The Journal of Neuroscience, December 1, 1998, 18(23):9954-9961
Nerve Terminal Currents Induced by Autoreception of
Acetylcholine Release
Wen-Mei
Fu,
Houng-Chi
Liou, and
Yu-Hwa
Chen
Pharmacological Institute, College of Medicine, National Taiwan
University, Taipei, Taiwan 100
The activation of autoreceptors is known to be important in the
modulation of presynaptic transmitter secretion in peripheral and
central neurons. Using whole-cell recordings made from the free growth
cone of myocyte-contact motoneurons of Xenopus cell cultures, we have observed spontaneous nerve terminal currents (NTCs).
These spontaneous NTCs are blocked by d-tubocurarine (d-TC) and
-bungarotoxin (-BuTx), indicating that endogenously released acetylcholine (ACh) can produce substantial membrane depolarization in
the nerve terminals. Local application of NMDA to the growth cone increased the frequency of spontaneous NTCs. When the electrical stimulations were applied at the soma to initiate evoked-release of
ACh, evoked ACh-induced potentials were recorded in the nerve terminals, which were inhibited by d-TC and hexamethonium but not by
atropine. Replacement of normal Ringer's solution with high-Mg2+, low-Ca2+ solution also
reversibly inhibited evoked ACh-induced potentials. The possible
regulatory role of presynaptic nicotinic autoreceptors on the synaptic
transmission was also examined. When the innervated myocyte was
whole-cell voltage-clamped to record synaptic currents, application of
hexamethonium inhibited the amplitude of evoked synaptic currents at a
higher degree than that of iontophoretic ACh-induced currents.
Furthermore, hexamethonium markedly reduced the frequency of
spontaneous synaptic currents at high-activity synapses. Pretreatment
of neurons with -BuTx also inhibited the evoked synaptic currents in
manipulated synapses. These results suggest that ACh released
spontaneously or by electrical stimulation may act on the presynaptic
nicotinic autoreceptors of the same nerve terminals to produce membrane
potential change and to regulate synaptic transmission.
Key words:
autoreceptor; neuronal nicotinic receptor; Xenopus
laevis; nerve terminal currents; synaptic transmission; acetylcholine
Copyright © 1998 Society for Neuroscience 0270-6474/98/18239954-08$05.00/0
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