Mechanoreceptor Potential Research Articles

NompC regulates locomotion and touch sensation in Bactrocera dorsalis.

No mechanoreceptor potential C (NompC) is a major mechanotransduction channel with an important role in sensing of external mechanical stimuli by insects, which help these organisms to avoid injury and adapt to environmental changes. To explore the biological functions of NompC in Bactrocera dorsalis, a notorious agricultural pest, we successfully generated NompC knockout strains using clustered regularly interspaced small palindromic repeats (CRISPR) / CRISPR-associated nuclease 9 (Cas9) technology. BdorNompC knockout led to an adult lethal phenotype, with approximately 100% mortality at 3 d after eclosion. Morphological observation revealed that the legs and wings of BdorNompC knockout insects were deformed, while behavioral assays showed that the locomotion was impaired in both adults and larvae, relative to that of the wild-type strain. Moreover, BdorNompC knockout reduced gentle-touch response in larvae. These results suggest that BdorNompC is critical for B. dorsalis survival, and that this mechanosensation channel represents a potential new target for pest control agents. Our findings also represent novel evidence indicating that insect NompC is involved in modulating adult wing and leg morphology.

The retrograde IFT dynein is required for normal function of diverse mechanosensory cilia in Drosophila.

Cilia biogenesis relies on intraflagellar transport (IFT), a conserved transport mechanism which functions bi-directionally to bring protein complexes to the growing ciliary tip and recycle signaling and transport proteins between the cilium and cell body. In Drosophila, anterograde IFT is critical for assembly of sensory cilia in the neurons of both chordotonal (ch) organs, which have relatively long ciliary axonemes, and external sensory (es) organs, which have short axonemal segments with microtubules in distal sensory segments forming non-axonemal bundles. We previously isolated the beethoven (btv) mutant in a mutagenesis screen for auditory mutants. Although many btv mutant flies are deaf, some retain a small residual auditory function as determined both by behavior and by auditory electrophysiology. Here we molecularly characterize the btv gene and demonstrate that it encodes the IFT-associated dynein-2 heavy chain Dync2h1. We also describe morphological changes in Johnston's organ as flies age to 30 days, and we find that morphological and electrophysiological phenotypes in this ch organ of btv mutants become more severe with age. We show that NompB protein, encoding the conserved IFT88 protein, an IFT complex B component, fails to be cleared from chordotonal cilia in btv mutants, instead accumulating in the distorted cilia. In macrochaete bristles, a class of es organ, btv mutants show a 50% reduction in mechanoreceptor potentials. Thus, the btv-encoded Dync2h1 functions as the retrograde IFT motor in the assembly of long ciliary axonemes in ch organs and is also important for normal function of the short ciliary axonemes in es organs.

The Voltage-Gated Sodium Channel in Drosophila, Para, Localizes to Dendrites As Well As Axons in Mechanosensitive Chordotonal Neurons.

The fruit fly Drosophila melanogaster has provided important insights into how sensory information is transduced by transient receptor potential (TRP) channels in the peripheral nervous system (PNS). However, TRP channels alone have not been able to completely model mechanosensitive transduction in mechanoreceptive chordotonal neurons (CNs). Here, we show that, in addition to TRP channels, the sole voltage-gated sodium channel (NaV) in Drosophila, Para, is localized to the dendrites of CNs. Para is localized to the distal tip of the dendrites in all CNs, from embryos to adults, and is colocalized with the mechanosensitive TRP channels No mechanoreceptor potential C (NompC) and Inactive/Nanchung (Iav/Nan). Para localization also demarcates spike initiation zones (SIZs) in axons and the dendritic localization of Para is indicative of a likely dendritic SIZ in fly CNs. Para is not present in the dendrites of other peripheral sensory neurons. In both multipolar and bipolar neurons in the PNS, Para is present in a proximal region of the axon, comparable to the axonal initial segment (AIS) in vertebrates, 40-60 μm from the soma in multipolar neurons and 20-40 μm in bipolar neurons. Whole-cell reduction of para expression using RNAi in CNs of the adult Johnston's organ (JO) severely affects sound-evoked potentials (SEPs). However, the duality of Para localization in the CN dendrites and axons identifies a need to develop resources to study compartment-specific roles of proteins that will enable us to better understand Para's role in mechanosensitive transduction.

