scholarly journals The female-specific VC neurons are mechanically activated, feed-forward motor neurons that facilitate serotonin-induced egg laying in C. elegans

2020 ◽  
Author(s):  
Richard J. Kopchock ◽  
Bhavya Ravi ◽  
Addys Bode ◽  
Kevin M. Collins
Keyword(s):  
Muscle Contraction ◽  
Motor Neurons ◽  
Neural Circuit ◽  
Egg Laying ◽  
Muscle Contractility ◽  
C Elegans ◽  
Optogenetic Stimulation ◽  
Vulval Muscle ◽  
Female Specific ◽  
Stimulation Of

AbstractSuccessful execution of behavior requires the coordinated activity and communication between multiple cell types. Studies using the relatively simple neural circuits of invertebrates have helped to uncover how conserved molecular and cellular signaling events shape animal behavior. To understand the mechanisms underlying neural circuit activity and behavior, we have been studying a simple circuit that drives egg-laying behavior in the nematode worm C. elegans. Here we show that the female-specific, Ventral C (VC) motoneurons are required for vulval muscle contractility and egg laying in response to serotonin. Ca2+ imaging experiments show the VCs are active during times of vulval muscle contraction and vulval opening, and optogenetic stimulation of the VCs promotes vulval muscle Ca2+ activity. However, while silencing of the VCs does not grossly affect steady-state egg-laying behavior, VC silencing does block egg laying in response to serotonin and increases the failure rate of egg-laying attempts. Signaling from the VCs facilitates full vulval muscle contraction and opening of the vulva for efficient egg laying. We also find the VCs are mechanically activated in response to vulval opening. Optogenetic stimulation of the vulval muscles is sufficient to drive VC Ca2+ activity and requires muscle contractility, showing the presynaptic VCs and the postsynaptic vulval muscles can mutually excite each other. Together, our results demonstrate that the VC neurons facilitate efficient execution of egg-laying behavior by coordinating postsynaptic muscle contractility in response to serotonin and mechanosensory feedback.

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.

Neural Circuit Mediating Tentacle Withdrawal in Helix aspersa, With Specific Reference to the Competence of the Motor Neuron C3

1997 ◽  
Vol 78 (6) ◽  
pp. 2951-2965 ◽  
Author(s):  
Steven A. Prescott ◽  
Nishi Gill ◽  
Ronald Chase
Keyword(s):  
Motor Neuron ◽  
Muscle Contraction ◽  
Motor Neurons ◽  
Neural Circuit ◽  
Helix Aspersa ◽  
Specific Reference ◽  
Stimulus Response ◽  
Withdrawal Reflex ◽  
Nerve Recordings ◽  
Stimulation Of

Prescott, Steven A., Nishi Gill, and Ronald Chase. Neural circuit mediating tentacle withdrawal in Helix aspersa, with specific reference to the competence of the motor neuron C3. J. Neurophysiol. 78: 2951–2965, 1997. The tentacle withdrawal reflex in the terrestrial snail Helix aspersa involves bending and retraction of the tentacles. When elicited by mechanical stimulation of the tentacle, the reflex is mediated by the conjoint action of the central and peripheral nervous systems. The neural circuit underlying the stimulus-response pathways was studied in vitro using a combination of morphological and physiological techniques. Sensory input caused by stimulation of the nose (situated at the superior tentacle's tip) first passes into the tentacle ganglion. Motor fibers are likely excited in the tentacle ganglion to form a peripheral stimulus-response pathway. While still in the tentacle ganglion, the excitation caused by a brief stimulus is transformed into a prolonged neuronal discharge. This modified signal travels, via the olfactory nerve, to the cerebral ganglion where it excites the giant motor neuron C3 along with numerous smaller motor neurons. Afferent input to C3 also arrives from several other sources. The afferent convergence is followed by a marked divergence of C3's output. C3 innervates the muscles mediating both tentacle retraction and tentacle bending through multiple cerebral nerves. Thus C3's pattern of effector innervation allows this single cell to elicit and coordinate both components of the tentacle withdrawal reflex. Lesion experiments indicate that C3 is responsible for 85% of the central contribution to tentacle retraction, though C3 is actually sufficient to mediate maximal muscle contraction as evidenced by intracellular stimulation. In addition to C3, three groups of putative central motor neurons were identified through nerve backfills and nerve recordings. The additional motor neurons mediating tentacle retraction are important for maximizing the rate of muscle contraction, whereas those mediating tentacle bending are likely more important for nondefensive behaviors. These neurons are arranged in parallel with C3, but unlike C3, each of these neurons innervates only a single effector or portion thereof. Given C3's direct innervation of multiple effectors and its sufficiency to evoke strong responses in those effectors, we conclude that C3 is paramount in eliciting and coordinating tentacle withdrawal.

