scholarly journals Temporally and spatially partitioned neuropeptide release from individual clock neurons

2021 ◽  
Vol 118 (17) ◽  
pp. e2101818118
Author(s):  
Markus K. Klose ◽  
Marcel P. Bruchez ◽  
David L. Deitcher ◽  
Edwin S. Levitan
Keyword(s):  
Locomotor Activity ◽  
Synaptic Transmission ◽  
Electrical Activity ◽  
Activity Period ◽  
Neuropeptide Release ◽  
Rhythmic Behavior ◽  
Rhythmic Behaviors ◽  
The Brain

Neuropeptides control rhythmic behaviors, but the timing and location of their release within circuits is unknown. Here, imaging in the brain shows that synaptic neuropeptide release by Drosophila clock neurons is diurnal, peaking at times of day that were not anticipated by prior electrical and Ca2+ data. Furthermore, hours before peak synaptic neuropeptide release, neuropeptide release occurs at the soma, a neuronal compartment that has not been implicated in peptidergic transmission. The timing disparity between release at the soma and terminals results from independent and compartmentalized mechanisms for daily rhythmic release: consistent with conventional electrical activity–triggered synaptic transmission, terminals require Ca2+ influx, while somatic neuropeptide release is triggered by the biochemical signal IP3. Upon disrupting the somatic mechanism, the rhythm of terminal release and locomotor activity period are unaffected, but the number of flies with rhythmic behavior and sleep–wake balance are reduced. These results support the conclusion that somatic neuropeptide release controls specific features of clock neuron–dependent behaviors. Thus, compartment-specific mechanisms within individual clock neurons produce temporally and spatially partitioned neuropeptide release to expand the peptidergic connectome underlying daily rhythmic behaviors.

scholarly journals Independently Regulated Multi-compartment Neuropeptide Release from a Clock Neuron Controls Circadian Behavior

2020 ◽  
Author(s):  
Markus K. Klose ◽  
Marcel P. Bruchez ◽  
David L. Deitcher ◽  
Edwin S. Levitan
Keyword(s):  
Locomotor Activity ◽  
Circadian Rhythms ◽  
Synaptic Transmission ◽  
Electrical Activity ◽  
Action Potentials ◽  
Single Neuron ◽  
Neuropeptide Release ◽  
Circadian Behavior ◽  
The Brain ◽  
Neuronal Compartments

Neuropeptides control many behaviors, including circadian rhythms. However, because monitoring neuropeptide release in the brain is challenging, analysis of peptidergic circuits often has relied on monitoring surrogates in the soma based on the paradigm that synaptic transmission is mediated exclusively by Ca2+ influx induced by propagating action potentials. Here live imaging demonstrates that neuropeptide release by Drosophila small ventrolateral (s-LNv) clock neurons does not conform to this paradigm. First, neuropeptide release from terminals peaks hours after sunrise, which was not evident from electrical and Ca2+ data. Second, inconsistent with global release by propagating action potentials, release from terminals is preceded by hours by release from the soma, a compartment not usually considered in peptidergic transmission. The timing of release from the two neuronal compartments reflects different mechanisms: terminals require Ca2+ influx, as expected with coupling to electrical activity, while somatic release is based on intracellular IP3 signaling. Upon cell specific disruption of the somatic mechanism, daily neuropeptide release from terminals remains rhythmic and the period of daily locomotor activity is unaffected, but behavioral rhythmicity is reduced. Thus, rhythmic bouts of anatomically, mechanistically and temporally distinct release from a single neuron control neuropeptide dependent features of circadian behavior.

The Effect of Some Drugs on the Electrical Activity of the Brain, and on Behaviour

1954 ◽  
Vol 100 (418) ◽  
pp. 125-128 ◽  
Author(s):  
J. Elkes ◽  
C. Elkes ◽  
P. B. Bradley
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Synaptic Transmission ◽  
Electrical Activity ◽  
Reference Points ◽  
Central Effects ◽  
System Form ◽  
The Central Nervous System ◽  
The Brain

Peripheral neuro-effector sites within and outside the autonomic nervous system form useful reference points for the study of the central effects of some agents. Nevertheless, ready analogies between peripheral neurohumoral mediation, and central synaptic transmission may be grossly misleading, and reliance must solely be placed on data derived from within the central nervous system itself.

Fit Vs Faint: Assessing Work Causation in “Idiopathic Fall” Cases

2014 ◽  
Vol 19 (5) ◽  
pp. 3-12
Author(s):  
Lorne Direnfeld ◽  
David B. Torrey ◽  
Jim Black ◽  
LuAnn Haley ◽  
Christopher R. Brigham
Keyword(s):  
Blood Flow ◽  
Electrical Activity ◽  
Loss Of Consciousness ◽  
Brain Electrical Activity ◽  
Medical Terminology ◽  
Scientific Analysis ◽  
Medical Causation ◽  
The Individual ◽  
The Brain ◽  
Current Science