Sugar sensation and mechanosensation in the egg-laying preference shift of Drosophila suzukii.

The agricultural pest Drosophila suzukii differs from most other Drosophila species in that it lays eggs in ripe, rather than overripe, fruit. Previously, we showed that changes in bitter taste sensation accompanied this adaptation (Dweck et al., 2021). Here, we show that D. suzukii has also undergone a variety of changes in sweet taste sensation. D. suzukii has a weaker preference than Drosophila melanogaster for laying eggs on substrates containing all three primary fruit sugars: sucrose, fructose, and glucose. Major subsets of D. suzukii taste sensilla have lost electrophysiological responses to sugars. Expression of several key sugar receptor genes is reduced in the taste organs of D. suzukii. By contrast, certain mechanosensory channel genes, including no mechanoreceptor potential C, are expressed at higher levels in the taste organs of D. suzukii, which has a higher preference for stiff substrates. Finally, we find that D. suzukii responds differently from D. melanogaster to combinations of sweet and mechanosensory cues. Thus, the two species differ in sweet sensation, mechanosensation, and their integration, which are all likely to contribute to the differences in their egg-laying preferences in nature.

A neural circuit integrates pharyngeal sensation to control feeding.

Swallowing is an essential step of eating and drinking. However, how the quality of a food bolus is sensed by pharyngeal neurons is largely unknown. Here we find that mechanical receptors along the Drosophila pharynx are required for control of meal size, especially for food of high viscosity. The mechanical force exerted by the bolus passing across the pharynx is detected by neurons expressing the mechanotransduction channel NOMPC (no mechanoreceptor potential C) and is relayed, together with gustatory information, to IN1 neurons in the subesophageal zone (SEZ) of the brain. IN1 (ingestion neurons) neurons act directly upstream of a group of peptidergic neurons that encode satiety. Prolonged activation of IN1 neurons suppresses feeding. IN1 neurons receive inhibition from DSOG1 (descending subesophageal neurons) neurons, a group of GABAergic neurons that non-selectively suppress feeding. Our results reveal the function of pharyngeal mechanoreceptors and their downstream neural circuits in the control of food ingestion.

Heterogeneous TRP Channel Model of a Chordotonal Neuron Might Explain Drosophila Hearing

Here, we propose a model for the Drosophila chordotonal neurons where the axoneme is an actively contracting wire, regulated by the calcium ion concentration. To date, which of Nanchung-inactive and no mechanoreceptor potential C channels are transient receptor potential channels (TRP) in chordotonal sensory cilia is still not clear. Our theory explains previous experimental findings, including non-linear gating compliance and spontaneous oscillation of the antenna. It also explains that neural signaling takes place only at amplitudes of mechanical stimulation much higher than those generating active amplification, which has not been explained so far within the conventional single-type TRP channel model.

Brv1 Is Required for Drosophila Larvae to Sense Gentle Touch

How we sense touch is fundamental for many physiological processes. However, the underlying mechanism and molecular identity for touch sensation arelargely unknown. Here, we report on defective gentle-touch behavioral responses in brv1 loss-of-function Drosophila larvae. RNAi and Ca2+ imaging confirmed the involvement of Brv1 in sensing touch and demonstrated that Brv1 mediates the mechanotransduction of class III dendritic arborization neurons. Electrophysiological recordings further revealed that the expression of Brv1 protein in HEK293T cells gives rise to stretch-activated cation channels. Purified Brv1 protein reconstituted into liposomes were found to sense stretch stimuli. In addition, co-expression studies suggested that Brv1 amplifies the response of mechanosensitive ion channel NOMPC (no mechanoreceptor potential C) to touch stimuli. Altogether, these findings demonstrate a molecular entity that mediates the gentle-touch response in Drosophila larvae, providing insights into the molecular mechanisms of touch sensation.