Muscle and nerve-specific regulation of a novel NK-2 class homeodomain factor in Caenorhabditis elegans

Development ◽  
1998 ◽  
Vol 125 (3) ◽  
pp. 421-429 ◽  
Author(s):  
B.D. Harfe ◽  
A. Fire
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Homeobox Gene ◽  
Cell Types ◽  
Egg Laying ◽  
Cis Acting ◽  
C Elegans ◽  
E Box ◽  
Vulval Muscle ◽  
Specific Regulation

We have identified a new Caenorhabditis elegans NK-2 class homeobox gene, designated ceh-24. Distinct cis-acting elements generate a complex neuronal and mesodermal expression pattern. A promoter-proximal enhancer mediates expression in a single pharyngeal muscle, the donut-shaped m8 cell at the posterior end of the pharynx. A second mesodermal enhancer is active in a set of eight nonstriated vulval muscles used in egg laying. Activation in the egg laying muscles requires an ‘NdE-box’ consensus motif (CATATG) which is related to, but distinct from, the standard E-box motif bound by the MyoD family of transcriptional activators. Ectodermal expression of ceh-24 is limited to a subset of sublateral motor neurons in the head of the animal; this activity requires a cis-acting activator element that is distinct from the control elements for pharyngeal and vulval muscle expression. Activation of ceh-24 in each of the three cell types coincides with the onset of differentiation. Using a set of transposon-induced null mutations, we show that ceh-24 is not essential for the formation of any of these cells. Although ceh-24 mutants have no evident defects under laboratory conditions, the pattern of ceh-24 activity is apparently important for Rhabditid nematodes: the related species C. briggsae contains a close homologue of C. elegans ceh-24 including a highly conserved and functionally equivalent set of cis-acting control signals.

Striatal dopamine mediates hallucination-like perception in mice

Science ◽  
2021 ◽  
Vol 372 (6537) ◽  
pp. eabf4740
Author(s):  
K. Schmack ◽  
M. Bosc ◽  
T. Ott ◽  
J. F. Sturgill ◽  
A. Kepecs
Keyword(s):  
Psychotic Disorders ◽  
Neural Circuit ◽  
Dopamine Neurons ◽  
Striatal Dopamine ◽  
Model Organisms ◽  
High Confidence ◽  
Optogenetic Stimulation ◽  
The Brain ◽  
Central Symptom ◽  
Stimulation Of

Hallucinations, a central symptom of psychotic disorders, are attributed to excessive dopamine in the brain. However, the neural circuit mechanisms by which dopamine produces hallucinations remain elusive, largely because hallucinations have been challenging to study in model organisms. We developed a task to quantify hallucination-like perception in mice. Hallucination-like percepts, defined as high-confidence false detections, increased after hallucination-related manipulations in mice and correlated with self-reported hallucinations in humans. Hallucination-like percepts were preceded by elevated striatal dopamine levels, could be induced by optogenetic stimulation of mesostriatal dopamine neurons, and could be reversed by the antipsychotic drug haloperidol. These findings reveal a causal role for dopamine-dependent striatal circuits in hallucination-like perception and open new avenues to develop circuit-based treatments for psychotic disorders.

