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Nitric oxide induces cGMP immunoreactivity and modulates membrane conductance in identified central neurons of Aplysia
Author(s) -
Koh H.Y.,
Jacklet J. W.
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2000.01416.x
Subject(s) - aplysia , neuron , soluble guanylyl cyclase , neuroscience , membrane potential , biology , afterhyperpolarization , depolarization , reversal potential , chemistry , nitric oxide , electrophysiology , patch clamp , biophysics , endocrinology , guanylate cyclase
Nitric oxide (NO) acts as an orthograde neurotransmitter in the central nervous system by stimulating guanylyl cyclase and increasing cGMP. We previously demonstrated this pathway for an identified synaptic follower neuron in the cerebral ganglion of the mollusc Aplysia californica . Here, we investigated the NO–cGMP pathway in other Aplysia central neurons using cGMP immunocytochemistry and intracellular recordings. NO‐induced cGMP immunoreactivity in a few neurons in the abdominal, pleural and buccal ganglia, including identified neurons L11 and R15 in the abdominal ganglion and neuron Bng in the buccal ganglion. NO depolarized all these neurons but none of the four nonimmunoreactive neurons tested. In neuron L11, NO‐induced depolarization, tonic spiking and a reduction in membrane conductance at resting potential. The NO effect was mimicked by applying the membrane permeable analogue, 8‐Br‐cGMP in L11. Neuron R15 was depolarized and its activity shifted from spike/bursts to tonic spiking. These NO effects were blocked by applying the guanylyl cyclase inhibitor ODQ and mimicked by 8‐Br‐cGMP. Neuron Bng was depolarized and produced spikes tonically. These results provide evidence that the NO–cGMP pathway is linked to membrane ionic channels in cGMP‐IR neurons, and the channels may be different in specific neurons.