Neurons controlling Aplysia feeding inhibit themselves by continuous NO production.
Neural activity can be affected by nitric oxide (NO) produced by spiking neurons. Can neural activity also be affected by NO produced in neurons in the absence of spiking?Applying an NO scavenger to quiescent Aplysia buccal ganglia initiated fictive feeding, indicating that NO production at rest inh...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2011-03-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3052382?pdf=render |
| _version_ | 1818988354605154304 |
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| author | Nimrod Miller Ravit Saada Shlomi Fishman Itay Hurwitz Abraham J Susswein |
| author_facet | Nimrod Miller Ravit Saada Shlomi Fishman Itay Hurwitz Abraham J Susswein |
| author_sort | Nimrod Miller |
| collection | DOAJ |
| description | Neural activity can be affected by nitric oxide (NO) produced by spiking neurons. Can neural activity also be affected by NO produced in neurons in the absence of spiking?Applying an NO scavenger to quiescent Aplysia buccal ganglia initiated fictive feeding, indicating that NO production at rest inhibits feeding. The inhibition is in part via effects on neurons B31/B32, neurons initiating food consumption. Applying NO scavengers or nitric oxide synthase (NOS) blockers to B31/B32 neurons cultured in isolation caused inactive neurons to depolarize and fire, indicating that B31/B32 produce NO tonically without action potentials, and tonic NO production contributes to the B31/B32 resting potentials. Guanylyl cyclase blockers also caused depolarization and firing, indicating that the cGMP second messenger cascade, presumably activated by the tonic presence of NO, contributes to the B31/B32 resting potential. Blocking NO while voltage-clamping revealed an inward leak current, indicating that NO prevents this current from depolarizing the neuron. Blocking nitrergic transmission had no effect on a number of other cultured, isolated neurons. However, treatment with NO blockers did excite cerebral ganglion neuron C-PR, a command-like neuron initiating food-finding behavior, both in situ, and when the neuron was cultured in isolation, indicating that this neuron also inhibits itself by producing NO at rest.Self-inhibitory, tonic NO production is a novel mechanism for the modulation of neural activity. Localization of this mechanism to critical neurons in different ganglia controlling different aspects of a behavior provides a mechanism by which a humeral signal affecting background NO production, such as the NO precursor L-arginine, could control multiple aspects of the behavior. |
| first_indexed | 2024-12-20T19:21:15Z |
| format | Article |
| id | doaj.art-10219c2c341742d88554fb219f75ed10 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-20T19:21:15Z |
| publishDate | 2011-03-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-10219c2c341742d88554fb219f75ed102022-12-21T19:28:59ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-03-0163e1777910.1371/journal.pone.0017779Neurons controlling Aplysia feeding inhibit themselves by continuous NO production.Nimrod MillerRavit SaadaShlomi FishmanItay HurwitzAbraham J SussweinNeural activity can be affected by nitric oxide (NO) produced by spiking neurons. Can neural activity also be affected by NO produced in neurons in the absence of spiking?Applying an NO scavenger to quiescent Aplysia buccal ganglia initiated fictive feeding, indicating that NO production at rest inhibits feeding. The inhibition is in part via effects on neurons B31/B32, neurons initiating food consumption. Applying NO scavengers or nitric oxide synthase (NOS) blockers to B31/B32 neurons cultured in isolation caused inactive neurons to depolarize and fire, indicating that B31/B32 produce NO tonically without action potentials, and tonic NO production contributes to the B31/B32 resting potentials. Guanylyl cyclase blockers also caused depolarization and firing, indicating that the cGMP second messenger cascade, presumably activated by the tonic presence of NO, contributes to the B31/B32 resting potential. Blocking NO while voltage-clamping revealed an inward leak current, indicating that NO prevents this current from depolarizing the neuron. Blocking nitrergic transmission had no effect on a number of other cultured, isolated neurons. However, treatment with NO blockers did excite cerebral ganglion neuron C-PR, a command-like neuron initiating food-finding behavior, both in situ, and when the neuron was cultured in isolation, indicating that this neuron also inhibits itself by producing NO at rest.Self-inhibitory, tonic NO production is a novel mechanism for the modulation of neural activity. Localization of this mechanism to critical neurons in different ganglia controlling different aspects of a behavior provides a mechanism by which a humeral signal affecting background NO production, such as the NO precursor L-arginine, could control multiple aspects of the behavior.http://europepmc.org/articles/PMC3052382?pdf=render |
| spellingShingle | Nimrod Miller Ravit Saada Shlomi Fishman Itay Hurwitz Abraham J Susswein Neurons controlling Aplysia feeding inhibit themselves by continuous NO production. PLoS ONE |
| title | Neurons controlling Aplysia feeding inhibit themselves by continuous NO production. |
| title_full | Neurons controlling Aplysia feeding inhibit themselves by continuous NO production. |
| title_fullStr | Neurons controlling Aplysia feeding inhibit themselves by continuous NO production. |
| title_full_unstemmed | Neurons controlling Aplysia feeding inhibit themselves by continuous NO production. |
| title_short | Neurons controlling Aplysia feeding inhibit themselves by continuous NO production. |
| title_sort | neurons controlling aplysia feeding inhibit themselves by continuous no production |
| url | http://europepmc.org/articles/PMC3052382?pdf=render |
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