Extracellular recording techniques have been used in the guinea pig hippocampal slice preparation to investigate the electrophysiological actions of the organophosphate (OP) anticholinesterase soman. When applied at a concentration of 100 nM, soman induced epileptiform activity in the CA1 region in approximately 75% of slices. This effect was mimicked by the anticholinesterases paraoxon (1 and 3 M), physostigmine (30 M), and neostigmine (30 M), thus providing indirect evidence that the epileptiform response was mediated by elevated acetylcholine levels. Soman-induced bursting was inhibited by the muscarinic receptor antagonists atropine (concentrations tested, 0

The presynaptic terminals of skate (Raja montagui) electric organ were tested for their sensitivity to calcium channel antagonists. Acetylcholine (ACh) release and the elevation of intraterminal Ca2+ concentrations triggered by K+ depolarisation were studied. ACh release was measured as 3H efflux from slices of organ prelabelled with [3H]choline. Depolarisation caused a marked, Ca2+‐dependent increase in 3H efflux that was completely blocked by 100 µM Cd2+ and by 300 nMω‐conotoxin‐MVIIC (MVIIC). Inhibition by MVIIC was concentration dependent (IC50 of ∼20 nM) and reversible. No inhibition was seen with nifedipine (5 µM) or the two other peptide antagonists studied: ω‐conotoxin‐GVIA (GVIA) at 5 µM and ω‐agatoxin‐IVA (Aga‐IVA) at 1 µM. In a “nerve plate” preparation (a presynaptic plexus of nerve fibres, Schwann cells, and nerve terminals) changes in intraterminal Ca2+ concentrations were measured by microfluorimetry using fluo‐3. An increase in fluorescence, indicating a rise in the free [Ca2+], rapidly followed K+ depolarisation, and this change was restricted to the nerve terminals. This response was insensitive to nifedipine (5 µM), GVIA (5 µM), and Aga‐IVA (300 nM) but almost completely abolished by MVIIC (1 µM). MVIIC inhibition was concentration dependent and partially reversible. These results show that the nerve terminals in skate electric organ have calcium channels with a pharmacological sensitivity that is markedly different from the established L, N, and P types in other systems but shares some, but not all, of the features of the recently described Q type.