The Journal of Neuroscience, May 15, 2002, 22(10):4175-4184
Nitric Oxide Selectively Tunes Inhibitory Synapses to Modulate
Vertebrate Locomotion
David L.
McLean and
Keith T.
Sillar
School of Biology, Division of Biomedical Sciences,
University of St. Andrews, St. Andrews, FIFE KY16 9TS, United
Kingdom
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 postembryonic 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 SNAP. 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.
Key words:
nitric oxide; GABA; glycine; spinal cord; release; locomotion
Copyright © 2002 Society for Neuroscience 0270-6474/02/22104175-10$05.00/0
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