in these sensory neurons the membrane potential is more negative than the reversal potential of the chloride current via the GABA_A receptor channels. The outcome of this primary afferent depolarization (PAD) is inhibitory in that whenever an action potential sweeps into the terminal its amplitude gets smaller, less Ca²⁺ influx takes place, therefore transmitter discharge from the terminal is decreased.

Presynaptic inhibition of Ia terminals is organized on a reciprocal basis in which the flexor afferents inhibit extensor afferents and vice-versa. At the begin of a movement presynaptic inhibition to Ia terminals going to agonist motor neurons is decreased while inhibition of antagonist muscle Ia terminals is increased. This means that spindle activity in the agonist is reinforced while that in the antagonist muscle is dampened. This makes sense; agonist action lengthens the antagonist muscle and this would incite it to contract were its stretch reflex not suppressed.The same circuitry is included in presynaptic inhibition of Ib and II afferents, permitting control of tension and tonic length signals separately of phasic length signals.