Highlights for the 6th International Ion Channel Conference: ion channel structure, function, disease and therapeutics

To foster communication and interactions amongst international scholars and scientists in the field of ion channel research, the 6th International Ion Channel Conference (IICC-2017) was held between June 23–27, 2017 in the eastern coastal city of Qingdao, China. The meeting consisted of 450 attendees and 130 speakers and poster presenters. The program consisted of research progress, new findings and ongoing studies that were focused on (1) Ion channel structure and function; (2) Ion channel physiology and human diseases; (3) Ion channels as targets for drug discovery; (4) Technological advances in ion channel research. An insightful overview was presented on the structure and function of the mechanotransduction channel Drosophila NOMPC (No mechanoreceptor potential C), a member of the transient receptor potential (TRP) channel family. Recent studies on Transmembrane protein 16 or Anoctamin-1 (TMEM16A, a member of the calcium-activated chloride channel [CaCC] family) were summarized as well. In addition, topics for ion channel regulation, homeostatic feedback and brain disorders were thoroughly discussed. The presentations at the IICC-2017 offer new insights into our understanding of ion channel structures and functions, and ion channels as targets for drug discovery.

NOMPC is likely a key component ofDrosophilamechanotransduction channels

Mechanotransduction is the basis of several sensory modalities, including touch, hearing, proprioception and gravity sensation. Despite its importance to sensory processing and behavior, the molecular mechanisms underlying mechanotransduction remain to be fully understood. In particular, the identity of the ion channels serving mechanotransduction is still unknown in many species. Drosophila melanogaster nompC (no mechanoreceptor potential C) has been shown to be essential for mechanotransduction in flies, yet there is no direct evidence demonstrating that NOMPC is indeed a mechanotransducing ion channel in Drosophila. To dissect the functional roles of NOMPC in mechanotransduction, we found that NOMPC-dependent transient adapting mechanoreceptor current (MRC) in the external bristle sensory organ was also chloride dependent. However, this chloride-dependent current was not necessary for spike generation. Furthermore, ectopic expression of wild-type NOMPC conferred mechanosensitivity on the interneurons in the antennal lobe (AL) and cation-mediated inward mechanocurrent was recorded, while a point mutation in the putative selective filter region of NOMPC failed to produce the mechanocurrent in the AL interneurons. These functional studies imply that NOMPC is likely to be a crucial component of mechanotransducers that accounts for mechanotransductions in mechanosensory neurons of Drosophila.

Drosophila NOMPC is a mechanotransduction channel subunit for gentle-touch sensation

Touch sensation is essential for behaviours ranging from environmental exploration to social interaction; however, the underlying mechanisms are largely unknown. In Drosophila larvae, two types of sensory neurons, class III and class IV dendritic arborization neurons, tile the body wall. The mechanotransduction channel PIEZO in class IV neurons is essential for sensing noxious mechanical stimuli but is not involved in gentle touch. On the basis of electrophysiological-recording, calcium-imaging and behavioural studies, here we report that class III dendritic arborization neurons are touch sensitive and contribute to gentle-touch sensation. We further identify NOMPC (No mechanoreceptor potential C), a member of the transient receptor potential (TRP) family of ion channels, as a mechanotransduction channel for gentle touch. NOMPC is highly expressed in class III neurons and is required for their mechanotransduction. Moreover, ectopic NOMPC expression confers touch sensitivity to the normally touch-insensitive class IV neurons. In addition to the critical role of NOMPC in eliciting gentle-touch-mediated behavioural responses, expression of this protein in the Drosophila S2 cell line also gives rise to mechanosensitive channels in which ion selectivity can be altered by NOMPC mutation, indicating that NOMPC is a pore-forming subunit of a mechanotransduction channel. Our study establishes NOMPC as a bona fide mechanotransduction channel that satisfies all four criteria proposed for a channel to qualify as a transducer of mechanical stimuli and mediates gentle-touch sensation. Our study also suggests that different mechanosensitive channels may be used to sense gentle touch versus noxious mechanical stimuli.

