Chemoreceptor Cells Research Articles

Acute Cardiovascular and Sympathetic Effects of Nicotine Replacement Therapy

Sympathetic overactivity is implicated in the increased cardiovascular risk of cigarette smokers. Excitatory nicotinic receptors are present on peripheral chemoreceptor cells. Chemoreceptors located in the carotid and aortic bodies increase ventilation (Ve), blood pressure (BP), heart rate (HR), and sympathetic nerve activity to muscle circulation (MSNA) in response to hypoxia. We tested the hypothesis that nicotine replacement therapy (NRT) increases MSNA and chemoreceptor sensitivity to hypoxia. Sixteen young healthy smokers were included in the study (8 women). After a randomized and blinded sublingual administration of a 4-mg tablet of nicotine or placebo, we measured minute Ve, HR, mean BP, and MSNA during normoxia and 5 minutes of isocapnic hypoxia. Maximal voluntary end-expiratory apneas were performed at baseline and at the end of the fifth minute of hypoxia. Nicotine increased HR by 7+/-3 bpm, mean BP by 5+/-2 mm Hg, and MSNA by 4+/-1 bursts/min, whereas subjects breathed room air (all P<0.05). During hypoxia, nicotine also raised HR by 8+/-2 bpm, mean BP by 2+/-1 mm Hg, and MSNA by 7+/-2 bursts/min (all P<0.05). Nicotine increased MSNA during the apneas performed in normoxia and hypoxia (P<0.05). Nicotine also raised the product of systolic BP and HR, a marker of cardiac oxygen consumption, during normoxia, hypoxia, and the apneas (P<0.05). Ve, apnea duration, and O2 saturation during hypoxia and the apneas remained unaffected. In conclusion, sympathoexcitatory effects of NRT are not because of an increased chemoreflex sensitivity to hypoxia. NRT increases myocardial oxygen consumption in periods of reduced oxygen availability.

Endothelins in the cat petrosal ganglion and carotid body: Effects and immunolocalization

In response to hypoxia, chemoreceptor cells of the carotid body (CB) release transmitters, which acting on the petrosal ganglion (PG) neuron terminals, increase the chemoafferent discharge. Additionally, vasoactive molecules produced within the CB may modulate hypoxic chemoreception by controlling blood flow and tissue PO 2. Endothelin-1 (ET-1) increases basal CB chemosensory discharges in situ, probably due to its vasoconstrictor action. However, the actions of ET-1 on PG neurons or its expression in the PG are not known. Using immunohistochemistry, we found that endothelin-like peptides are expressed in the cat PG and CB under normoxic conditions. Exogenous applications of ET-1 increased the chemosensory activity in the vascularly perfused CB but were ineffective on either the CB or PG superfused preparations, both of which are devoid of vascular control. Thus, our data indicate that the excitatory effect of ET-1 in the carotid chemoreceptor system appears to be mainly due to a vasoconstrictor effect in the CB blood vessels.

Activity modulation in cockroach sensillum: The role of octopamine

The plasticity of sensory perception is provided partially by modulation of receptor cells. The electrical activity of American cockroach chemoreceptor cells in response to sex pheromone was measured under the influence of octopamine treatment and tracheal anoxia. Both experimental procedures caused decreased electroantennograms but affected spike activity differently: octopamine treatment increased firing rate, whereas anoxia decreased it. Spike frequency under octopamine treatment was elevated in response to pheromone stimulation and at background activity. Experiments with perfusion of isolated antennae showed a direct effect of octopamine on spike activity of pheromone sensilla, and excluded the possibility of indirect effects via octopamine-dependent release of other biologically active substances. The suggested mechanism of octopamine action is receptor cell membrane depolarization.

