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Nitric Oxide as a Putative Transmitter in Aplysia: Neural Circuits and Membrane Effects

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image of Netherlands Journal of Zoology
For more content, see Archives Néerlandaises de Zoologie (Vol 1-17) and Animal Biology (Vol 53 and onwards).

Nitric oxide (NO) is proposed as a neurotransmitter in the mammalian CNS. Histochemical staining and physiological studies suggest that it may be used as a transmitter in invertebrates as well. We stained the CNS of Aplysia using NADPH-diaphorase as a marker for nitric oxide synthase (NOS) to identify neurons, fibre tracts, neuropil and synaptic terminals where NO may be produced. We found a few (3-6) densely stained neurons in most central ganglia and 30 or so bilaterally represented neurons in the cerebral ganglion. Axons, as well as cell bodies, were stained. They joined well defined stained fibre tracts in the ganglia and interganglionic connectives. Several conspicuous synaptic glomeruli were stained, including the lateral terminus of the optic tract. Antiserum to myomodulin, a transmitter/modulator, also stained the lateral terminus. Peripheral nerves including the optic, tentacular and lip nerves contained stained fibres. Select cerebral E-cluster neurons, impaled with micropipettes, responded to the NO generating compounds SIN-1 (3 morpholino-sydnonimine) and s-nitrosocysteine (S-NC). The membrane potential depolarized ca 10 mV, membrane resistance increased and spike activity increased. Degassed solutions had no effect. 8-bromo-cGMP mimicked the effect of SIN-1 and S-NC, suggesting that NO effects may be mediated by activation of guanylate cyclase. NADPH-diaphorase positive neurons were impaled and found to produce synaptic depolarization of follower neurons that also were responsive to SIN-1 and S-NC. The combined evidence identifies NO as a putative transmitter/ modulator in the Aplysia nervous system.

Affiliations: 1: Department of Biological Sciences, State University of New York at Albany, Albany, NY 12222, U.S.A.

10.1163/156854293X00593
/content/journals/10.1163/156854293x00593
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/content/journals/10.1163/156854293x00593
1993-01-01
2016-12-03

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