scholarly journals Glia actively sculpt sensory neurons by controlled phagocytosis to tune animal behavior

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Stephan Raiders ◽  
Erik Calvin Black ◽  
Andrea Bae ◽  
Stephen MacFarlane ◽  
Mason Klein ◽  
...  
Keyword(s):  
Animal Behavior ◽  
Sensory Input ◽  
Single Neuron ◽  
Sense Organ ◽  
Neuron Activity ◽  
Photoreceptor Outer Segments ◽  
C Elegans ◽  
Rac1 Gtpase ◽  
The Central Nervous System ◽  
Sensory Endings

Glia in the central nervous system engulf neuron fragments to remodel synapses and recycle photoreceptor outer-segments. Whether glia passively clear shed neuronal debris, or actively prune neuron fragments is unknown. How pruning of single-neuron endings impacts animal behavior is also unclear. Here we report our discovery of glia-directed neuron pruning in C. elegans. Adult C. elegans AMsh glia engulf sensory endings of the AFD thermosensory neuron by repurposing components of the conserved apoptotic corpse phagocytosis machinery. The phosphatidylserine (PS) flippase TAT-1/ATP8A, functions with glial PS-receptor PSR-1/PSR and PAT-2/α-integrin to initiate engulfment. This activates glial CED-10/Rac1 GTPase through the ternary GEF complex of CED-2/CrkII, CED-5/DOCK180, CED-12/ELMO. Execution of phagocytosis uses the actin-remodeler WSP-1/nWASp. This process dynamically tracks AFD activity and is regulated by temperature, the AFD sensory input. Importantly, glial CED-10 levels regulate engulfment rates downstream of neuron activity, and engulfment-defective mutants exhibit altered AFD-ending shape and thermosensory behavior. Our findings reveal a molecular pathway underlying glia-dependent engulfment in a peripheral sense-organ, and demonstrate that glia actively engulf neuron-fragments, with profound consequences on neuron shape and animal sensory behavior.

scholarly journals Glia actively sculpt sensory neurons by controlled phagocytosis to tune animal behavior

2020 ◽  
Author(s):  
Stephan Raiders ◽  
Erik Calvin Black ◽  
Andrea Bae ◽  
Stephen MacFarlane ◽  
Shai Shaham ◽  
...  
Keyword(s):  
Animal Behavior ◽  
Sensory Input ◽  
Single Neuron ◽  
Sense Organ ◽  
Photoreceptor Outer Segments ◽  
C Elegans ◽  
Rac1 Gtpase ◽  
The Central Nervous System ◽  
Membrane Sealing ◽  
Sensory Endings

ABSTRACTGlia in the central nervous system engulf neuron fragments during synapse remodeling and recycling of photoreceptor outer-segments. Whether glia passively clear shed neuronal debris, or actively remove neuron fragments is unknown. How pruning of single-neuron endings impacts animal behavior is also unclear. Here we report that adult C. elegans AMsh glia engulf sensory endings of the AFD thermosensory neuron. Engulfment is regulated by temperature, AFD’s sensory input, and tracks AFD activity. Phosphatidylserine (PS) flippase TAT-1/ATP8A, functions with glial PS-receptor PSR-1/PSR and PAT-2/α-integrin to initiate engulfment. Glial CED-10/Rac1 GTPase, acting through a conserved GEF complex, executes phagocytosis using the actin-remodeler WSP-1/nWASp and the membrane-sealing factor EFF-1 fusogen. CED-10 levels determine engulfment rates, and engulfment-defective mutants exhibit altered AFD-ending shape and thermosensory behavior. Our findings reveal a molecular pathway underpinning glia-dependent phagocytosis in a peripheral sense-organ, and demonstrate that glia actively engulf neuron-fragments, with profound consequences on neuron shape and animal behavior.

scholarly journals QLCA and Entangled States as Single-Neuron Activity Generators

2021 ◽  
Vol 15 ◽  
Author(s):  
Yehuda Roth
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cellular Automaton ◽  
Single Neuron ◽  
Entangled States ◽  
Neuron Activity ◽  
Input Information ◽  
The Central Nervous System ◽  
Single Neuron Activity

