We have explored the possible modulation by nitric oxide (NO) of inhibitory synaptic transmission mediated by either glycine or GABA during episodes of rhythmic fictive swimming in postem-bryonic Xenopus laevis tadpoles. Extracellular ventral-root recordings suggest a stage-dependent increase in the reliability and extent of the NO donor S-nitroso-n-acetylpenicillamine (SNAP; 0.1-1 mM) to inhibit swimming by reducing the frequency and shortening the duration of swim episodes. These effects of SNAP on the swimming rhythm at both developmental stages are corroborated by intracellular recordings from presumed motor neurons with sharp microelectrodes, which also suggest that NO inhibits swimming by facilitating both glycinergic and GABAergic inhibition. However, we found no evidence for NO modulation of the excitatory drive for swimming. In addition to presynaptic effects on inhibitory transmitter release, a pronounced postsynaptic membrane depolarization (∼5-10 mV) and conductance decrease (∼10-20%) are associated with bath application of SNAR Hence, NO exerts inhibitory effects on swimming through multiple but selective actions on both the electrical properties of spinal neurons and on particular synaptic interconnections. The presynaptic and postsynaptic effects of NO act in concert to tune inhibitory synapses.
|Original language||English (US)|
|Number of pages||10|
|Journal||Journal of Neuroscience|
|State||Published - May 15 2002|
- Nitric oxide
- Spinal cord
ASJC Scopus subject areas