Dendritic Filopodia, Ripped Pocket, NOMPC, and NMDARs Contribute to the Sense of Touch in Drosophila Larvae

Among the Aristotelian senses, the subcellular and molecular mechanisms involved in the sense of touch are the most poorly understood. We demonstrate that specialized sensory neurons, the class II and class III multidendritic (md) neurons, are gentle touch sensors of Drosophila larvae. Genetic silencing of these cells significantly impairs gentle touch responses, optogenetic activation of these cells triggers behavioral touch-like responses, and optical recordings from these neurons show that they respond to force. The class III neurons possess highly dynamic dendritic protrusions rich in F-actin. Genetic manipulations that alter actin dynamics indicate that the actin-rich protrusions (termed sensory filopodia) on the class III neurons are required for behavioral sensitivity to gentle touch. Through a genome-wide RNAi screen of ion channels, we identified Ripped Pocket (rpk), No Mechanoreceptor Potential C (nompC), and NMDA Receptors 1 and 2 (Nmdars) as playing critical roles in both behavioral responses to touch and in the formation of the actin-rich sensory filopodia. Consistent with this requirement, reporters for rpk and nompC show expression in the class III neurons. A genetic null allele of rpk confirms its critical role in touch responses. Output from class II and class III md neurons of the Drosophila larvae is necessary and sufficient for eliciting behavioral touch responses. These cells show physiological responses to force. Ion channels in several force-sensing gene families are required for behavioral sensitivity to touch and for the formation of the actin-rich sensory filopodia.

The role of Drosophila Piezo in mechanical nociception

Transduction of mechanical stimuli by receptor neurons is essential for senses such as hearing, touch, and pain1–4. Ion channels play a role in neuronal mechanotransduction in invertebrates1; however, functional conservation of these ion channels in mammalian mechanotransduction is not observed. For example, NOMPC, a TRP ion channel, acts as a mechanotransducer in Drosophila melanogaster5 and Caenorhabditis elegans6,7; however, it has no orthologues in mammals. DEG/ENaC family members are mechanotransducers in C. elegans8 and potentially in D. melanogaster9; however, a direct role of its mammalian homologues in sensing mechanical force is not shown. Recently, Piezo1 and Piezo2 were identified as components of mechanically activated (MA) channels in mammals10. Piezos represent an evolutionary conserved family of transmembrane proteins. It is unknown whether Piezos function in mechanical sensing in vivo, and if they do, which mechanosensory modalities they mediate. Here, we study the physiological role of the single Piezo member in D. melanogaster (dpiezo). dpiezo expression in human cells induces mechanically activated currents, similar to its mammalian counterparts [Coste et al., accompanying paper11]. Behavioral responses to noxious mechanical stimuli were severely reduced in dpiezo knockout larvae, while responses to another noxious stimulus or touch were not affected. Knocking down dpiezo in sensory neurons that mediate nociception and express the DEG/ENaC ion channel pickpocket (ppk) was sufficient to impair responses to noxious mechanical stimuli. Furthermore, expression of dpiezo in these same neurons rescued the phenotype of the constitutive dpiezo knockout larvae. Accordingly, electrophysiological recordings from ppk-positive neurons revealed a dpiezo dependent, mechanically-activated current. Finally, we found that dpiezo and ppk function in parallel pathways in ppk-positive cells, and that mechanical nociception is abolished in the absence of both channels. These data demonstrate physiological relevance of Piezo family in mechanotransduction in vivo, supporting a role of Piezo proteins in mechanosensory nociception.

