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The Journal of Neuroscience, November 4, 2009, 29(44):13945-13951; doi:10.1523/JNEUROSCI.3841-09.2009

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Behavioral/Systems/Cognitive
The Nitric Oxide/cGMP Pathway Tunes the Thermosensitivity of Swimming Motor Patterns in Xenopus laevis Tadpoles

R. Meldrum Robertson^1,2 and Keith T. Sillar²

¹Department of Biology, Queen's University, Kingston, Ontario K7L 3N6, Canada, and ²School of Biology, University of St. Andrews, Fife KY16 9TS, United Kingdom

Correspondence should be addressed to R. Meldrum Robertson, 3118 Biosciences Complex, Queen's University, Kingston, ON K7L 3N6, Canada. Email: robertrm{at}queensu.ca

We investigated the role of the nitric oxide (NO)/cGMP pathway in setting thresholds for failure and recovery during hyperthermic stress of the swimming central pattern generator of immobilized Xenopus tadpoles (stage 42). We recorded swimming motor patterns induced by tail skin stimulation (TS) (1 ms current pulse) or by bath application of 50 µM NMDA. Swimming rhythm frequency increased in a linear manner with increasing temperature. In the presence of the NO donor S-nitroso-N-acetylpenicillamine (SNAP), recovery from hyperthermic failure was greatly slowed, often taking longer than the duration of the experiment. Pharmacological activation of the NO/cGMP pathway using SNAP or 8-bromo-cGMP (1) decreased the duration of TS-evoked swim episodes; (2) decreased the temperature threshold for hyperthermic circuit failure; (3) decreased the temperature at which the circuit recovered; and (4) increased the time taken to recover. Pharmacological inhibition of the NO/cGMP pathway using the NO scavenger CPTIO, the nitric oxide synthase (NOS) inhibitor L-NAME or the guanylyl cyclase inhibitor ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) had the opposite effects. NMDA rhythms were more resistant to hyperthermic failure than TS-evoked swim episodes, but the effects of SNAP on the temperature sensitivity of swimming evoked by NMDA were similar to those on TS-evoked swimming, suggesting that drug effects occur on central pattern-generating networks rather than sensory pathways. We conclude that the NO/cGMP pathway is involved in setting the threshold temperatures for hyperthermic failure and subsequent recovery of fictive swimming in tadpoles, and we suggest that this is part of a variable response to prevent overexcitation during abiotic stress under different environmental conditions.

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Received Aug. 6, 2009; revised Sept. 10, 2009; accepted Sept. 11, 2009.

Correspondence should be addressed to R. Meldrum Robertson, 3118 Biosciences Complex, Queen's University, Kingston, ON K7L 3N6, Canada. Email: robertrm{at}queensu.ca

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