An investigation of primary or direct inhibition

Experiments With Perfused Frog's Spinal Cord

“…The results with strychnine agree with those of Bradley, Easton, and Eccles (1953) and of Bunzl et al (1954). The inhibitory effect of the contralateral stimulation appeared to be converted into an excitatory effect.…”

Cholinergic and inhibitory synapses in a pathway from motor‐axon collaterals to motoneurones

“…4B), which may become very large. This (Bradley, Easton & Eccles, 1953). The identity of the antidromic hyperpolarization and an IPSP is also indicated by the similar changes produced in them when the membrane potential of the motoneurone has been changed over a wide range by extrinsic currents .…”

“…These investigations lead to the conclusion that the antidromic hyperpolarization is produced by ionic movements across the motoneuronal membrane which are identical with those giving the IPSP of direct inhibition. It is probable that strychnine depresses direct inhibition by blocking the postsynaptic receptors for the inhibitory transmitting substance (Bradley et al 1953); hence the similar depressant action of strychnine on antidromic hyperpolarization indicates that it is caused by mediation of the same transmitting substance. It is therefore justifiable to identify the antidromic hyperpolarization as a true IPSP and to attribute it to the action of a synaptic mechanism similar to that giving the direct IPSP.…”

The specific ionic conductances and the ionic movements across the motoneuronal membrane that produce the inhibitory post‐synaptic potential

“…of motoneurones. It has been found that identical ionic mechanisms are concerned in five types of inhibitory synaptic action that are exerted on motoneurones in the spinal cord: direct inhibition of antagonist motoneurones by group Ia impulses from the annulo-spiral endings of muscle spindles (Lloyd, 1941(Lloyd, , 1946Laporte & Lloyd, 1952;Bradley, Easton & Eccles, 1953); the disynaptic inhibition by group Ib impulses from Golgi tendon organs (cf. Granit, 1950;Laporte & Lloyd, 1952); the polysynaptic inhibition by group III muscle impulses (Lloyd, 1943); the polysynaptic inhibition by cutaneous impulses (Renshaw, 1942;Hagbarth, 1952); and the disynaptic inhibition by impulses in the motor axon collaterals, which will henceforth be called antidromic inhibition because it can be evoked by antidromic volleys (Renshaw, 1941;Eccles, Fatt & Koketsu, 1954).…”