Mechanoreception in motile flagella of Chlamydomonas

Ciliates and flagellates temporarily swim backwards on collision by generating a mechanoreceptor potential. Although this potential has been shown to be associated with cilia in Paramecium, the molecular entity of the mechanoreceptor has remained unknown. Here we show that Chlamydomonas cells express TRP11, a member of the TRP (transient receptor potential) subfamily V, in the proximal region of the flagella, and that suppression of TRP11 expression results in loss of the avoiding reaction. The results indicate that Chlamydomonas flagella exhibit mechanosensitivity, despite constant motility, by localizing the mechanoreceptor in the proximal region, where active bending is restricted.

A general mathematical model of transduction events in mechano-sensory stretch receptors

Crayfish (Astacus astacus) muscle stretch receptors show strong homology to mammalian muscle spindles and bipolar neurons in D. melanogaster. All are typical, non-ciliated, stretch-sensitive, afferent neurons. Such receptors are observed in many species and perform an important sensory role. However, they are poorly characterised. A previous study reported a bio-mechanical and behavioural model of A. astacus stretch receptors, which used the principles of elasticity and tension in a spring to describe the adaptation of a mechano-sensory ending. This model described the changing mechano-sensory currents in the receptor when subjected to a stretch protocol. Here, we re-implement and extend this model. Notably, we introduce additional descriptions of voltage-gated channels that are suggested to contribute to stretch receptor mechano-transduction. Our model presents a more complete picture of the initiation of the mechano-receptor potential in response to a stretching stimulus. The inclusion of voltage-dependent sodium and potassium currents in addition to the initial mechano-sensitive sodium current allowed the model to account for most of the initial stretch response of the receptor. This preliminary model has potential for extension to describe fully the behaviour of non-ciliated mechano-sensors across species and predict the molecular mediators of mechano-transduction.

Drosophila TRPN( = NOMPC) Channel Localizes to the Distal End of Mechanosensory Cilia

BackgroundA TRPN channel protein is essential for sensory transduction in insect mechanosensory neurons and in vertebrate hair cells. The Drosophila TRPN homolog, NOMPC, is required to generate mechanoreceptor potentials and currents in tactile bristles. NOMPC is also required, together with a TRPV channel, for transduction by chordotonal neurons of the fly's antennal ear, but the TRPN or TRPV channels have distinct roles in transduction and in regulating active antennal mechanics. The evidence suggests that NOMPC is a primary mechanotransducer channel, but its subcellular location—key for understanding its exact role in transduction—has not yet been established.Methodology/Principal FindingsHere, by immunostaining, we locate NOMPC at the tips of mechanosensory cilia in both external and chordotonal sensory neurons, as predicted for a mechanotransducer channel. In chordotonal neurons, the TRPN and TRPV channels are respectively segregated into distal and proximal ciliary zones. This zonal separation is demarcated by and requires the ciliary dilation, an intraciliary assembly of intraflagellar transport (IFT) proteins.ConclusionsOur results provide a strong evidence for NOMPC as a primary transduction channel in Drosophila mechansensory organs. The data also reveals a structural basis for the model of auditory chordotonal transduction in which the TRPN and TRPV channels play sequential roles in generating and amplifying the receptor potential, but have opposing roles in regulating active ciliary motility.