Abstract When an individual falls due to a nonwork-related episode of dizziness, hits their head and sustains injury, do workers’ compensation laws consider such injuries to be compensable? Bearing in mind that each state makes its own laws, the answer depends on what caused the loss of consciousness, and the second asks specifically what happened in the fall that caused the injury? The first question speaks to medical causation, which applies scientific analysis to determine the cause of the problem. The second question addresses legal causation: Under what factual circumstances are injuries of this type potentially covered under the law? Much nuance attends this analysis. The authors discuss idiopathic falls, which in this context means “unique to the individual” as opposed to “of unknown cause,” which is the familiar medical terminology. The article presents three detailed case studies that describe falls that had their genesis in episodes of loss of consciousness, followed by analyses by lawyer or judge authors who address the issue of compensability, including three scenarios from Arizona, California, and Pennsylvania. A medical (scientific) analysis must be thorough and must determine the facts regarding the fall and what occurred: Was the fall due to a fit (eg, a seizure with loss of consciousness attributable to anormal brain electrical activity) or a faint (eg, loss of consciousness attributable to a decrease in blood flow to the brain? The evaluator should be able to fully explain the basis for the conclusions, including references to current science.

The Electrical Activity of the Brain

1954 ◽  
Vol 190 (6) ◽  
pp. 54-63 ◽  
Author(s):  
W. Grey Walter
Keyword(s):  
Electrical Activity ◽  
The Brain

scholarly journals Identification of Brain Electrical Activity Related to Head Yaw Rotations

Sensors ◽  
2021 ◽  
Vol 21 (10) ◽  
pp. 3345
Author(s):  
Enrico Zero ◽  
Chiara Bersani ◽  
Roberto Sacile
Keyword(s):  
Electrical Activity ◽  
Electrical Stimulus ◽  
Head Movements ◽  
Brain Electrical Activity ◽  
Output Function ◽  
Input Output ◽  
Eeg Signals ◽  
Head Turning ◽  
Identification Technique ◽  
The Brain

Automatizing the identification of human brain stimuli during head movements could lead towards a significant step forward for human computer interaction (HCI), with important applications for severely impaired people and for robotics. In this paper, a neural network-based identification technique is presented to recognize, by EEG signals, the participant’s head yaw rotations when they are subjected to visual stimulus. The goal is to identify an input-output function between the brain electrical activity and the head movement triggered by switching on/off a light on the participant’s left/right hand side. This identification process is based on “Levenberg–Marquardt” backpropagation algorithm. The results obtained on ten participants, spanning more than two hours of experiments, show the ability of the proposed approach in identifying the brain electrical stimulus associate with head turning. A first analysis is computed to the EEG signals associated to each experiment for each participant. The accuracy of prediction is demonstrated by a significant correlation between training and test trials of the same file, which, in the best case, reaches value r = 0.98 with MSE = 0.02. In a second analysis, the input output function trained on the EEG signals of one participant is tested on the EEG signals by other participants. In this case, the low correlation coefficient values demonstrated that the classifier performances decreases when it is trained and tested on different subjects.

Electrical activity of the brain: Mechanisms and interpretation

1983 ◽  
Vol 26 (9) ◽  
pp. 801-828 ◽  
Author(s):  
S M Osovets ◽  
D A Ginzburg ◽  
V S Gurfinkel' ◽  
L P Zenkov ◽  
L P Latash ◽  
...  
Keyword(s):  
Electrical Activity ◽  
The Brain

Central and Peripheral Clock Control of Circadian Feeding Rhythms

2021 ◽  
pp. 074873042110458
Author(s):  
Carson V. Fulgham ◽  
Austin P. Dreyer ◽  
Anita Nasseri ◽  
Asia N. Miller ◽  
Jacob Love ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Circadian Clock ◽  
Feeding Behavior ◽  
Molecular Clock ◽  
Fat Body ◽  
Molecular Clocks ◽  
Central Brain ◽  
Feeding Rhythms ◽  
Free Running ◽  
The Brain

Many behaviors exhibit ~24-h oscillations under control of an endogenous circadian timing system that tracks time of day via a molecular circadian clock. In the fruit fly, Drosophila melanogaster, most circadian research has focused on the generation of locomotor activity rhythms, but a fundamental question is how the circadian clock orchestrates multiple distinct behavioral outputs. Here, we have investigated the cells and circuits mediating circadian control of feeding behavior. Using an array of genetic tools, we show that, as is the case for locomotor activity rhythms, the presence of feeding rhythms requires molecular clock function in the ventrolateral clock neurons of the central brain. We further demonstrate that the speed of molecular clock oscillations in these neurons dictates the free-running period length of feeding rhythms. In contrast to the effects observed with central clock cell manipulations, we show that genetic abrogation of the molecular clock in the fat body, a peripheral metabolic tissue, is without effect on feeding behavior. Interestingly, we find that molecular clocks in the brain and fat body of control flies gradually grow out of phase with one another under free-running conditions, likely due to a long endogenous period of the fat body clock. Under these conditions, the period of feeding rhythms tracks with molecular oscillations in central brain clock cells, consistent with a primary role of the brain clock in dictating the timing of feeding behavior. Finally, despite a lack of effect of fat body selective manipulations, we find that flies with simultaneous disruption of molecular clocks in multiple peripheral tissues (but with intact central clocks) exhibit decreased feeding rhythm strength and reduced overall food intake. We conclude that both central and peripheral clocks contribute to the regulation of feeding rhythms, with a particularly dominant, pacemaker role for specific populations of central brain clock cells.

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