{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T13:55:54Z","timestamp":1774446954511,"version":"3.50.1"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2004,3,9]],"date-time":"2004-03-09T00:00:00Z","timestamp":1078790400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurobiol."],"published-print":{"date-parts":[[2004,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In crayfish, movement of the tailfan causes stimulation of exteroceptive sensory hairs located on its surface. Movement is monitored by a proprioceptor, the protopodite\u2010endopodite 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\u2010application of the NO\u2010precursor <jats:sc>L<\/jats:sc>\u2010arginine, the NO donor SNAP, the NOS\u2010inhibitor L\u2010NAME, and the NO scavenger PTIO, while changes in PAD amplitude were measured. Application of <jats:sc>L<\/jats:sc>\u2010arginine or SNAP resulted in consistent decreases in PAD amplitude, whereas L\u2010NAME 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. \u00a9 2004 Wiley Periodicals, Inc. 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