An IFT-A Protein Is Required to Delimit Functionally Distinct Zones in Mechanosensory Cilia

Conserved intraflagellar transport (IFT) particle proteins and IFT-associated motors are needed to assemble most eukaryotic cilia and flagella. Proteins in an IFT-A subcomplex are generally required for dynein-driven retrograde IFT, from the ciliary tip to the base. We describe novel structural and functional roles for IFT-A proteins in chordotonal organs, insect mechanosensory organs with cilia that are both sensory and motile. The reduced mechanoreceptor potential A (rempA) locus of Drosophila encodes the IFT-A component IFT140. Chordotonal cilia are shortened in rempA mutants and an IFT-B protein accumulates in the mutant cilia, consistent with a defect in retrograde IFT. A functional REMPA-YFP fusion protein concentrates at the site of the ciliary dilation (CD), a highly structured axonemal inclusion of hitherto unknown composition and function. The CD is absent in rempA mutants, and REMPA-YFP is undetectable in the absence of another IFT-A protein, IFT122. In a mutant lacking the IFT dynein motor, the CD is disorganized and REMPA-YFP is mislocalized. A TRPV ion channel, required to generate sensory potentials and regulate ciliary motility, is normally localized in the cilia, proximal to the CD. This channel spreads into the distal part of the cilia in dynein mutants and is undetectable in rempA mutants. IFT-A proteins are located at and required by the ciliary dilation, which separates chordotonal cilia into functionally distinct zones. A requirement for IFT140 in stable TRPV channel expression also suggests that IFT-A proteins may mediate preciliary transport of some membrane proteins.

Hydrozoan nematocytes send and receive synaptic signals induced by mechano-chemical stimuli

Nematocytes, the stinging cells of Hydrozoa, can be considered as prototypic mechanosensory hair cells bearing a concentric hair bundle, the cnidocil apparatus. These cells produce typical mechanoreceptor potentials in response to deflection of their cnidocil. Here we show that mechanosensory signals are relayed to neighbouring nematocytes via chemical neurotransmission and that nematocytes receive synaptic input from surrounding nematocytes, hair cells and probably from epithelial cells. Intracellular voltage recordings from stenotele nematocytes of capitate hydroid polyps showed two distinct types of responses when other nematocytes within the same tentacle were mechanically stimulated: (i) graded depolarizations of variable duration ('L-potentials'), and (ii) uniform impulse-like, often repetitive depolarizations ('T-potentials') that occurred in correlation with contractions of epitheliomuscular cells. Voltage clamp experiments showed that despite the stereotyped time course of T-potentials, their generation did not involve electrically excitable conductances. Instead, time course, post-stimulus delay, susceptibility to blockers of neurotransmission and gap junctions, and induction by electrical stimulation of other nematocytes indicate that L- and T-potentials are postsynaptic, most likely glutamatergic potentials. Both result from different presynaptic pathways: L-potentials are induced monosynaptically by presynaptic receptor potentials, T-potentials are most likely triggered by presynaptic action potentials propagating through the ectodermal epithelium via gap junctions. Moreover, contact-chemosensory (phospholipid) stimulation of the presynaptic nematocyte is a positive modulator of the nematocyte's afferent synaptic efficacy and of cnidocyst discharge, both triggered by mechanoreceptor potentials. The results reveal that hydrozoan nematocytes act as bimodal sensory cells, signalling coincident chemical and mechanical stimuli indicative of prey, and receive signals from other nematocytes and sensory cells.