scholarly journals Optogenetic activation of muscle contraction in vivo

2020 ◽  
Author(s):  
Elahe Ganji ◽  
C. Savio Chan ◽  
Christopher W. Ward ◽  
Megan L. Killian
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Fluorescent Imaging ◽  
Triceps Surae ◽  
Light Activation ◽  
Non Invasive ◽  
Optogenetic Stimulation ◽  
Stimulation Of

AbstractOptogenetics is an emerging alternative to traditional electrical stimulation to initiate action potentials in activatable cells both ex vivo and in vivo. Optogenetics has been commonly used in mammalian neurons and more recently, it has been adapted for activation of cardiomyocytes and skeletal muscle. Therefore, the aim of this study was to evaluate the stimulation feasibility and sustain isometric muscle contraction and limit decay for an extended period of time (1s), using non-invasive transdermal light activation of skeletal muscle (triceps surae) in vivo. We used inducible Cre recombination to target expression of Channelrhodopsin-2 (ChR2(H134R)-EYFP) in skeletal muscle (Acta1-Cre) in mice. Fluorescent imaging confirmed that ChR2 expression is localized in skeletal muscle and does not have specific expression in sciatic nerve branch, therefore, allowing for non-nerve mediated optical stimulation of skeletal muscle. We induced muscle contraction using transdermal exposure to blue light and selected 10Hz stimulation after controlled optimization experiments to sustain prolonged muscle contraction. Increasing the stimulation frequency from 10Hz to 40Hz increased the muscle contraction decay during prolonged 1s stimulation, highlighting frequency dependency and importance of membrane repolarization for effective light activation. Finally, we showed that optimized pulsed optogenetic stimulation of 10 Hz resulted in comparable ankle torque and contractile functionality to that of electrical stimulation. Our results demonstrate the feasibility and repeatability of non-invasive optogenetic stimulation of muscle in vivo and highlight optogenetic stimulation as a powerful tool for non-invasive in vivo direct activation of skeletal muscle.

scholarly journals Neuropeptide VF neurons promote sleep via the serotonergic raphe

2019 ◽  
Author(s):  
Daniel A. Lee ◽  
Grigorios Oikonomou ◽  
Tasha Cammidge ◽  
Young Hong ◽  
David A. Prober
Keyword(s):  
Calcium Imaging ◽  
Neural Circuit ◽  
Raphe Nuclei ◽  
Hypothalamic Neurons ◽  
Optogenetic Stimulation ◽  
Genetic Epistasis ◽  
Normal Sleep ◽  
Genetic Labeling ◽  
Raphé Nuclei ◽  
Stimulation Of

ABSTRACTAlthough several sleep-regulating neurons have been identified, little is known about how they interact with each other for sleep/wake control. We previously identified neuropeptide VF (NPVF) and the hypothalamic neurons that produce it as a sleep-promoting system (Lee et al., 2017). Here we use zebrafish to describe a neural circuit in which neuropeptide VF (npvf)-expressing neurons control sleep via the serotonergic raphe nuclei (RN), a hindbrain structure that promotes sleep in both diurnal zebrafish and nocturnal mice. Using genetic labeling and calcium imaging, we show that npvf-expressing neurons innervate and activate serotonergic RN neurons. We additionally demonstrate that optogenetic stimulation of npvf-expressing neurons induces sleep in a manner that requires NPVF and is abolished when the RN are ablated or lack serotonin. Finally, genetic epistasis demonstrates that NPVF acts upstream of serotonin in the RN to maintain normal sleep levels. These findings reveal a novel hypothalamic-hindbrain circuit for sleep/wake control.

scholarly journals Release-dependent feedback inhibition by a presynaptically localized ligand-gated anion channel

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Seika Takayanagi-Kiya ◽  
Keming Zhou ◽  
Yishi Jin
Keyword(s):  
Motor Neurons ◽  
Neurotransmitter Release ◽  
Neural Circuit ◽  
Feedback Inhibition ◽  
Release Kinetics ◽  
Anion Channel ◽  
C Elegans ◽  
Release Of Acetylcholine ◽  
Presynaptic Release

