[Block of presynaptic inhibition of spinal cord reflexes by ammonium acetate]

In experiments on cats ammonium acetate (AA) injected intravenously (2--4 mM/kg body weight) depressed the process of primary afferent depolarization (PAD) which were thought to be responsible for presynaptic inhibition of spinal reflexes. PAD depression is reversible and proceeds in parallel to depression of postsynaptic inhibition of monosynaptic reflexes. The ammonium depression of PAD is not connected with the block of the negative postsynaptic potential recorded from the dorsal surface of the spinal cord or with the block of the reflex electrical discharges from the ventral roots. A conclusion was drawn that one of the possible mechanisms for convulsive action of AA consists in depression of presynaptic inhibition. It is supposed that the depression of PAD by AA results from the block of the chloride ion pump existing in primary afferent terminals. The block of the pump leads to abolition of the EMF for the outwardly directed transmembrane chloride current producing PAD.