Diazepam inhibits post tetanic potentiation of fast excitatory post synaptic potentials in bullfrog sympathetic ganglia, without altering the responses to single shocks. In addition, diazepam, like GABA and dibutyryl GMP depolarizes presynaptic nerve terminals, that can be antagonized by picrotoxin and not by tubocurarine or atropine. The bullfrog and rat superior cervical ganglion (SCG) accumlate exogenous radiolabelled GABA presumably in the glial cells. This radioactive GABA can be released by dibutyryl cGMP, high concentration of K ion, and diazepam. Rat SCG contains endogenous GABA that can be altered by various drugs and other treatments, such s amino-oxyacetic acid, urethane, decentralization and electrical stimulation. We postulate that diazepam acts presumably by releasing glial GABA which depolarizes presynpatic terminals and inhibits transmitter release, thus inhibiting post tetanic potentiation.