The olfactory pathway for individual recognition in the American lobsterHomarus americanus

Individual recognition in the lobster Homarus americanus (Milne-Edwards), is based on detection of urine pheromones via chemoreceptors of the lateral antennular flagellum. The specific sensory pathway mediating this recognition is not known. Most of the chemoreceptor cells of this flagellum are found in the unimodal aesthetasc sensilla and project specifically to the glomeruli of the olfactory lobe in the brain. Additional chemoreceptor cells are located among mechanoreceptor cells in bimodal sensilla, including the guard hairs; they do not project to the olfactory lobe. This neuroanatomy suggested that aesthetascs were essential to all complex chemosensory tasks until it was shown that spiny lobsters Panulirus argus can still perform complex food odor discrimination and localization tasks without aesthetascs. Here, we demonstrate that the aesthetascs of H. americanus contain the chemoreceptors necessary for individual recognition of familiar opponents. In contrast to intact and guard hair-shaved animals, lobsters with aesthetascs removed did not recognize previous opponents as shown by second encounters statistically similar in length and aggression to first-encounter fights. Non-aesthetasc chemosensory pathways were incapable of rescuing opponent recognition. Subsequent lesion of all remaining chemoreceptor cells (by immersion in distilled water) abolished recognition and renewed fighting.

Down regulation of Kv3.4 channels by chronic hypoxia increases acute oxygen sensitivity in rabbit carotid body

The carotid body (CB) chemoreceptors participate in the ventilatory responses to acute and chronic hypoxia (CH). Arterial hypoxaemia increases breathing within seconds, and CB chemoreceptors are the principal contributors to this reflex hyperventilatory response. Acute hypoxia induces depolarization of CB chemoreceptors by inhibiting certain K+ channels, but the role of these channels in CH, as in high-altitude acclimatization, is less known. Here we explored the effects of prolonged (24-48 h) hypoxic exposure of rabbit CB chemoreceptor cells in primary cultures on the voltage-dependent K+ currents and on their response to acute hypoxia. We found that CH induces a decrease in the amplitude of outward K+ currents due to a reduction in a fast-inactivating BDS- and highly TEA-sensitive component of the current. In spite of this effect, acute hypoxic inhibition of K+ currents is increased in CH cultures, as well as hypoxia-induced depolarization. These data suggest that downregulation of this component (that does not contribute to the oxygen-sensitive K+ current (IKO2) participates in the hypoxic sensitization. Pharmacological, immunocytochemical and quantitative PCR (qPCR) experiments demonstrate that CH-induced decrease in outward K+ currents is due to a downregulation of the expression of Kv3.4 channels. Taken together, our results suggest that CH sensitization in rabbit CB could be achieved by an increase in the relative contribution of IKO2 to the outward K+ current as a consequence of the decreased expression of the oxygen-insensitive component of the current. We conclude that acute and chronic hypoxia can exert their effects acting on different molecular targets.

What Is a Pheromone? Mammalian Pheromones Reconsidered

Pheromone communication is a two-component system: signaling pheromones and receiving sensory neurons. Currently, pheromones remain enigmatic bioactive compounds, as only a few have been identified, but classical bioassays have suggested that they are nonvolatile, activate vomeronasal sensory neurons, and regulate innate social behaviors and neuroendocrine release. Recent discoveries of potential pheromones reveal that they may be more structurally and functionally diverse than previously defined.

Neurotransmitters in carotid body development

This review examines the possible role of neurotransmitters present in the carotid body on the functional expression of chemosensory activity during postnatal development. In particular, dopamine, acetylcholine, adenosine and neuropeptides are reviewed. Evidence to date shows involvement of these transmitters in signal transmission from the chemoreceptor cells to chemosensory afferent fibers of the sinus nerve, with clear age- or maturation-dependence of some aspects. However, it remains unresolved whether these neurotransmitters, some of which are expressed in the carotid body before birth, are directly involved in the maturation of the functional properties of the carotid chemoreceptors in sensing oxygen or other stimuli during postnatal development.

Solitary chemoreceptor cell proliferation in adult nasal epithelium

Nasal trigeminal chemosensitivity in mice and rats is mediated in part by solitary chemoreceptor cells (SCCs) in the nasal epithelium (Finger et al., 2003). Many nasal SCCs express the G-protein alpha-gustducin as well as other elements of the bitter-taste signaling cascade including phospholipase Cbeta2, TRPM5 and T2R bitter-taste receptors. While some populations of sensory cells are replaced throughout life (taste and olfaction), others are not (hair cells and carotid body chemoreceptors). These experiments were designed to test whether new SCCs are generated within the epithelium of adult mice. Wild type C57/B6 mice were injected with the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label dividing cells. At various times after injection (1-40 days), the mice were perfused with 4% paraformaldehyde and prepared for dual-label immunocytochemistry. Double labeled cells were detected as early as 3 days post BrdU injection and remained for as long as 12 days post-injection suggesting that SCCs do undergo turnover like the surrounding nasal epithelium. No BrdU labeled cells were detected after 24 days suggesting relatively rapid replacement of the SCCs.

