| Title | Nitric oxide potentiation of locomotor activity in the spinal cord of the lamprey. | | Author(s) | Kyriakatos A, Molinari M, Mahmood R, Grillner S, Sillar KT, El Manira A | | Institution | Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. | | Source | J Neurosci 2009 Oct 21; 29(42):13283-91. | | MeSH | Action Potentials
Animals
Benzoates
Enzyme Inhibitors
Excitatory Amino Acid Antagonists
Hydrazines
Imidazoles
Lampreys
Locomotion
NADPH Dehydrogenase
NG-Nitroarginine Methyl Ester
Neuroglia
Neurons
Nitric Oxide
Nitric Oxide Donors
Nitric Oxide Synthase Type I
Patch-Clamp Techniques
Sodium Channel Blockers
Spinal Cord
Synaptic Transmission
Tetrodotoxin
| | Abstract | To understand the intrinsic operation of spinal networks generating locomotion, we need to not only characterize the constituent neurons and their connectivity, but also determine the role of intrinsic modulation in shaping the final motor output. We have focused on the effects of nitric oxide (NO) on the locomotor frequency and the underlying synaptic mechanisms in the lamprey spinal cord. To identify the source of NO, we used NADPH-diaphorase histochemistry and nNOS immunocytochemistry. Gray matter and sensory neurons were positively labeled using both methods. Preparations preincubated with NO synthase inhibitors displayed slower locomotor frequency that increased upon washout of the inhibitors, suggesting that NO is an endogenous neuromodulator in the spinal cord. Application of NO donors increased the locomotor frequency that was blocked by an NO scavenger and partially reduced by an inhibitor of sGC. To analyze the synaptic modulation underlying the NO-induced increase of the locomotor frequency we performed intracellular recordings from motoneurons and interneurons. The NO-induced increase in locomotor frequency was associated with a decrease in the midcycle inhibition and an increase in on-cycle excitation. To determine the site of action of NO, we examined the effect of NO donors on miniature PSCs. NO increased both the frequency and amplitude of mEPSCs while it only decreased the frequency of mIPSCs, suggesting the increased excitation is mediated by both presynaptic and postsynaptic mechanisms, while the decrease in inhibition involves only presynaptic mechanisms. Our results demonstrate a significant role of NO in adult vertebrate motor control which, via modulation of both excitatory and inhibitory transmission, increases the locomotor burst frequency. | | Language | eng | | Pub Type(s) | In Vitro
Journal Article
Research Support, Non-U.S. Gov't
| | PubMed ID | 19846716 |
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