Nitric oxide modulates presynaptic afferent depolarization of mechanosensory neurons

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Description/Abstract

In crayfish, movement of the tailfan causes stimulation of exteroceptive sensory hairs located
on its surface. Movement is monitored by a proprioceptor,
the protopodite-endopodite chordotonal organ
within the tailfan. Proprioceptive afferents provide indirect
presynaptic inhibitory inputs to sensory hair afferents
in the form of primary afferent depolarizations
(PADs). Bath application of nitric oxide (NO) substrates,
donors and scavengers, and nitric oxide synthase (NOS)
inhibitors had no effect on the responses of proprioceptive
afferents during imposed movements of the chordotonal
organ. In contrast, the amplitude of PADs in
exteroceptive hair afferents was dependent on NO levels.
NO levels were altered by bath-application of the NOprecursor
L-arginine, the NO donor SNAP, the NOSinhibitor
L-NAME, and the NO scavenger PTIO, while
changes in PAD amplitude were measured. Application
of L-arginine or SNAP resulted in consistent decreases in
PAD amplitude, whereas L-NAME and PTIO induced
increases in PAD amplitude. These results suggest that
endogenous NO decreases inhibitory inputs to exteroceptive
neurons, thus enhancing transmitter release at
their output synapses.