Barium ions fail to support neurotransmission at a central synapse.

Synaptic transmission in the CA1 area of the hippocampal slice preparation in vitro was studied in bathing media containing different levels of divalent cations. Transmission was abolished by replacing the normal levels (2.5 mM) of Ca2+ with 3 mM Mg. Transmission was not permanently restored by subsequent addition of Ba2+ but added Ca2+ was effective. Transient reappearance of synaptic currents were seen when Ba2+ was added at a time when contaminating levels of Ca2+ were still present, but neurotransmission waned as [Ca2+]e declined with protracted washout. In accordance with this interpretation, Ba2+ potentiated the transmission observed in the presence of low concentrations (0.25 mM) of Ca2+. Little evidence was found for Ba2+ effects at axonal sites but the potentiation of synaptic transmission by Ba2+ could be accounted for in terms of a blockade of terminal K-channels.