Touch Circuit Research Articles

Behavioral adjustment of C. elegans to mechanosensory loss requires intact mechanosensory neurons.

Sensory neurons specialize in detecting and signaling the presence of diverse environmental stimuli. Neuronal injury or disease may undermine such signaling, diminishing the availability of crucial information. Can animals distinguish between a stimulus not being present and the inability to sense that stimulus in the first place? To address this question, we studied Caenorhabditis elegans nematode worms that lack gentle body touch sensation due to genetic mechanoreceptor dysfunction. We previously showed that worms can compensate for the loss of touch by enhancing their sense of smell, via an FLP-20 neuropeptide pathway. Here, we find that touch-deficient worms exhibit, in addition to sensory compensation, also cautious-like behavior, as if preemptively avoiding potential undetectable hazards. Intriguingly, these behavioral adjustments are abolished when the touch neurons are removed, suggesting that touch neurons are required for signaling the unavailability of touch information, in addition to their conventional role of signaling touch stimulation. Furthermore, we found that the ASE taste neurons, which similarly to the touch neurons, express the FLP-20 neuropeptide, exhibit altered FLP-20 expression levels in a touch-dependent manner, thus cooperating with the touch circuit. These results imply a novel form of neuronal signaling that enables C. elegans to distinguish between lack of touch stimulation and loss of touch sensation, producing adaptive behavioral adjustments that could overcome the inability to detect potential threats.

Microbiota and Diapause-Induced Neuroprotection Share a Dependency on Calcium But Differ in Their Effects on Mitochondrial Morphology.

The balance between the degeneration and regeneration of damaged neurons depends on intrinsic and environmental variables. In nematodes, neuronal degeneration can be reversed by intestinal GABA and lactate-producing bacteria, or by hibernation driven by food deprivation. However, it is not known whether these neuroprotective interventions share common pathways to drive regenerative outcomes. Using a well established neuronal degeneration model in the touch circuit of the bacterivore nematode Caenorhabditis elegans, we investigate the mechanistic commonalities between neuroprotection offered by the gut microbiota and hunger-induced diapause. Using transcriptomics approaches coupled to reverse genetics, we identify genes that are necessary for neuroprotection conferred by the microbiota. Some of these genes establish links between the microbiota and calcium homeostasis, diapause entry, and neuronal function and development. We find that extracellular calcium as well as mitochondrial MCU-1 and reticular SCA-1 calcium transporters are needed for neuroprotection by bacteria and by diapause entry. While the benefits exerted by neuroprotective bacteria require mitochondrial function, the diet itself does not affect mitochondrial size. In contrast, diapause increases both the number and length of mitochondria. These results suggest that metabolically induced neuronal protection may occur via multiple mechanisms.

Active in‐cell touch circuit using floating common electrode as sensing pad for the large size in‐plane‐switching liquid crystal displays

AbstractIn this paper, we propose an in‐cell active touch circuit using the concept of floating common electrode for large size in‐plane‐switching liquid crystal displays. Compared with the conventional passive in‐cell touch circuit, the proposed method can greatly reduce the readout channel numbers by sharing the sensing bus for one column. Because the touch signal is amplified in the pixel, the touch panel can be easily scaled up in size. Simulation results show that the difference between touch and no‐touch signals can be as large as 10 μA even with threshold voltage shift of ±1 V. The possible issues of the proposed method are experimentally verified.

49‐3: In‐Cell Active Touch Circuit Using a‐Si TFT for Large Size Panel

In this paper, we present an advanced in‐cell active touch circuit using a‐Si thin film transistors (TFTs) for large size panel. The circuit design is different from traditional mutual‐capacitance and self‐capacitance in‐cell touch panel which are so‐called passive touch circuit. The touch capacitance formed between the touching finger and the common electrode of IPS LC is used to share the charge with the couple capacitance on common electrode. The sensing line is used to sense the current of the active device for different charging status to determine whether an external object are touched or approached.

