scholarly journals Presynaptic Gαo (GOA-1) signals to depress command neuron excitability and allow stretch-dependent modulation of egg laying in Caenorhabditis elegans

2019 ◽  
Author(s):  
Bhavya Ravi ◽  
Jian Zhao ◽  
Sana Chaudhry ◽  
Mattingly Bartole ◽  
Richard J. Kopchock ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Feedback ◽  
Sensory Input ◽  
Stable State ◽  
Egg Laying ◽  
Active State ◽  
Neuroendocrine Cells ◽  
Electrical Excitability ◽  
State Behavior ◽  
Nematode Worm

AbstractEgg laying in the nematode worm Caenorhabditis elegans is a two-state behavior modulated by internal and external sensory input. We have previously shown that homeostatic feedback of embryo accumulation in the uterus regulates bursting activity of the serotonergic HSN command neurons that sustains the egg-laying active state. How sensory feedback of egg release signals to terminate the egg-laying active state is less understood. We find that Gαo, a conserved Pertussis Toxin-sensitive G protein, signals within HSN to inhibit egg-laying circuit activity and prevent entry into the active state. Gαo signaling hyperpolarizes HSN, reducing HSN Ca2+ activity and input onto the postsynaptic vulval muscles. Loss of inhibitory Gαo signaling uncouples presynaptic HSN activity from a postsynaptic, stretch-dependent homeostat, causing precocious entry into the egg-laying active state when only a few eggs are present in the uterus. Feedback of vulval opening and egg release activates the uv1 neuroendocrine cells which release NLP-7 neuropeptides which signal to inhibit egg laying through Gαo-independent mechanisms in the HSNs and Gαo-dependent mechanisms in cells other than the HSNs. Thus, neuropeptide and inhibitory Gαo signaling maintains a bi-stable state of electrical excitability that dynamically controls circuit activity in response to both external and internal sensory input to drive a two-state behavior output.

scholarly journals Presynaptic Gαo (GOA-1) signals to depress command neuron excitability and allow stretch-dependent modulation of egg laying in Caenorhabditis elegans

Genetics ◽  
2021 ◽  
Author(s):  
Bhavya Ravi ◽  
Jian Zhao ◽  
I Chaudhry ◽  
Rossana Signorelli ◽  
Mattingly Bartole ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Feedback ◽  
Sensory Input ◽  
Stable State ◽  
Egg Laying ◽  
Active State ◽  
Neuroendocrine Cells ◽  
State Behavior ◽  
Nematode Worm ◽  
Worm Caenorhabditis Elegans

Abstract Egg laying in the nematode worm Caenorhabditis elegans is a two-state behavior modulated by internal and external sensory input. We have previously shown that homeostatic feedback of embryo accumulation in the uterus regulates bursting activity of the serotonergic HSN command neurons that sustains the egg-laying active state. How sensory feedback of egg release signals to terminate the egg-laying active state is less understood. We find that Gαo, a conserved Pertussis Toxin-sensitive G protein, signals within HSN to inhibit egg-laying circuit activity and prevent entry into the active state. Gαo signaling hyperpolarizes HSN, reducing HSN Ca2+ activity and input onto the postsynaptic vulval muscles. Loss of inhibitory Gαo signaling uncouples presynaptic HSN activity from a postsynaptic, stretch-dependent homeostat, causing precocious entry into the egg-laying active state when only a few eggs are present in the uterus. Feedback of vulval opening and egg release activates the uv1 neuroendocrine cells which release NLP-7 neuropeptides which signal to inhibit egg laying through Gαo-independent mechanisms in the HSNs and Gαo-dependent mechanisms in cells other than the HSNs. Thus, neuropeptide and inhibitory Gαo signaling maintains a bi-stable state of electrical excitability that dynamically controls circuit activity in response to both external and internal sensory input to drive a two-state behavior output.

scholarly journals Activity of the C. elegans egg-laying behavior circuit is controlled by competing activation and feedback inhibition

2016 ◽  
Author(s):  
Kevin M. Collins ◽  
Addys Bode ◽  
Robert W. Fernandez ◽  
Jessica E. Tanis ◽  
Jacob Brewer ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Neural Circuit ◽  
Feedback Inhibition ◽  
Rhythmic Activity ◽  
Egg Laying ◽  
The Body ◽  
Active State ◽  
Neuroendocrine Cells ◽  
C Elegans ◽  
Discrete Signals

AbstractLike many behaviors, Caenorhabditis elegans egg laying alternates between inactive and active states. To understand how the underlying neural circuit turns the behavior on and off, we optically recorded circuit activity in behaving animals while manipulating circuit function using mutations, optogenetics, and drugs. In the active state, the circuit shows rhythmic activity phased with the body bends of locomotion. The serotonergic HSN command neurons initiate the active state, but accumulation of unlaid eggs also promotes the active state independent of the HSNs. The cholinergic VC motor neurons slow locomotion during egg-laying muscle contraction and egg release. The uv1 neuroendocrine cells mechanically sense passage of eggs through the vulva and release tyramine to inhibit egg laying, in part via the LGC-55 tyramine-gated Cl− channel on the HSNs. Our results identify discrete signals that entrain or detach the circuit from the locomotion central pattern generator to produce active and inactive states.