Role of voltage‐dependent calcium channels in stimulus–secretion coupling in rabbit carotid body chemoreceptor cells

We have defined Ca2+ channel subtypes expressed in rabbit carotid body (CB) chemoreceptor cells and their participation in the stimulus-evoked catecholamine (CA) release. Ca2+ currents (I(Ca)) activated at -30 mV, peaked at +10 mV and were fully blocked by 200 microm Cd2+. L-type channels (sensitive to 2 microm nisoldipine) activated at -30 mV and carried 21 +/- 2% of total I(Ca). Non-L-type channels activated at potentials positive to -10 mV and carried: N channels (sensitive to 1 microM omega-conotoxin-GVIA) 16 +/- 1% of total I(Ca), P/Q channels (sensitive to 3 microM omega-conotoxin-MVIIC after nisoldipine plus GVIA) 23 +/- 3% of total I(Ca) and R channels (resistant to all blockers combined) 40 +/- 3% of total I(Ca). CA release induced by hypoxia, hypercapnic acidosis, dinitrophenol (DNP) and high K(+)(o) in the intact CB was inhibited by 79-98% by 200 microm Cd2+. Hypoxia, hypercapnic acidosis and DNP, depolarized chemoreceptor cells and eventually generated repetitive action potential discharge. Nisoldipine plus MVIIC nearly abolished the release of CAs induced by hypoxia and hypercapnic acidosis and reduced by 74% that induced by DNP. All these secretory responses were insensitive to GVIA. 30 and 100 mm K(+)(o) brought resting membrane potential (E(m)) of chemoreceptor cells (-48.1 +/- 1.2 mV) to -22.5 and +7.2 mV, respectively. Thirty millimolar K(+)(o)-evoked release was abolished by nisoldipine but that induced by 100 mm K(+)(o) was mediated by activation of L, N, and P/Q channels. Data show that tested stimuli depolarize rabbit CB chemoreceptor cells and elicit CA release through Ca2+ entry via voltage-activated channels. Only L and P/Q channels are tightly coupled to the secretion of CA.

Postnatal development of E-4031-sensitive potassium current in rat carotid chemoreceptor cells

The O2 sensitivity of dissociated type I cells from rat carotid body increases with age until approximately 14-16 days. Hypoxia-induced depolarization appears to be mediated by an O2-sensitive K+ current, but other K+ currents may modulate depolarization. We hypothesized that membrane potential may be stabilized in newborn type I cells by human ether-a-go-go-related gene (HERG)-like K+ currents that inhibit hypoxia-induced depolarization and that a decrease in this current with age could underlie, in part, the developmental increase in type I cell depolarization response to hypoxia. In dissociated type I cells from 0- to 1- and 11- to 16-day-old rats, using perforated patch-clamp and 70 mM K+ extracellular solution, we measured repolarization-induced inward K+ tail currents in the absence and presence of E-4031, a specific HERG channel blocker. This allowed isolation of the E-4031-sensitive HERG-like current. E-4031-sensitive peak currents in type I cells from 0- to- 1-day-old rats were 2.5-fold larger than in cells from 11- to 16-day-old rats. E-4031-sensitive current density in newborn type I cells was twofold greater than in cells from 11- to 16-day-old rats. Under current clamp conditions, E-4031 enhanced hypoxia-induced depolarization in type I cells from 0- to- 1-day-old but not 11- to 16-day-old rats. With use of fura 2 to measure intracellular Ca2+, E-4031 increased the cytosolic Ca2+ concentration response to anoxia in cells from 0- to- 1-day-old but not cells from 11- to 16-day-old rats. E-4031-sensitive K+ currents are present in newborn carotid body type I cells and decline with age. These findings are consistent with a role for E-4031-sensitive K+ current, and possibly HERG-like K+ currents, in the type I cell hypoxia response maturation.