A Gap Junction Circuit Enhances Processing of Coincident Mechanosensory Inputs

SummaryElectrical synapses have been shown to be important for enabling and detecting neuronal synchrony in both vertebrates [1–4] and invertebrates [5, 6]. Hub-and-spoke circuits, in which a central hub neuron is electrically coupled to several input neurons, are an overrepresented motif in the C. elegans nervous system [7] and may represent a conserved functional unit. The functional relevance of this configuration has been demonstrated for circuits mediating aggregation behavior [8] and nose touch perception [9]. Modeling approaches have been useful for understanding structurally and dynamically more complex electrical circuits [10, 11]. Therefore, we formulated a simple analytical model with minimal assumptions to obtain insight into the properties of the hub-and-spoke microcircuit motif. A key prediction of the model is that an active input neuron should facilitate activity throughout the network, whereas an inactive input should suppress network activity through shunting; this prediction was supported by cell ablation and in vivo neuroimaging experiments in the C. elegans nose touch circuit. Thus, the hub-and-spoke architecture may implement an analog coincidence detector enabling distinct responses to distributed and localized patterns of sensory input.

Real-time multimodal optical control of neurons and muscles in freely behaving Caenorhabditis elegans.

The ability to optically excite or silence specific cells using optogenetics has provided a powerful tool to interrogate the nervous system. Optogenetic experiments in small organisms have mostly been performed using whole-field illumination and genetic targeting, but these strategies do not always provide adequate cellular specificity. Targeted illumination can be a valuable alternative but to date it has only been shown in non-moving animals without the ability to observe behavior output. We present a real-time multimodal illumination technology that allows both tracking and recording the behavior of freely moving Caenorhabditis elegans while stimulating specific cells that express Channelrhodopsin-2 or MAC. We use this system to optically manipulate nodes within the C. elegans touch circuit and study the roles of sensory and command neurons and the ultimate behavioral output. This technology significantly enhances our ability to control, alter, observe, and investigate how neurons, muscles, and circuits ultimately produce behavior in animals using optogenetics.

Developmental analysis of habituation in the nematodeC. elegans

Habituation and spontaneous recovery from habituation to tap were studied across development in C. elegans. Unlike adult worms, larval worms do not consistently swim backwards to tap, but reverse half of the time and accelerate forward half of the time. In adult worms, the tap response is produced by the integration of two competing circuits: The head touch circuit, mediated by ALM and AVM sensory neurons, produces backward movement (reversals); the tail touch circuit, mediated by PLM neurons, produces forward movement (accelerations). Because the response type changes over development, habituation of each of the subcircuits was studied separately. Habituation of the head touch circuit was studied by laser ablating PLM, and habituation of the tail circuit was studied by ablating ALM. Worms were tested at six stages of development at either 10- or 60-s interstimulus intervals. All stages of development showed normal habituation and spontaneous recovery at both interstimulus intervals.

Integration of mechanosensory stimuli in Caenorhabditis elegans

The tap withdrawal reflex in Caenorhabditis elegans demonstrates various forms of nonassociative learning. A first step in determining the cellular mechanisms of this learning is to identify the neuronal circuitry that underlies this reflex. Studies by Chalfie et al. (1985) have defined the touch-circuit that mediates the response to a stimulus related to tap--a light touch. We used the touch circuit as a starting point in the identification of the tap withdrawal circuitry. Here we report the effects of lesions of identified neurons on the tap withdrawal reflex. Ablations of the sensory neurons and interneurons of the touch circuit produce effects on the tap withdrawal response that generally confirm and expand upon the roles of these cells in mechanosensory integration as proposed by Chalfie et al. (1985). However, no role for the LUA interneurons could be identified in the production of the tap withdrawal response. Furthermore, the effects of ablating some neurons outside the touch circuit suggest roles for two of these cells in the integration of the tap withdrawal response. Ablation of either the midline neuron DVA or the PVD neurons resulted in a decrease in both the frequency and magnitude of reversals that were elicited by tap. Additionally, the ablation of either cell decreased the magnitude of accelerations produced by animals in response to tap.

A multi-purpose photocell and touch circuit amplifier

A simple and inexpensive multiple channel amplifier based on the TLC374 quad comparator is described. The unit can be used in behavioral studies to amplify photocell signals and as a drinkometer.