Presynaptic ligand-gated ion channels (LGICs) have long been proposed to affect neurotransmitter release and to tune the neural circuit activity. However, the understanding of their in vivo physiological action remains limited, partly due to the complexity in channel types and scarcity of genetic models. Here we report that C. elegans LGC-46, a member of the Cys-loop acetylcholine (ACh)-gated chloride (ACC) channel family, localizes to presynaptic terminals of cholinergic motor neurons and regulates synaptic vesicle (SV) release kinetics upon evoked release of acetylcholine. Loss of lgc-46 prolongs evoked release, without altering spontaneous activity. Conversely, a gain-of-function mutation of lgc-46 shortens evoked release to reduce synaptic transmission. This inhibition of presynaptic release requires the anion selectivity of LGC-46, and can ameliorate cholinergic over-excitation in a C. elegans model of excitation-inhibition imbalance. These data demonstrate a novel mechanism of presynaptic negative feedback in which an anion-selective LGIC acts as an auto-receptor to inhibit SV release.

scholarly journals A conserved neuropeptide system links head and body motor circuits to enable adaptive behavior

2020 ◽  
Author(s):  
Shankar Ramachandran ◽  
Navonil Banerjee ◽  
Raja Bhattacharya ◽  
Denis Touroutine ◽  
Christopher M. Lambert ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Adaptive Behavior ◽  
Environmental Conditions ◽  
Body Wall ◽  
Behavioral Responses ◽  
Physiological Changes ◽  
C Elegans ◽  
Motor Circuits ◽  
Concerted Activity ◽  
Stimulation Of

SUMMARYNeuromodulators promote adaptive behaviors in response to either environmental or internal physiological changes. These responses are often complex and may involve concerted activity changes across circuits that are not physically connected. It is not well understood how neuromodulatory systems act across circuits to elicit complex behavioral responses. Here we show that the C. elegans NLP-12 neuropeptide system shapes responses to food availability by selectively modulating the activity of head and body wall motor neurons. NLP-12 modulation of the head and body wall motor circuits is generated through conditional involvement of alternate GPCR targets. The CKR-1 GPCR is highly expressed in the head motor circuit, and functions to enhance head bending and increase trajectory reorientations during local food searching, primarily through stimulatory actions on SMD head motor neurons. In contrast, NLP-12 activation of CKR-1 and CKR-2 GPCRs regulates body bending under basal conditions, primarily through actions on body wall motor neurons. Thus, locomotor responses to changing environmental conditions emerge from conditional NLP-12 stimulation of head or body wall motor neuron targets.

scholarly journals GABAergic motor neurons bias locomotor decision-making in C. elegans

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Ping Liu ◽  
Bojun Chen ◽  
Zhao-Wen Wang
Keyword(s):  
Decision Making ◽  
Motor Neurons ◽  
Gaba Receptor ◽  
Single Neuron ◽  
Neural Circuit ◽  
Electrical Coupling ◽  
C Elegans ◽  
Sensory Modalities ◽  
Motor Information ◽  
Molecular Bases

Abstract Proper threat-reward decision-making is critical to animal survival. Emerging evidence indicates that the motor system may participate in decision-making but the neural circuit and molecular bases for these functions are little known. We found in C. elegans that GABAergic motor neurons (D-MNs) bias toward the reward behavior in threat-reward decision-making by retrogradely inhibiting a pair of premotor command interneurons, AVA, that control cholinergic motor neurons in the avoidance neural circuit. This function of D-MNs is mediated by a specific ionotropic GABA receptor (UNC-49) in AVA, and depends on electrical coupling between the two AVA interneurons. Our results suggest that AVA are hub neurons where sensory inputs from threat and reward sensory modalities and motor information from D-MNs are integrated. This study demonstrates at single-neuron resolution how motor neurons may help shape threat-reward choice behaviors through interacting with other neurons.

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