Long‐term potentiation of transmitter release induced by adrenaline in bull‐frog sympathetic ganglia.

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Abstract
1. Long-term potentiation (l.t.p.) of transmitter release induced by adrenaline in bull-frog sympathetic ganglia was studied using intracellular recording techniques. 2. The quantal content of the fast excitatory post-synaptic potentials (fast e.p.s.p.s: evoked by the nicotinic action of acetylcholine) was potentiated for more than several hours after treatment with adrenaline (1-100 .mu.M). 3. A similar l.t.p. of quantal content was produced consistently by isoprenaline (10 .mu.M) and only in a certain fraction of cells by dopamine (10 .mu.M). The l.t.p. induced by adrenaline (10 .mu.M) was blocked by a .beta.-antagonist, propranolol (1 .mu.M), but not by an .alpha.-antagonist, phenoxybenzamine (1 .mu.M). 4. Dibutyryl adenosine 3'',5''-phosphate (dibutyryl cyclic AMP) (0.8-1.0 mM), adenosine 3'',5''-phosphate (cyclic AMP) (4 mM), 3-isobutyl-1-methylxanthine (10 .mu.M), caffeine (1-2 mM), and cholera toxin (2 .mu.g ml-1) applied for 20-30 min, all caused the l.t.p. of quantal content. by contrast, adenosine 5''-phosphate (AMP) (4 mM) and adenosine (4 mM) had no potentiating action. 5. Treatment of the ganglion with adrenaline (2.5-160 .mu.M) or dibutyryl cyclic AMP (4 mM) for 15-30 min resulted in the l.t.p. of the frequency of miniature e.p.s.p.s. 6. The l.t.p. of quantal content induced by adrenaline was markedly suppressed by lowering temperature from 20-25.degree. C to 11-13.degree. C, and blocked by dibutyryl guanosine 3'',5''-phosphate (dibutyryl cyclic GMP) (100 .mu.M) consistently when applied together, but inconsistently when given after adrenaline. 7. The post-synaptic sensitivity to acetylcholine was unchanged for at least 1 h after exposure to adrenaline (2.5-160 .mu.m) or dibutyryl cyclic AMP (0.8-4 mM). 8. It can be concluded that adrenaline produces l.t.p. of transmitter release by activating a cyclic-AMP-dependent metabolic process through the activation of .beta.-adrenoceptors, and that this mechanism is presumably regulated by a process involving endogenous guanosine 3'',5''-phosphate (cyclic GMP).