Endothelins and Nitric Oxide: Vasoactive Modulators of Carotid Body Chemoreception

The carotid body (CB) is the main arterial chemoreceptor that senses arterial PO2, PCO2 and pH. The structural unit of the CB is the glomoid, which is formed by clusters of chemoreceptor (glomus) cells located around the capillaries. The glomus cells are synaptically connected to nerve terminals of petrosal ganglion (PG) neurons and surrounded by sustentacular cells. The most accepted model of CB chemoreception states that glomus cells are the primary sensors. In response to hypoxia, hypercapnia and acidosis, glomus cells release one or more transmitters, which acting on the nerve terminals of sensory PG neurons, increase the chemosensory discharge. The CB has a high blood flow and an elevated metabolism that correlate to its oxygen-sensing function. Thus, vasoactive molecules produced within the CB may modulate the chemosensory process by controlling the CB blood flow and tissue PO2. In this review, we examine recent evidence supporting the idea that endothelins (ETs) and nitric oxide (NO) modulate the CB function acting upon chemoreceptor cells and chemosensory neurons or by regulating the blood flow through the CB parenchyma.

?-Gustducin immunoreactivity in the airways

The G-protein subunit alpha-gustducin is a marker of chemoreceptive cells. In the present study, we examined the immunohistochemical localization of alpha-gustducin in rat airway epithelium both by light and electron microscopy. alpha-Gustducin immunoreactivity was found in solitary cells that presented ultrastructural features of chemoreceptor cells, i.e. flask-shaped or pear-shaped, with an apical process with thin microvilli protruding into the lumen. The immunostaining was mainly concentrated in the apical process and along the basolateral cell surface. To investigate whether alpha-gustducin-immunoreactive cells represented a distinct cell subset in rat airways, we performed double-label immunocytochemistry with antibodies to protein gene groduct (PGP) 9.5, a marker of neuroendocrine cells, and to phospholipase C beta2 (PLCbeta2), a component of the bitter signalling pathway. alpha-Gustducin-immunoreactive cells were present in a subset of PGP-9.5-immunoreactive elements, although not all alpha-gustducin-positive cells expressed PGP 9.5 labelling. In addition, a subset of alpha-gustducin-expressing cells colocalized PLCbeta2. This work thus demonstrates that solitary alpha-gustducin-immunoreactive cells exist throughout the airways and represent a specialized cell type with morphological and immunohistochemical characteristics of chemoreceptor cells.

Laryngeal chemosensory clusters.

The expression of molecules involved in the transductory cascade of the sense of taste (TRs, alpha-gustducin, PLCbeta2, IP3R3) has been described in lingual taste buds or in solitary chemoreceptor cells located in different organs. At the laryngeal inlet, immunocytochemical staining at the light and electron microscope levels revealed that alpha-gustducin and PLCbeta2 are mainly localized in chemosensory clusters (CCs), which are multicellular organizations differing from taste buds, being generally composed of two or three chemoreceptor cells. Compared with lingual taste buds, CCs are lower in height and smaller in diameter. In laryngeal CCs, immunocytochemistry using the two antibodies identified a similar cell type which appears rather unlike the alpha-gustducin-immunoreactive (IR) and PLCbeta2-IR cells visible in lingual taste buds. The laryngeal IR cells are shorter than the lingual ones, with poorly developed basal processes and their apical process is shorter and thicker. Some cells show a flask-like shape due to the presence of a large body and the absence of basal processes. CCs lack pores and their delimitation from the surrounding epithelium is poorly evident. The demonstration of the existence of CCs strengthens the hypothesis of a phylogenetic link between gustatory and solitary chemosensory cells.

Detection of hypoxia-evoked ATP release from chemoreceptor cells of the rat carotid body

The carotid body (CB) is a chemosensory organ that detects changes in chemical composition of arterial blood and maintains homeostasis via reflex control of ventilation. Thus, in response to a fall in arterial PO 2 (hypoxia), CB chemoreceptors (type I cells) depolarize, and release neurotransmitters onto afferent sensory nerve endings. Recent studies implicate ATP as a key excitatory neurotransmitter released during CB chemoexcitation, but direct evidence is lacking. Here we use the luciferin–luciferase bioluminescence assay to detect ATP, released from rat chemoreceptors in CB cultures, fresh tissue slices, and whole CB. Hypoxia evoked an increase in extracellular ATP, that was inhibited by L-type Ca 2+channel blockers and reduced by the nucleoside hydrolase, apyrase. Additionally, iberiotoxin (IbTX; 100 nM), a blocker of O 2-sensitive Ca 2+-dependent K + (BK) channels, stimulated ATP release and largely occluded the effect of hypoxia. These data strongly support a neurotransmitter role for ATP in carotid body function.

