PT  - JOURNAL ARTICLE
AU  - G A Montoya
AU  - W K Riker
AU  - N J Russell
TI  - Stimulus-bound repetitive synaptic firing caused by ethanol in sympathetic ganglion.
DP  - 1977 Feb 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 320--327
VI  - 200
IP  - 2
4099  - http://jpet.aspetjournals.org/content/200/2/320.short
4100  - http://jpet.aspetjournals.org/content/200/2/320.full
SO  - J Pharmacol Exp Ther1977 Feb 01; 200
AB  - The effects of ethanol, 0.1 to 1.0 M, on synaptic transmission, preganglionic axonal fibers and the ganglion cell were examined by extracellular and intracellular recording in isolated bullfrog sympathetic ganglia. Within the concentration range 0.2 to 0.8 M ethanol caused stimulus-bound repetitive postganglionic responses (SBR) to single preganglionic stimuli. The presynaptic origin of ethanol-induced SBR was confirmed by recordings of repetitive synaptic potential responses to single stimuli, and by absence of repetitive responses in myelinated preganglionic axons and in ganglion cells stimulated antidromically. Ethanol acted synergistically with Cs+ to produce SBR more intense than that caused by either agent alone. The postganglionic SBR caused by ethanol was suppressed by concentrations of d-tubocurarine, lidocaine, or tetraethylammonium that had little or no effect on synaptic transmission. Ethanol also blocked synaptic transmission, but this occurred secondary to the initial excitatory effects, and in the concentration range 0.4 to 1.0 M. The present data, together with previous studies of ethanol at neuromuscular junction, indicate that synaptic excitatory effects of ethanol are unrelated to hyperosmolarity or cholinesterase inhibition and represent a primary action of ethanol on prejunctional nerve endings.