SPONTANEOUS electrical activity in the isolated hemisected frog spinal
cord increased in the presence of the SH reductant dithiothreitol (DT
T) was reversibly suppressed by the oxidant 5-5'-dithio-bis-(2-nitrobe
nzoic acid) (DTNB) and was irreversibly suppressed by the sulphydryl m
odifying agents N-ethyl-maleimide (NEM) and monobromotrimethylammonio
bimane. Glutathione (GSH), an important natural low molecular weight t
hiol, reversibly suppressed spontaneous activity. Cords pretreated wit
h glutathione and successively exposed to NEM or bimane maintained the
ir normal electrical activity. This indicates tht GSH had interacted w
ith the exposed sulphydryls and prevented their reaction with NEM or b
imane. Incubation with bimane resulted in fluorescence-labelled neuron
es in the dorsal and ventral horns, whereas samples pretreated with NE
M or with GSH were not labelled. Neurones appeared again fluorescent i
n cords preincubated with GSH and sequentially exposed to NEM or biman
e. Both electrophysiological and histochemical methods indicate that e
xposed membrane sulphydryls are involved in the genesis and/or modulat
ion of spontaneous electrical potentials.