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Abstract
Intracellular recordings showed that administration of pulses of tryptamine mimicked
one of the actions of serotonin (a slow depolarization associated with an increased
input resistance) on type II/AH neurons of the myenteric plexus. After superfusion
at high concentration tryptamine initially acted like serotonin, but then blocked
the action of serotonin on these cells. Measurements of the release of preloaded [3H]serotonin
or [3H]norepinephrine revealed that tryptamine is a potent releaser of these labeled
amines; this release is Ca2+ independent but temperature dependent. Moreover, incubation
with tryptamine depleted the myenteric plexus of endogenous serotonin. Since tryptamine
has previously been demonstrated not to inhibit the binding of [3H]serotonin to its
enteric neural receptor we framed the hypothesis that the serotonin-releasing action
of tryptamine is responsible for its ability to mimic serotonin when given in pulses
or to desensitize serotonin receptors through the prolonged release of serotonin when
it is superfused. This hypothesis was tested by examining the action of tryptamine
on the serotonin-mediated slow excitatory postsynaptic potentials evoked in type II/AH
neurons by fiber tract stimulation. Tryptamine superfusion antagonized these slow
potentials as predicted. Moreover, after a long time when endogenous serotonin was
depleted, the response of type II/AH neurons to exogenous serotonin recovered but
the slow synaptic potential did not. The action of tryptamine on this neuron was relatively
specific. When the slow synaptic potential and serotonin responses were blocked by
tryptamine the type II/AH neurons still responded to acetylcholine. Fast excitatory
postsynaptic potentials were not affected by tryptamine. Furthermore, other types
of neurons (I/S) and other neuronal responses to serotonin (such as a fast depolarization
with decreased input resistance or presynaptic inhibition of acetylcholine release)
were not blocked by tryptamine. Finally, radioautographic studies revealed a neural
uptake of tryptamine in the chemically sympathectomized myenteric plexus; however,
the distribution of tryptamine in the plexus was different from that of serotonin
and was not blocked by excess non-radioactive serotonin. Therefore tryptamine does
not enter myenteric neurons via the specific serotonin uptake mechanism; however,
zimelidine, found to be a selective inhibitor of the enteric uptake of serotonin,
antagonized the release of serotonin by tryptamine and attenuated the effect of tryptamine
on responses to serotonin.(ABSTRACT TRUNCATED AT 400 WORDS)