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.

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 Minireview: The Neuroendocrinology of the Suprachiasmatic Nucleus as a Conductor of Body Time in Mammals

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5640-5647 ◽  
Author(s):  
Ilia N. Karatsoreos ◽  
Rae Silver
Keyword(s):  
Circadian Rhythms ◽  
Suprachiasmatic Nucleus ◽  
Hormone Secretion ◽  
Gonadal Hormone ◽  
Multiple Levels ◽  
And Behavior ◽  
Circadian Behavior ◽  
The Brain ◽  
Indirect Route ◽  
Photic Input

Circadian rhythms in physiology and behavior are regulated by a master clock resident in the suprachiasmatic nucleus (SCN) of the hypothalamus, and dysfunctions in the circadian system can lead to serious health effects. This paper reviews the organization of the SCN as the brain clock, how it regulates gonadal hormone secretion, and how androgens modulate aspects of circadian behavior known to be regulated by the SCN. We show that androgen receptors are restricted to a core SCN region that receives photic input as well as afferents from arousal systems in the brain. We suggest that androgens modulate circadian behavior directly via actions on the SCN and that both androgens and estrogens modulate circadian rhythms through an indirect route, by affecting overall activity and arousal levels. Thus, this system has multiple levels of regulation; the SCN regulates circadian rhythms in gonadal hormone secretion, and hormones feed back to influence SCN functions.

scholarly journals Temporal Event Association and Output-Dependent Learning: A Proposed Scheme of Neural Molecular Connections

1999 ◽  
Vol 3 (4) ◽  
pp. 234-244 ◽  
Author(s):  
Yukifumi Shigematsu ◽  
◽  
Hiroshi Okamoto ◽  
Kazuhisa Ichikawa ◽  
Gen Matsumoto ◽  
...  
Keyword(s):  
Action Potentials ◽  
Single Neuron ◽  
Calcium Concentration ◽  
Molecular Mechanisms ◽  
Learning Algorithm ◽  
Learning Rule ◽  
Voltage Dependent ◽  
Temporal Events ◽  
Dependent Learning ◽  
The Brain

We introduce a model of temporal-event-associated and output-dependent learning rule, genetically acquired and expressed in a single neuron. This is essentially indispensable for the brain to acquire algorithms, how to process its self-selected information, by itself. This proposed learning rule is revised-Hebbian with a synaptic history trace to correlate one temporal event to others. Temporal events are memorized to be expressed at the synaptic site of inputs and in the form of the asymmetric neural strength corrections associated with temporal events. This learning algorithm has an advantage to associate one temporal event with others, resulting in the neuron with predictability but also makes recalling flexible. Re ’ calling is, according to this learning, independent of timing, supposed to be crucial in learning. Underlying molecular mechanisms for our proposed learning rule are discussed and we identify three important factors: 1) the back-propagating action potentials experimentally observed a single neuron play a crucial role for outputdependent learning, 2) temporally associated, nonlinear couplings are modeled at molecular levels with glutamate receptors, voltage-dependent channels, intracellular calcium concentration, protein kinases and phosphatase, and 3) intracellular concentration of inositol-tri-phosphate [IP3] is the memory substrate of synaptic history.

scholarly journals Dissection of central clock function in Drosophila through cell-specific CRISPR-mediated clock gene disruption

2019 ◽  
Author(s):  
Rebecca Delventhal ◽  
Meghan Pantalia ◽  
Reed M. O’Connor ◽  
Matthew Ulgherait ◽  
Han X. Kim ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Circadian Rhythms ◽  
Molecular Clock ◽  
Gene Disruption ◽  
Clock Gene ◽  
Distributed Network ◽  
Circadian Activity ◽  
Clock Proteins ◽  
Central Clock ◽  
Circadian Behavior

AbstractIn Drosophila, ~150 neurons expressing molecular clock proteins regulate circadian behavior. Sixteen of these clock neurons secrete the neuropeptide Pdf and have been called “master pacemakers” because they are essential for circadian rhythms. A subset of Pdf+ neurons (the morning oscillator) regulates morning activity and communicates with other non-Pdf+ neurons, including a subset called the evening oscillator. It is assumed that the molecular clock in Pdf+ neurons is required for these functions. To test this, we developed and validated Gal4-UAS based CRISPR tools for cell-specific disruption of key molecular clock components, period and timeless. While loss of the molecular clock in both the morning and evening oscillators eliminates circadian locomotor activity, the molecular clock in either oscillator alone is sufficient for circadian locomotor activity. This suggests that clock neurons do not act in a hierarchy but as a distributed network to regulate circadian activity.