Each neuron in the central nervous system has many dendrites, which provide input information through impulses. Assuming that a neuron's decision to continue or stop firing is made by rules applied to the dendrites' inputs, we associate neuron activity with a quantum like-cellular automaton (QLCA) concepts. Following a previous study that related the CA description with entangled states, we provide a quantum-like description of neuron activity. After reviewing and presenting the entanglement concept expressed by QLCA terminology, we propose a model that relates quantum-like measurement to consciousness. Then, we present a toy model that reviews the QLCA theory, which is adapted to our terminology. The study also focuses on implementing QLCA formalism to describe a single neuron activity.

scholarly journals C. elegans REMO-1, a glial GPCR, regulates stress-induced nervous system remodeling and behavior

2020 ◽  
Author(s):  
In Hae Lee ◽  
Carl Procko ◽  
Yun Lu ◽  
Shai Shaham
Keyword(s):  
Nervous System ◽  
Animal Behavior ◽  
Single Neuron ◽  
Structural Changes ◽  
C Elegans ◽  
Stress Dependent ◽  
Favorable Conditions ◽  
And Behavior ◽  
G Protein Coupled ◽  
Shape Changes

Animal nervous systems remodel following stress. Although global stress-dependent changes are well documented, contributions of individual neuron remodeling events to animal behavior modification are challenging to study. In response to environmental insults, C. elegans become stress-resistant dauers. Dauer entry induces amphid sensory-organ remodeling, in which bilateral AMsh glial cells expand and fuse, allowing embedded AWC chemosensory neurons to extend sensory receptive endings. We show that amphid remodeling accelerates dauer exit upon exposure to favorable conditions, and identify a G protein-coupled receptor, REMO-1, driving AMsh glia fusion, AWC neuron remodeling, and dauer exit. REMO-1 is expressed in and localizes to AMsh glia tips, is dispensable for other remodeling events, and promotes stress-induced expression of the remodeling receptor tyrosine kinase VER-1. Our results demonstrate how single-neuron structural changes affect animal behavior, identify key glial roles in stress-induced nervous system shape changes, and demonstrate that remodeling primes animals to respond to favorable conditions.

Peripheral control of the gain of a central synaptic connection between antagonistic motor neurones in the locust

1996 ◽  
Vol 199 (3) ◽  
pp. 613-625
Author(s):  
T Jellema ◽  
W Heitler
Keyword(s):  
Muscle Contraction ◽  
Sensory Input ◽  
Sense Organ ◽  
Gain Control ◽  
Motor Neurone ◽  
Extensor Muscle ◽  
Chordotonal Organ ◽  
Excitatory Postsynaptic Potential ◽  
Motor Neurones ◽  
Peripheral Sensory

The metathoracic fast extensor tibiae (FETi) motor neurone of locusts is unusual amongst insect motor neurones because it makes output connections within the central nervous system as well as in the periphery. It makes excitatory chemical synaptic connections to most if not all of the antagonist flexor tibiae motor neurones. The gain of the FETi-flexor connection is dependent on the peripheral conditions at the time of the FETi spike. This dependency has two aspects. First, sensory input resulting from the extensor muscle contraction can sum with the central excitatory postsynaptic potential (EPSP) to augment its falling phase if the tibia is restrained in the flexed position (initiating a tension-dependent reflex) or is free to extend (initiating a movement-dependent resistance reflex). This effect is thus due to simple postsynaptic summation of the central EPSP with peripheral sensory input. Second, the static tibial position at the time of the FETi spike can change the amplitude of the central EPSP, in the absence of any extensor muscle contraction. The EPSP can be up to 30 % greater in amplitude if FETi spikes with the tibia held flexed rather than extended. The primary sense organ mediating this effect is the femoral chordotonal organ. Evidence is presented suggesting that the mechanism underlying this change in gain may be specifically localised to the FETi-flexor connection, rather than being due to general position-dependent sensory feedback summing with the EPSP. The change in the amplitude of the central EPSP is probably not caused by general postsynaptic summation with tonic sensory input, since a diminution in the amplitude of the central EPSP caused by tibial extension is often accompanied by overall tonic excitation of the flexor motor neurone. Small but significant changes in the peak amplitude of the FETi spike have a positive correlation with changes in the EPSP amplitude, suggesting a likely presynaptic component to the mechanism of gain control. The change in amplitude of the EPSP can alter its effectiveness in producing flexor motor output and, thus, has functional significance. The change serves to augment the effectiveness of the FETi-flexor connection when the tibia is fully flexed, and thus to increase its adaptive advantage during the co-contraction preceding a jump or kick, and to reduce the effectiveness of the connection when the tibia is partially or fully extended, and thus to reduce its potentially maladaptive consequences during voluntary extension movements such as thrusting.