Identification and characterization of a specific sensory epithelium in the rat larynx.

A specific laryngeal sensory epithelium (SLSE), which includes arrays of solitary chemoreceptor cells, is described in the supraglottic region of the rat. Two plates of SLSE were found, one on each side of the larynx. The first plate was located in the ventrolateral wall of the larynx, and the second was located in the interarytenoidal region. In SLSE, immunoblotting showed the presence of alpha-gustducin and phospholipase C beta2 (PLCbeta2), which are two markers of chemoreceptor cells. At immunocytochemistry, laryngeal immunoreactivity for alpha-gustducin was localized mainly in solitary chemosensory cells. Double-label immunocytochemistry using confocal microscopy demonstrated that alpha-gustducin-expressing cells in large part colocalize type III IP3 receptor (IP3R3), another key molecule in bitter taste perception. However, some IP3R3-expressing cells do not colocalize alpha-gustducin. At ultrastructural immunocytochemistry, these cells showed packed apical microvilli, clear cytoplasmic vesicles, and cytoneural junctions. SLSE was characterized by high permeability to a tracer due to poorly developed junctional contacts between superficial cells. Junctions were short in length and showed little contact with the terminal web. Ultrastructural analysis showed deep pits among the superficial cells. In SLSE, high density of intraepithelial nerve fibers was found. The lamina propria of the SLSE appeared thicker than that in other supraglottic regions. It was characterized by the presence of a well-developed subepithelial nerve plexus. The immunocytochemical and ultrastructural data suggested that SLSE is a chemoreceptor located in an optimal position for detecting substances entering the larynx from the pharynx or the trachea.

Espins are multifunctional actin cytoskeletal regulatory proteins in the microvilli of chemosensory and mechanosensory cells.

Espins are associated with the parallel actin bundles of hair cell stereocilia and are the target of mutations that cause deafness and vestibular dysfunction in mice and humans. Here, we report that espins are also concentrated in the microvilli of a number of other sensory cells: vomeronasal organ sensory neurons, solitary chemoreceptor cells, taste cells, and Merkel cells. Moreover, we show that hair cells and these other sensory cells contain novel espin isoforms that arise from a different transcriptional start site and differ significantly from other espin isoforms in their complement of ligand-binding activities and their effects on actin polymerization. The novel espin isoforms of sensory cells bundled actin filaments with high affinity in a Ca(2+)-resistant manner, bound actin monomer via a WASP (Wiskott-Aldrich syndrome protein) homology 2 domain, bound profilin via a single proline-rich peptide, and caused a dramatic elongation of microvillus-type parallel actin bundles in transfected epithelial cells. In addition, the novel espin isoforms of sensory cells differed from other espin isoforms in that they potently inhibited actin polymerization in vitro, did not bind the Src homology 3 domain of the adapter protein insulin receptor substrate p53, and did not bind the acidic, signaling phospholipid phosphatidylinositol 4,5-bisphosphate. Thus, the espins constitute a family of multifunctional actin cytoskeletal regulatory proteins with the potential to differentially influence the organization, dimensions, dynamics, and signaling capabilities of the actin filament-rich, microvillus-type specializations that mediate sensory transduction in various mechanosensory and chemosensory cells.

Characterization of the Kv channels of mouse carotid body chemoreceptor cells and their role in oxygen sensing.

