The effects of convulsant doses of penicillin on primary afferents, dorsal root ganglion cells, and on ‘presynaptic’ inhibition in the spinal cord

Intracellular recordings were made from neurons in dorsal root ganglia (DRG) of rats, isolated in vitro. The depolarization of DRG cells caused by the application of gamma-aminobutyric acid (GABA) diminished reversibly when penicillin (0.08–2.0 mM) was added to the bathing fluid. The decrease of the input resistance of DRG cells measured during GABA perfusion was also depressed in the presence of penicillin, but no evidence of a shift of the reversal potential of the GABA-induced depolarization was found. Nor did penicillin (up to 10 mM) cause a change in the voltage-current function, in electrical excitability, in the inclination to repetitive firing, bursting discharge, or after discharge. In decapitate cat preparation the amplitude of the negative dorsal root potential (DRP or DR V) diminished by 0–50% after the i.v. administration of 0.5–1.0 × 10⁶I.U./kg (the convulsant dose) of penicillin. Post-tetanic depression of the DRP was aggravated by penicillin. The degree of depression of the DRP bore no relationship to the promptness of the eruption, and to the intensity, of the seizure activity induced by penicillin. The rates of rise and fall of the negative DRP (DR V) were consistently slowed, the positive DRP (DR V) reduced, and the dorsal root reflex (DRR) blocked by penicillin. Inhibitory reflex effects presumed to be presynaptic were either enhanced or unchanged, never depressed by penicillin. This was seen when inhibitory function was gauged by monosynaptic reflex amplitude, and also from the inhibition of ventral root electronic excitatory postsynaptic potentials (VR EPSPs). Possible explanations of these seemingly paradoxical findings are discussed, with arguments in favor and against each.