[Depolarization of primary afferents and presynaptic inhibition of monosynaptic reflexes].

In experiments on anesthetized spinal cats, perfusion of the lumbosacral spinal cord through the central canal with artificial cerebrospinal fluid containing ammonium ions led to reversible suppression of slow negative dorsal root potentials (DRP). The suppression of DRP proceeded in parallel to suppression of postsynaptic inhibition of motoneurons but was not related to a marked weakening of prolonged "presynaptic" inhibition of extensor monosynaptic reflexes produced by repetitive impulse volleys in group I flexor muscle afferents. It is concluded that primary afferent depolarization alone does not lead to presynaptic inhibition of synaptic transmission. A decisive factor for the inhibition might be the GABA-induced increase in chloride conductance of the presynaptic membrane, which, however, does not result in the terminal depolarizing current flow after the blockade of chloride pump with ammonium ions.