Nitric oxide modulates sodium taste via a cGMP-independent pathway.
Insects, like other animals, require sodium chloride (NaCl) as part of their normal diet and detect it with contact chemoreceptors on the body surface. By adjusting the responsiveness of the chemosensory neurons within these receptors insects can modify the intake of salt and other nutrients, and it has been hypothesized that the responsiveness of chemosensory neurons is regulated by nitric oxide (NO). To identify potential sources of NO in the periphery, the authors applied the NO-sensitive fluorescent probe 4,5-diaminofluorescein and the universal NO synthase antibody, and found that in locusts NO is synthesized within one particular class of cells of the epidermis, the glandular cells, from where it may diffuse to neighboring chemosensory neurons. The effects of NO on chemosensory neurons were investigated by recording from contact chemoreceptors on the leg while perfusing it with drugs that interfere with NO signaling. Results showed that both endogenous and exogenous NO decreased the frequency of action potentials in chemosensory neurons in response to stimulation with NaCl by acting via a cyclic guanosine monophosphate-independent pathway. Variation of the NaCl concentration in the perfusion solution demonstrated that the synthesis of NO in glandular cells depends on the NaCl concentration in the hemolymph. By contrast NO increased the frequency of action potentials in chemosensory neurons in response to sucrose stimulation. The authors suggest that NO released from glandular cells modulates the responsiveness of chemosensory neurons to regulate NaCl intake, and hypothesize that NO may play a key role in the signaling of salt and sugars.
Schuppe
H
H
Southampton Neuroscience Group, School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, United Kingdom. hs8@soton/ac/uk
Cuttle
M
M
Newland
P L
PL
D000200:Action Potentials / Q000187:drug effects; D000704:Analysis of Variance; D000818:Animals; D006152:Cyclic GMP / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004791:Enzyme Inhibitors / Q000494:pharmacology; D000078404:Epidermal Cells; D004817:Epidermis / Q000648:ultrastructure; D019793:Fluorescein / Q000378:metabolism; D006110:Grasshoppers; D006834:Hydrazines / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009475:Neurons, Afferent / Q000187:drug effects; D009569:Nitric Oxide / Q000378:metabolism* / Q000494:pharmacology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D012964:Sodium; D012965:Sodium Chloride / Q000494:pharmacology; D013649:Taste / Q000187:drug effects / Q000502:physiology*
C111205:4,5-diaminofluorescein; D004791:Enzyme Inhibitors; D006834:Hydrazines; D020030:Nitric Oxide Donors; C112653:PAPA NONOate; D009569:Nitric Oxide; D012965:Sodium Chloride; D012964:Sodium; D019001:Nitric Oxide Synthase; D006152:Cyclic GMP; D019793:Fluorescein; D019331:NG-Nitroarginine Methyl Ester