As there are wide interspecies variations in the molecular nature of the O(2)-sensitive Kv channels in arterial chemoreceptors, we have characterized the expression of these channels and their hypoxic sensitivity in the mouse carotid body (CB). CB chemoreceptor cells were obtained from a transgenic mouse expressing green fluorescent protein (GFP) under the control of tyrosine hydroxylase (TH) promoter. Immunocytochemical identification of TH in CB cell cultures reveals a good match with GFP-positive cells. Furthermore, these cells show an increase in [Ca(2+)](i) in response to low P(O(2)), demonstrating their ability to engender a physiological response. Whole-cell experiments demonstrated slow-inactivating K(+) currents with activation threshold around -30 mV and a bi-exponential kinetic of deactivation (tau of 6.24 +/- 0.52 and 32.85 +/- 4.14 ms). TEA sensitivity of the currents identified also two different components (IC(50) of 17.8 +/- 2.8 and 940.0 +/- 14.7 microm). Current amplitude decreased reversibly in response to hypoxia, which selectively affected the fast deactivating component. Hypoxic inhibition was also abolished in the presence of low (10-50 microm) concentrations of TEA, suggesting that O(2) interacts with the component of the current most sensitive to TEA. The kinetic and pharmacological profile of the currents suggested the presence of Kv2 and Kv3 channels as their molecular correlates, and we have identified several members of these two subfamilies by single-cell PCR and immunocytochemistry. This report represents the first functional and molecular characterization of Kv channels in mouse CB chemoreceptor cells, and strongly suggests that O(2)-sensitive Kv channels in this preparation belong to the Kv3 subfamily.

Role of Glutathione Redox State in Oxygen Sensing by Carotid Body Chemoreceptor Cells

This chapter discusses the role of glutathione redox state in oxygen sensing by carotid body (CB) chemoreceptor cells. The basic structural traits of the carotid body CB arterial chemoreceptors are presented to understand the relationship between the arterial blood PO 2 and the activation of chemoreceptor cells, which are the O 2 sensing structures of the CB. The threshold for the detection of the hypoxic stimulus, and the glutathione system causing modifications in the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio are discussed.The relationship between GSH/GSSG and the oxygen chemoreception is approached from two different points of view. The GSH/ GSSG levels are measured, followed by calculation of the redox environment of the cells and correlation with the activity of chemoreceptor cells in normoxia and in hypoxia. Data is presented on pharmacological manipulation of the redox environment of the cells, as assessed by GSH/GSSG quotients, and possible correlations with the level of activity of chemoreceptor cells. The possible mechanisms of coupling between ROS and the GSH/GSSG system to the cellular effector machineries are also reviewed.

Molecular Strategies for Studying Oxygen-Sensitive K+ Channels

Publisher Summary This chapter focuses on the molecular strategies for studying oxygen-sensitive K + channels. It discusses about environmental hypoxia that evokes a rapid reflex increase in the respiration rate. This reflex is initiated in the carotid bodies located at the bifurcation of the carotid arteries. Upon a decrease in arterial pO 2 , chemoreceptor type I carotid body cells release neurotransmitters that activate afferent sensory fibers of the sinus nerve stimulating the brain stem respiratory centers and provoking a reflex increase in ventilation. In this chapter, various methods employed to study O 2 -sensitive ion channels in chemosensitive cells are described. The chapter discusses technical issues including: (i) isolation and culture of chemosensitive cells, (ii) methods for detecting and visualizing ion channel mRNAs and proteins in chemoreceptor cells, (iii) electrophysiological techniques for studying O 2 -sensitive K + channels, (iv) molecular strategies to interfere with O 2 -sensitive K + channels, and (v) the functional role of one such ion channel, the TASK-like K + channel, which plays a key role in O 2 sensing in carotid body type I cells.

Intrinsic nitric oxide regulates the taste response of the sugar receptor cell in the blowfly, Phormia regina.

The taste organ in insects is a hair-shaped taste sensory unit having four functionally differentiated contact chemoreceptor cells. In the blowfly, Phormia regina, cGMP has been suggested to be a second messenger for the sugar receptor cell. Generally, cGMP is produced by membranous or soluble guanylyl cyclase (sGC), which can be activated by nitric oxide (NO). In the present paper, we electrophysiologically showed that an NO scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-3-oxide-1-oxyl (PTIO), an NO donor, 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC 7) or an NO synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) specifically affected the response in the sugar receptor cell, but not in other receptor cells. PTIO, when introduced into the receptor cells in a sensillum aided by sodium deoxycholate (DOC, pH 7.2), depressed the response of sugar receptor cells to sucrose but did not affect those of the salt or water receptor cells. NOC 7, given extracellularly, latently induced the response of sugar receptor cells; and L-NAME, when introduced into the receptor cells, depressed the response of sugar receptor cells. The results clearly suggest that NO, which may be produced by intrinsic NOS in sugar receptor cells, participates in the transduction cascade of these cells in blowfly.