scholarly journals The Informational Underload (Sensory Deprivation) Model in Contemporary Psychiatry

1967 ◽  
Vol 12 (2) ◽  
pp. 105-124
Author(s):  
Peter Brawley ◽  
Robert Pos
Keyword(s):  
Sensory Input ◽  
Genetic Factors ◽  
Sensory Deprivation ◽  
Critical Factor ◽  
Good Evidence ◽  
Psychotic Experience ◽  
Common Pathway ◽  
The Central Nervous System ◽  
Deprivation Model ◽  
The Brain

To summarize briefly: Converging data from many disciplines — psychology, psychiatry, social theory, biochemistry, neuropharmacology, neurophysiology — point to the sensory input regulating mechanism of the central nervous system as a critical factor in the production of hallucinoses and psychotic experience. There is good evidence that what we have called the informational underload model ‘holds considerable promise for improving our understanding of many clinical and non-clinical phenomena of interest to psychiatry. The evidence suggests that a neurophysiological, internal informational underload syndrome may be a final common pathway of psychotic experience. The question as to where such a syndrome might occur in the brain, together with the question of whether such an informational underload syndrome might be due to toxins, genetic factors, conditioning processes, anxiety or dissociation, or other causes, has to be left open. What is needed now, is research directed at these two questions: 1) does such an internal informational underload syndrome occur in the brain, 2) when, where, and under what circumstances does it occur?

scholarly journals On The Hormonal and Neural Control of the Release of Gametes in Ascidians

1951 ◽  
Vol 28 (4) ◽  
pp. 463-472
Author(s):  
D. B. CARLISLE
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neural Control ◽  
Sense Organ ◽  
Chorionic Gonadotrophin ◽  
Gamete Release ◽  
The Central Nervous System ◽  
Neural Region

1. It is argued that the neural gland (+ciliated pit) of ascidians is homologous with the entire pituitary of vertebrates, adenohypophysis as well as neurohypophysis. 2. Ciona and Phallusia are shown to respond to an injection of chorionic gonadotrophin by the release of gametes. 3. They respond in the same way to feeding with eggs and sperm of their own species but not to those of other species. 4. This response is prevented in both cases by section of the nerves from the ganglion to the region of the gonads. 5. Destruction of the heart and removal of the blood does not prevent the response to feeding with gametes, nor to injection of gonadotrophin into the neural region; this operation does prevent the reaction if the site of injection is elsewhere. 6. Destruction of the neural gland, leaving the ganglion intact, prevents the response to feeding with gametes, but does not prevent its following an injection of chorionic gonadotrophin. 7. The hypothesis is advanced that the neural gland (+ciliated pit) is the sense organ involved in this response to feeding, and that it produces gonadotrophin and passes it to the ganglion by a non-vascular route; the ganglion then stimulates by nervous pathways the gonads to release gametes. 8. It is suggested that gonadotrophin is here fulfilling a sensory role in passing information from sense organ to the central nervous system. It may be contrasted with adrenalin which passes instructions from the central nervous system to effectors. 9. Phallusia is shown to respond with gamete release to an injection of an extract of the neural complex of Ciona.

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