Abstract

Isotonic lithium (154 mM) substituted temporarily for sodium (154 mM) in synapses of mammalian sympathetic ganglia. Ganghionic transmission and the responses to injected acetylchohine (ACh) were initally supported and then abolished during perfusion with lithium. Time blockade by lithium of time ganglionic responses to stimulation and injected ACh was accelerated by repetitive stimulation of time preganglionic trunk or by previous exposure to a sodium-deficient (40 mM) medium. Recovery of transmission and of ACh-evoked responses was directly related to the concentration of sodium in the perfusing solution. By contrast, potassium-induced depolarization was not affected by lithium. Lithium-induced abolition of both ganglionic transmission and the responses to injected ACh appears to be due primarily to impairment of postsynaptic processes.