Calcium Activates a Chloride Conductance Likely Involved in Olfactory Receptor Neuron Repolarization in the Moth<i>Spodoptera littoralis</i>

Pezier, Adeline; Grauso, Marta; Acquistapace, Adrien; Monsempes, Christelle; Rospars, Jean-Pierre; Lucas, Philippe

doi:10.1523/jneurosci.0261-10.2010

Cited by 17 publications

(21 citation statements)

References 57 publications

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“…Inhibition by FFA has also been observed in other native CaCCs in rabbit portal vein, pig ventricular cardiomyocytes, as well as olfactory receptors neurons from moth Spodoptera littoralis (Greenwood & Large, 1995; Gwanyanya et al, 2010; Pezier et al, 2010). FFA appears to exert an open-channel block like in CFTR (Greenwood & Large, 1995).…”

Section: Flufenamic Acid As An Ion Channel Modulatormentioning

confidence: 68%

Flufenamic acid as an ion channel modulator

Guinamard

Simard

Negro

2013

Pharmacology & Therapeutics

119

113

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Flufenamic acid has been known since the 1960s to have anti-inflammatory properties attributable to the reduction of prostaglandin synthesis. Thirty years later, flufenamic acid appeared to be an ion channel modulator. Thus, while its use in medicine diminished, its use in ionic channel research expanded. Flufenamic acid commonly affects non-selective cation channels and chloride channels, but also modulates potassium, calcium and sodium channels with effective concentrations ranging from 10-6 M in TRPM4 channel inhibition to 10-3 M in two-pore outwardly rectifying potassium channel activation. Because flufenamic acid effects develop and reverse rapidly, it is a convenient and widely used tool. However, given the broad spectrum of its targets, experimental results have to be interpreted cautiously. Here we provide an overview of ion channels targeted by flufenamic acid to aid in interpreting its effects at the molecular, cellular, and systems levels. If it is used with good practices, flufenamic acid remains a useful tool for ion channel research. Understanding the targets of FFA may help reevaluate its physiological impacts and revive interest in its therapeutic potential.

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Section: Flufenamic Acid As An Ion Channel Modulatormentioning

confidence: 68%

Flufenamic acid as an ion channel modulator

Guinamard

Simard

Negro

2013

Pharmacology & Therapeutics

119

113

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“…It is known that aedeskinins hyperpolarize the basolateral membrane voltage by increasing the chloride conductance of Malpighian tubule cells in A. aegypti (8,40). A simple speculative explanation is that, acting via the Aedae-KR, analog 1728 changes the chloride concentration in the sensillum lymph, thus affecting the chloride channels involved in the repolarization of gustatory neurons and making the sucrose receptor cells insensitive (41). There is a lack of knowledge regarding chemosensory reception in mosquito leg sensilla.…”

Section: Discussionmentioning

confidence: 99%

Leucokinin mimetic elicits aversive behavior in mosquito Aedes aegypti (L.) and inhibits the sugar taste neuron

Kwon

Agha

Smith

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Insect kinins (leucokinins) are multifunctional peptides acting as neurohormones and neurotransmitters. In females of the mosquito vector Aedes aegypti (L.), aedeskinins are known to stimulate fluid secretion from the renal organs (Malpighian tubules) and hindgut contractions by activating a G protein-coupled kinin receptor designated "Aedae-KR." We used protease-resistant kinin analogs 1728, 1729, and 1460 to evaluate their effects on sucrose perception and feeding behavior. In no-choice feeding bioassays (capillary feeder and plate assays), the analog 1728, which contains α-amino isobutyric acid, inhibited females from feeding on sucrose. It further induced quick fly-away or walk-away behavior following contact with the tarsi and the mouthparts. Electrophysiological recordings from single long labellar sensilla of the proboscis demonstrated that mixing the analog 1728 at 1 mM with sucrose almost completely inhibited the detection of sucrose. Aedae-KR was immunolocalized in contact chemosensory neurons in prothoracic tarsi and in sensory neurons and accessory cells of long labellar sensilla in the distal labellum. Silencing Aedae-KR by RNAi significantly reduced gene expression and eliminated the feeding-aversion behavior resulting from contact with the analog 1728, thus directly implicating the Aedae-KR in the aversion response. To our knowledge, this is the first report that kinin analogs modulate sucrose perception in any insect. The aversion to feeding elicited by analog 1728 suggests that synthetic molecules targeting the mosquito Aedae-KR in the labellum and tarsi should be investigated for the potential to discover novel feeding deterrents of mosquito vectors.neuropeptide GPCR | sucrose taste | sensory neuron | chemical target validation | feeding deterrent

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“…Rising intracellular Ca 2+ concentrations and increasing depolarization then might open voltage- and Ca 2+ -dependent cation and Cl − channels found in ORNs (Zufall et al, 1991a; Dolzer et al, 2008; Pézier et al, 2010). Possibly, these ion channel openings might underlie the elementary receptor potentials (bumps) observed in moth ORNs (Minor and Kaissling, 2003).…”

Section: Subthreshold Membrane Potential Oscillations Of Orns and Temmentioning

confidence: 99%

Pheromone Transduction in Moths

Stengl

2010

Front. Cell. Neurosci.

137

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Calling female moths attract their mates late at night with intermittent release of a species-specific sex-pheromone blend. Mean frequency of pheromone filaments encodes distance to the calling female. In their zig-zagging upwind search male moths encounter turbulent pheromone blend filaments at highly variable concentrations and frequencies. The male moth antennae are delicately designed to detect and distinguish even traces of these sex pheromones amongst the abundance of other odors. Its olfactory receptor neurons sense even single pheromone molecules and track intermittent pheromone filaments of highly variable frequencies up to about 30 Hz over a wide concentration range. In the hawkmoth Manduca sexta brief, weak pheromone stimuli as encountered during flight are detected via a metabotropic PLCβ-dependent signal transduction cascade which leads to transient changes in intracellular Ca2+ concentrations. Strong or long pheromone stimuli, which are possibly perceived in direct contact with the female, activate receptor-guanylyl cyclases causing long-term adaptation. In addition, depending on endogenous rhythms of the moth's physiological state, hormones such as the stress hormone octopamine modulate second messenger levels in sensory neurons. High octopamine levels during the activity phase maximize temporal resolution cAMP-dependently as a prerequisite to mate location. Thus, I suggest that sliding adjustment of odor response threshold and kinetics is based upon relative concentration ratios of intracellular Ca2+ and cyclic nucleotide levels which gate different ion channels synergistically. In addition, I propose a new hypothesis for the cyclic nucleotide-dependent ion channel formed by insect olfactory receptor/coreceptor complexes. Instead of being employed for an ionotropic mechanism of odor detection it is proposed to control subthreshold membrane potential oscillation of sensory neurons, as a basis for temporal encoding of odors.

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Calcium Activates a Chloride Conductance Likely Involved in Olfactory Receptor Neuron Repolarization in the MothSpodoptera littoralis

Cited by 17 publications

References 57 publications

Flufenamic acid as an ion channel modulator

Flufenamic acid as an ion channel modulator

Leucokinin mimetic elicits aversive behavior in mosquito Aedes aegypti (L.) and inhibits the sugar taste neuron

Pheromone Transduction in Moths

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