scholarly journals Activity of the C. elegans egg-laying behavior circuit is controlled by competing activation and feedback inhibition

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Kevin M Collins ◽  
Addys Bode ◽  
Robert W Fernandez ◽  
Jessica E Tanis ◽  
Jacob C Brewer ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Neural Circuit ◽  
Feedback Inhibition ◽  
Rhythmic Activity ◽  
Egg Laying ◽  
The Body ◽  
Active State ◽  
Neuroendocrine Cells ◽  
C Elegans ◽  
Discrete Signals

Like many behaviors, Caenorhabditis elegans egg laying alternates between inactive and active states. To understand how the underlying neural circuit turns the behavior on and off, we optically recorded circuit activity in behaving animals while manipulating circuit function using mutations, optogenetics, and drugs. In the active state, the circuit shows rhythmic activity phased with the body bends of locomotion. The serotonergic HSN command neurons initiate the active state, but accumulation of unlaid eggs also promotes the active state independent of the HSNs. The cholinergic VC motor neurons slow locomotion during egg-laying muscle contraction and egg release. The uv1 neuroendocrine cells mechanically sense passage of eggs through the vulva and release tyramine to inhibit egg laying, in part via the LGC-55 tyramine-gated Cl- channel on the HSNs. Our results identify discrete signals that entrain or detach the circuit from the locomotion central pattern generator to produce active and inactive states.

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

scholarly journals Effect of a Neuropeptide Gene on Behavioral States in Caenorhabditis elegans Egg-Laying

Genetics ◽  
2000 ◽  
Vol 154 (3) ◽  
pp. 1181-1192 ◽  
Author(s):  
Laura E Waggoner ◽  
Laura Anne Hardaker ◽  
Steven Golik ◽  
William R Schafer
Keyword(s):  
Caenorhabditis Elegans ◽  
Active Phase ◽  
Egg Laying ◽  
Sensory Cues ◽  
Nematode Caenorhabditis Elegans ◽  
Inactive State ◽  
Recessive Mutations ◽  
Inactive Phase ◽  
Behavioral States ◽  
Stimulation Of

Abstract Egg-laying behavior in the nematode Caenorhabditis elegans involves fluctuation between alternative behavioral states: an inactive state, during which eggs are retained in the uterus, and an active state, during which eggs are laid in bursts. We have found that the flp-1 gene, which encodes a group of structurally related neuropeptides, functions specifically to promote the switch from the inactive to the active egg-laying state. Recessive mutations in flp-1 caused a significant increase in the duration of the inactive phase, yet egg-laying within the active phase was normal. This pattern resembled that previously observed in mutants defective in the biosynthesis of serotonin, a neuromodulator implicated in induction of the active phase. Although flp-1 mutants were sensitive to stimulation of egg-laying by serotonin, the magnitude of their serotonin response was abnormally low. Thus, the flp-1-encoded peptides and serotonin function most likely function in concert to facilitate the onset of the active egg-laying phase. Interestingly, we observed that flp-1 is necessary for animals to down-regulate their rate of egg-laying in the absence of food. Because flp-1 is known to be expressed in interneurons that are postsynaptic to a variety of chemosensory cells, the FLP-1 peptides may function to regulate the activity of the egg-laying circuitry in response to sensory cues.

scholarly journals The emulation theory of representation: Motor control, imagery, and perception

2004 ◽  
Vol 27 (3) ◽  
pp. 377-396 ◽  
Author(s):  
Rick Grush
Keyword(s):  
Motor Control ◽  
Sensory Feedback ◽  
Sensory Input ◽  
Neural Circuits ◽  
Sensory Information ◽  
The Body ◽  
Feedback Delay ◽  
Run Off ◽  
Effects Of Feedback ◽  
The Brain

The emulation theory of representation is developed and explored as a framework that can revealingly synthesize a wide variety of representational functions of the brain. The framework is based on constructs from control theory (forward models) and signal processing (Kalman filters). The idea is that in addition to simply engaging with the body and environment, the brain constructs neural circuits that act as models of the body and environment. During overt sensorimotor engagement, these models are driven by efference copies in parallel with the body and environment, in order to provide expectations of the sensory feedback, and to enhance and process sensory information. These models can also be run off-line in order to produce imagery, estimate outcomes of different actions, and evaluate and develop motor plans. The framework is initially developed within the context of motor control, where it has been shown that inner models running in parallel with the body can reduce the effects of feedback delay problems. The same mechanisms can account for motor imagery as the off-line driving of the emulator via efference copies. The framework is extended to account for visual imagery as the off-line driving of an emulator of the motor-visual loop. I also show how such systems can provide for amodal spatial imagery. Perception, including visual perception, results from such models being used to form expectations of, and to interpret, sensory input. I close by briefly outlining other cognitive functions that might also be synthesized within this framework, including reasoning, theory of mind phenomena, and language.

