PubMed · 5750171
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J J Kanski. 1968. Miotics.. https://doi.org/10.1136/bjo.52.12.936
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It is not yet understood how the molecular mechanisms controlling the release of neuropeptides differ from those controlling the release of classical transmitters, mainly because there are few peptidergic synapses in which the environment at the presynaptic release sites can be manipulated. Using Aplysia californica neuron B2, which synthesizes both peptide and classical transmitters, we have established two synaptic types. When B2 is cocultured with a sensory neuron, a peptidergic synapse is formed. In contrast, when B2 is cocultured with neuron B6, a classical synapse is formed. In contrast to a common assumption, single action potentials can release both types of transmitters. The secretion of peptide and classical transmitters by B2 is inhibited by the presynaptic injection of tetanus toxin, but not by an inactive mutant. Thus a synaptobrevin-like molecule is involved in the secretion of these two types of transmitters.
Neurotrophic factors derived from postsynaptic muscle cells may play important roles in the development of presynaptic neuronal functions. In 3-d-old Xenopus nerve-muscle cultures, embryonic spinal neurons that had made natural contact with co-cultured myocytes exhibited spontaneous release of larger packets of acetylcholine (ACh) quanta than those released by the isolated neurons having no contact with any myocyte. Treatment of isolated neurons with neurotrophin-3 (NT-3) for 2 d increased the average sizes of quantal ACh packets at newly formed nerve-muscle synapses, whereas treatment with antibody against NT-3 or with K252a, a specific inhibitor of tyrosine kinase receptors, decreased the quantal size at existing synapses, which suggests that NT-3 supplied by the postsynaptic muscle cell may be responsible for the development and maintenance of the quantal packets. The muscle effect seems to depend on synaptic activities mediated by postsynaptic ACh receptor channels, because chronic treatment of the culture with D-tubocurarine (D-Tc) for 2 d resulted in a marked reduction of the quantal sizes, when assayed after extensive washing of the culture with Ringer's solution. The curare treatment did not affect the postsynaptic ACh receptor sensitivity, because iontophoretically applied ACh induced current responses similar to those of control. Finally, co-treatment of the culture with NT-3 and D-Tc reversed the effect of D-Tc on the quantal size, and this reversal effect was abolished when K252a was also applied concomitantly. Our results suggest that muscle-derived NT-3 participates in the maturation of normal transmitter packets in developing neurons, and the secretion of NT-3 depends on spontaneous synaptic activity.
The dominant efferent innervation of the cochlea terminates on outer hair cells (OHCs), with acetylcholine (ACh) being its principal neurotransmitter. OHCs respond with a somatic shape change to alterations in their membrane potential, and this electromotile response is believed to provide mechanical feedback to the basilar membrane. We examine the effects of ACh on electromotile responses in isolated OHCs and attempt to deduce the mechanism of ACh action. Axial electromotile amplitude and cell compliance increase in the presence of the ligand. This response occurs with a significantly greater latency than membrane current and potential changes attributable to ACh and is contemporaneous with Ca2+ release from intracellular stores. It is likely that increased axial compliance largely accounts for the increase in motility. The mechanical responses are probably related to a recently demonstrated slow efferent effect. The implications of the present findings related to commonly assumed efferent behavior in vivo are considered.