Electrophysiological analysis of the presynaptic action of β-bungarotoxin in the central nervous system

Abstract

In view of previously reported actions of β-bungarotoxin (β-BuTX) on central brain synaptosomes, the effects of this toxin on the electrical activity of two brain slice preparations have been examined in vitro. β-BuTX initially suppresses the synaptic component of the field responses to electrical stimulation in olfactory cortex and hippocampal slices. Intracellular recordings demonstrate that this synaptic depression occurs without detectable reduction in the sensitivity of the postsynaptic neuron to putative neurotransmitters. Following longer exposure to the toxin, reduced neuronal excitability is observed both pre- and post-synaptically. Elimination of the phospholipase A 2 activity of β-BuTX, by chemical modification or removing the Ca 2+ necessary for enzymic activity, greatly reduces but does not totally eradicate the toxin's ability to block neurotransmission in the olfactory cortex. In the absence of enzymic activity β-BuTX has no obvious effect on axonal conduction. Pure phospholipases A 2, such as that from Naja melanoleuca mimic the transmission-blocking action of β-BuTX, but with lower potency and without the effects on fibre excitability. Collectively, these results are taken as evidence that β-BuTX initially suppresses transmitter release, a notion supported by the observed loss of spontaneous synaptic activity in hippocampal cells. Prolonged exposure to the toxin induces apparently less specific effects on neuronal excitability which are dependent on phospholipase A 2 activity and are discussed with reference to the selective action of β-BuTX on hippocampal fibre systems which possess release sites.