Electricity Works

2019 ◽  
pp. 123-140
Author(s):  
Alan J. McComas
Keyword(s):  
Human Brain ◽  
Electrical Activity ◽  
Single Neuron ◽  
Impulse Activity ◽  
Slow Waves ◽  
Rabbit Brain ◽  
The Impact ◽  
The Brain

This chapter focuses on the electrical activity of the brain. It first highlights Richard Caton’s demonstration of slow waves in the rabbit brain before an audience of physicians in Edinburgh in 1875. Then the chapter turns to the impact of Hans Berger’s discovery of similar slow waves in the human brain and of the advent of electroencephalography. The chapter finishes with the remarkable technical accomplishment of Mircea Steriade in being able to record from the same single neuron during periods of sleep and wakefulness, thereby showing the enormous range of impulse firing frequencies possible. From here, the chapter considers if it is possible that it is simply the intensity of the cortical discharge, with its thalamic underpinning, that determines whether or not impulse activity enters into consciousness.

Pineal transplantation to the brain of pinealectomized lizards: Effects of circadian rhythms of locomotor activity.

1997 ◽  
Vol 111 (5) ◽  
pp. 1123-1132 ◽  
Author(s):  
Augusto Foà ◽  
Cristiano Bertolucci ◽  
Andrea Marsanich ◽  
Augusto Innocenti
Keyword(s):  
Locomotor Activity ◽  
Circadian Rhythms ◽  
The Brain

Ketamine Differentially Blocks Sensory Afferent Synaptic Transmission in Medial Nucleus Tractus Solitarius (mNTS)

2003 ◽  
Vol 98 (1) ◽  
pp. 121-132 ◽  
Author(s):  
Young-Ho Jin ◽  
Timothy W. Bailey ◽  
Mark W. Doyle ◽  
Bai-yan Li ◽  
Kyoung S. K. Chang ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Sensory Neurons ◽  
Action Potentials ◽  
Nucleus Tractus Solitarius ◽  
Solitary Tract ◽  
Medial Nucleus ◽  
Conduction Velocities ◽  
Autonomic Reflexes ◽  
Synaptic Failure ◽  
The Brain

Background Ketamine increases blood pressure and heart rate by unknown mechanisms, but studies suggest that an intact central nervous system and arterial baroreceptors are required. In the brain stem, medial nucleus tractus solitarius receives afferents from nodose neurons that initiate cardiovascular autonomic reflexes. Here, the authors assessed ketamine actions on afferent medial nucleus tractus solitarius synaptic transmission. Methods Ketamine was applied to horizontally sliced brain stems. Solitary tract (ST) stimulation evoked excitatory postsynaptic currents (eEPSCs) in medial nucleus tractus solitarius neurons. Capsaicin (200 nm) block of ST eEPSCs sorted neurons into sensitive (n = 19) and resistant (n = 23). In nodose ganglion slices, shocks to the peripheral vagal trunk activated afferent action potentials in sensory neurons classified by conduction velocities and capsaicin. Results Ketamine potently (10-100 mciro m) blocked small, ST-evoked -methyl-d-aspartate synaptic currents found only in a subset of capsaicin-resistant neurons (6 of 12). Surprisingly, ketamine reversibly inhibited ST eEPSC amplitudes and induced synaptic failure at lower concentrations in capsaicin-sensitive than in capsaicin-resistant neurons (P < 0.005; n = 11 and 11). Spontaneous EPSCs using non- -methyl-d-aspartate receptors were insensitive even to 1-3 mm ketamine, suggesting that ST responses were blocked presynaptically. Similarly, ketamine blocked C-type action potential conduction at lower concentrations than A-type nodose sensory neurons. Conclusion The authors conclude that ketamine inhibits postsynaptic -methyl-d-aspartate receptors and presynaptic afferent processes in medial nucleus tractus solitarius. Unexpectedly, capsaicin-sensitive (C-type), unmyelinated afferents are significantly more susceptible to block than capsaicin-resistant (A-type), myelinated afferents. This differentiation may be related to tetrodotoxin-resistant sodium currents. Since C-type afferents mediate powerful arterial baroreflexes effects, these differential actions may contribute to ketamine-induced cardiovascular dysfunction.

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.

Electroencephalogram during arousal from hibernation in the birchmouse

1960 ◽  
Vol 199 (3) ◽  
pp. 535-538 ◽  
Author(s):  
Per Andersen ◽  
Kjell Johansen ◽  
John Krog
Keyword(s):  
Oxygen Consumption ◽  
Body Temperature ◽  
Electrical Activity ◽  
Action Potentials ◽  
Sensory Stimulation ◽  
The Body ◽  
Muscle Action ◽  
Oral Temperature ◽  
Body Temperatures ◽  
The Brain

In the birchmouse, Sicista betulina, electrical activity of the brain was recorded at an oral temperature as low as 2.5°C. At body temperatures below about 10°C the activity consisted of bursts of slow waves separated by silent intervals. On increasing body temperature during the arousal this pattern was gradually replaced by activity of higher frequency until a normal electroencephalogram was recorded at about 30°C. No typical desynchronization of the EEG in response to sensory stimulation was noted until the body temperature reached that same level. The vocalization at low body temperatures induced by faint stimulation therefore seems to be unrelated to EEG desynchronization. The increase of recorded muscle-action potentials during the arousal from hibernation paralleled the increase in oxygen consumption and body temperature described previously (1).

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