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Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/4112

Title: Nitric oxide is a volume transmitter regulating postsynaptic excitability at a glutamatergic synapse.
Authors: Steinert, Joern R.
Kopp-Scheinpflug, Cornelia
Baker, Claire
Challiss, R.A. John
Mistry, Raj
Haustein, Martin D.
Griffin, Sarah J.
Tong, Huaxia
Graham, Bruce P.
Forsythe, Ian D.
Issue Date: 26-Nov-2008
Publisher: Elsevier.
Citation: Neuron, 2008, 60 (4), pp. 642-656.
Abstract: Neuronal nitric oxide synthase (nNOS) is broadly expressed in the brain and associated with synaptic plasticity through NMDAR -mediated calcium influx. However, its physiological activation and the mechanisms by which nitric oxide (NO) influences synaptic transmission have proved elusive. Here, we exploit the unique input-specificity of the calyx of Held to characterize NO modulation at this glutamatergic synapse in the auditory pathway. NO is generated in an activity-dependent manner by principle neurons receiving a calyceal synaptic input. It acts in the target and adjacent inactive neurons to modulate excitability and synaptic efficacy, inhibiting postsynaptic Kv3 potassium currents (via phosphorylation), reducing EPSCs and so increasing action potential duration and reducing the fidelity of transmission. We conclude that NO serves as a volume transmitter and slow dynamic modulator, integrating spontaneous and evoked neuronal firing, providing an index of global activity and regulating information transmission across a population of active and inactive neurons.
ISSN: 0896-6273
Links: http://www.cell.com/neuron/home
http://dx.doi.org/10.1016/j.neuron.2008.08.025
http://hdl.handle.net/2381/4112
Type: Article
Description: This is the author’s final draft of the paper published as Neuron, 2008, 60 (4), pp. 642-656. The final published version is available at http://www.cell.com/neuron/home, Doi: 10.1016/j.neuron.2008.08.025.
Appears in Collections:Published Articles, MRC Toxicology Unit

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