From taste to touch: sensory signaling in model organisms

The ability to perceive our environment has fascinated scientists and philosophers for thousands of years. According to some interpretations of Aristotle’s writings, the sense organs are able to perceive the environment by being transformed so that they are more like the object they are detecting. An eye can see a specific color by taking on that color; an animal can perceive warmth by becoming warm, and so forth. In recent years, our understanding of the inner workings of the Aristotelian senses of sight, smell, taste, touch, and hearing has gone through a revolution, and many of the key insights have emerged through analyses of model organisms. The reviews in this special issue of Pflugers Archiv highlight the progress achieved through work in genetically tractable metazoan animals ranging from worms to flies and mice. Although the various sensory modalities operate through a diversity of activation mechanisms and timescales, a recurring theme is that members of the transient receptor potential (TRP) superfamily of cation channels function broadly in sensory physiology and throughout animal phylogeny. The most ancient among the five classical senses are touch, taste, and smell. These three sensory modalities are present in the worm, Caenorhabditis elegans, and all metazoan organisms analyzed. In fact, the first mutations to affect touch were identified in the worm, and a review by Alexander Bounoutas and Martin Chalfie describes the current state of knowledge of the cells and proteins that function in the response to gentle touch. The fruitfly, Drosophila melanogaster, has also been invaluable for dissecting the genetics of gentle and noxious touch, and Maurice Kernan reviews the functions and development of the various types of sense organs in flies and the proteins essential for mechanotransduction. Among the players identified is no mechanoreceptor potential C (NOMPC), which is required for light touch and is the first TRP channel shown to function in mechanotransduction. The other of the primordial sensory modalities, taste and smell are important not only for identifying nutrient-rich sources but for avoiding noxious chemicals and predators. In many animals, the pheromone response contributes to mate selection, mating behavior, aggressiveness, and other behaviors. In worms, chemosensation impacts on a developmental program as the animals arrest at a nonreproductive, nonfeeding stage in environments with a paucity of food or food-derived odors. The perception of chemical cues in the environment can also impact lifespan, at least in invertebrates. Four reviews in the current special issue focus on the responses to volatile (olfactory) and nonvolatile (gustatory) chemical stimuli. These include a contribution by Piala Sengupta, outlining the cells, circuitry, and molecules involved in chemically induced behaviors in worms. Michelle Ebbs and Hubert Amrien provide an overview of the anatomical sites and receptors required for the taste and pheromone responses in Drosophila. In addition, they review fly taste transduction and the behaviors controlled by nonvolatile chemicals. As outlined in a separate review by Dean Smith, Drosophila has also provided important insights into the detection and processing of olfactory stimuli. While most pheromones are nonvolatile, at least one volatile chemical serves as a pheromone in flies, and this latter review describes the requirement for this pheromone for mating and for aggressive behavior. Pflugers Arch Eur J Physiol (2007) 454:689–690 DOI 10.1007/s00424-007-0265-8

NompC TRP channel required for vertebrate sensory hair cell mechanotransduction.

The senses of hearing and balance in vertebrates rely on the sensory hair cells (HCs) of the inner ear. The central element of the HC's transduction apparatus is a mechanically gated ion channel of unknown identity. Here we report that the zebrafish ortholog of Drosophila no mechanoreceptor potential C (nompC), which encodes a transient receptor potential (TRP) channel, is critical for HC mechanotransduction. In zebrafish larvae, nompC is selectively expressed in sensory HCs. Morpholino-mediated removal of nompC function eliminated transduction-dependent endocytosis and electrical responses in HCs, resulting in larval deafness and imbalance. These observations indicate that nompC encodes a vertebrate HC mechanotransduction channel.

Effects of gadolinium on electrical membrane properties and behaviour in Paramecium tetraurelia

Summary Low concentrations (4 to 10 μM) of the trivalent cation gadolinium raised the input resistance and altered the membrane potential of Paramecium tetraurelia suggesting an interference with membrane channels. Current-clamp conditions revealed a concentration-dependent reduction of membrane rectification, in particular in the hyperpolarizing direction. The graded action potential and the early inward current seen under voltage-clamp conditions were depressed. Standardized applications of probes for focal mechanostimulation showed a reduction in mechanoreceptor potentials. Reversal responses of downward swimming cells in gadolinium transiently rose to higher frequency and settled at a reduced level thereafter explaining observations of a transient increase in gravitaxis. Vertical swimming speed was reduced, whereas the horizontal speed was largely unchanged. Gravity-induced modulation of swimming speed (gravikinesis) was depressed. The data indicate that gadolinium at micromolar concentrations effectively interferes with various types of membrane channels in Paramecium and is therefore no specific channel inhibitor to characterize graviresponses in this ciliate.