Pre- and postsynaptic effects of zinc on in vitro prepyriform neurones.

Intracellular recordings from guinea-pig olfactory cortex neurones revealed a dual effect of zinc: firstly (at 100-500 microM), the responses to bath-applied GABA, muscimol and 3-aminopropanesulphonate were reversibly enhanced, and secondly (at 25-500 microM), the excitatory postsynaptic potential was dramatically prolonged. At Zn2+ doses higher than 50 microM, transmission was eventually blocked irreversibly. These effects of zinc were not produced by 4-aminopyridine, or other divalent cations. The GABA-enhancement is suggested to occur via an interaction of Zn2+ with the post-synaptic GABA receptor, and the prolonged transmitter release probably via blockade of an outward current in nerve terminals. The latter effect may be a contributory factor in the epileptogenic activity of zinc.