scholarly journals Screening for Presenilin Inhibitors Using the Free-Living Nematode, Caenorhabditis elegans

2004 ◽  
Vol 9 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Brenda R. Ellerbrock ◽  
Eileen M. Coscarelli ◽  
Mark E. Gurney ◽  
Timothy G. Geary
Keyword(s):  
Caenorhabditis Elegans ◽  
High Throughput Screening ◽  
Screening Method ◽  
Genetic System ◽  
Body Cavity ◽  
Egg Laying ◽  
The Body ◽  
Loss Of Function ◽  
C Elegans ◽  
Automated Method

Caenorhabditis elegans contains 3 homologs of presenilin genes that are associated with Alzheimer s disease. Loss-of-function mutations in C. elegans genes cause a defect in egg laying. In humans, loss of presenilin-1 (PS1) function reduces amyloid-beta peptide processing from the amyloid protein precursor. Worms were screened for compounds that block egg laying, phenocopying presenilin loss of function. To accommodate even relatively high throughput screening, a semi-automated method to quantify egg laying was devised by measuring the chitinase released into the culture medium. Chitinase is released by hatching eggs, but little is shed into the medium from the body cavity of a hermaphrodite with an egg laying deficient ( egl) phenotype. Assay validation involved measuring chitinase release from wild-type C. elegans (N2 strain), sel-12 presenilin loss-of-function mutants, and 2 strains of C. elegans with mutations in the egl-36K+ channel gene. Failure to find specific presenilin inhibitors in this collection likely reflects the small number of compounds tested, rather than a flaw in screening strategy. Absent defined biochemical pathways for presenilin, this screening method, which takes advantage of the genetic system available in C. elegans and its historical use for anthelminthic screening, permits an entry into mechanism-based discovery of drugs for Alzheimer s disease. ( Journal of Biomolecular Screening 2004:147-152)

Central patterning and reflex control of antennular flicking in the hermit crab Pagurus alaskensis (Benedict)

1975 ◽  
Vol 63 (1) ◽  
pp. 17-32
Author(s):  
P. J. Snow
Keyword(s):  
Hermit Crab ◽  
Functional Significance ◽  
Sensory Feedback ◽  
Sensory Input ◽  
Spike Frequency ◽  
Joint Movement ◽  
Trigger System ◽  
System A ◽  
Joint Flexion ◽  
Reflex Control

1. The effects of altering sensory input on the motoneuronal activity underlying antennular flicking have been tested. 2. Removal of the short segments of the outer flagellum results in a reduction of the number of spikes/burst in the fast flexor motoneurones A31F and A32F. 3. During a flick the delay between the burst in motoneurone A31F and the burst in motoneurone A32F is insensitive to alteration of sensory input. 4. Sensory feedback from the flexion phase of a flick is necessary for the activation of either extensor motoneurone. Evidence is presented to suggest that this feedback is primarily from joint-movement receptors at the MS-DS and DS-OF joints. 5. The results are incorporated into a model in which the patterns of flexor activity result from some specified properties of three components: a trigger system, a follower system, and the spike initiating zone of the flexor motoneurones. The trigger system determines when a flick will occur. The follower system determines the number of flexor spikes during a flick. Properties of the spike initiating zone determine the spike frequency and the timing between bursts in the flexor motoneurones. Extensor activity in the model is reflexively elicited by feedback from phasic, unidirectional receptors sensitive to joint flexion. 6. The functional significance of reflex control of extensor activity is discussed in relation to the form and proposed function of antennular flicking. It is suggested that this form of control is adapted to the function of antennular flicking because flexion at the MS-DS joint is not always necessary for the fulfilment of the fuction of a flick.

The terminal differentiation factor LIN-29 is required for proper vulval morphogenesis and egg laying in Caenorhabditis elegans

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4333-4342 ◽  
Author(s):  
J.C. Bettinger ◽  
S. Euling ◽  
A.E. Rougvie
Keyword(s):  
Caenorhabditis Elegans ◽  
Terminal Differentiation ◽  
Egg Laying ◽  
Small Subset ◽  
Wild Type ◽  
Vulval Development ◽  
Genetic Mosaics ◽  
Hypodermal Cell ◽  
Heterochronic Gene ◽  
Final Molt

Caenorhabditis elegans vulval development culminates during exit from the L4-to-adult molt with the formation of an opening through the adult hypodermis and cuticle that is used for egg laying and mating. Vulva formation requires the heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the final molt. lin-29 mutants are unable to lay eggs or mate because no vulval opening forms; instead, a protrusion forms at the site of the vulva. We demonstrate through analysis of genetic mosaics that lin-29 is absolutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying. However, lin-29 function is not strictly limited to the lateral hypodermis. First, LIN-29 accumulates in many non-hypodermal cells with known roles in vulva formation or egg laying. Second, animals homozygous for one lin-29 allele, ga94, have the vulval defect and cannot lay eggs, despite having a terminally differentiated adult lateral hypodermis. Finally, vulval morphogenesis and egg laying requires lin-29 activity within the EMS lineage, a lineage that does not generate hypodermal cells.

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