scholarly journals Integration of sleep homeostasis and navigation in Drosophila

2020 ◽  
Author(s):  
Andres Flores Valle ◽  
Pedro J. Gonçalves ◽  
Johannes D. Seelig
Keyword(s):  
Structural Changes ◽  
Brain Area ◽  
Network Connectivity ◽  
Central Complex ◽  
Head Direction ◽  
Sleep Phase ◽  
Plasticity Mechanism ◽  
Sleep Homeostasis ◽  
The Face ◽  
The Brain

ABSTRACTDuring sleep, the brain undergoes dynamic and structural changes. In Drosophila, such changes have been observed in the central complex, a brain area important for sleep control and navigation. The connectivity of the central complex raises the question about how navigation, and specifically the head direction system, can operate in the face of sleep related plasticity.To address this question, we develop a model that integrates sleep homeostasis and head direction. We show that by introducing plasticity, the head direction system can function in a stable way by balancing plasticity in connected circuits that encode sleep pressure. With increasing sleep pressure, the head direction system nevertheless becomes unstable and a sleep phase with a different plasticity mechanism is introduced to reset network connectivity.The proposed integration of sleep homeostasis and head direction circuits captures features of their neural dynamics observed in flies and mice.

scholarly journals Integration of sleep homeostasis and navigation in Drosophila

2021 ◽  
Vol 17 (7) ◽  
pp. e1009088
Author(s):  
Andres Flores-Valle ◽  
Pedro J. Gonçalves ◽  
Johannes D. Seelig
Keyword(s):  
Structural Changes ◽  
Brain Area ◽  
Network Connectivity ◽  
Central Complex ◽  
Head Direction ◽  
Sleep Phase ◽  
Plasticity Mechanism ◽  
Sleep Homeostasis ◽  
The Face ◽  
The Brain

During sleep, the brain undergoes dynamic and structural changes. In Drosophila, such changes have been observed in the central complex, a brain area important for sleep control and navigation. The connectivity of the central complex raises the question about how navigation, and specifically the head direction system, can operate in the face of sleep related plasticity. To address this question, we develop a model that integrates sleep homeostasis and head direction. We show that by introducing plasticity, the head direction system can function in a stable way by balancing plasticity in connected circuits that encode sleep pressure. With increasing sleep pressure, the head direction system nevertheless becomes unstable and a sleep phase with a different plasticity mechanism is introduced to reset network connectivity. The proposed integration of sleep homeostasis and head direction circuits captures features of their neural dynamics observed in flies and mice.

scholarly journals The head direction circuit of two insect species

2019 ◽  
Author(s):  
Ioannis Pisokas ◽  
Stanley Heinze ◽  
Barbara Webb
Keyword(s):  
Fruit Fly ◽  
Central Complex ◽  
Insect Species ◽  
Comparative Approach ◽  
Head Direction ◽  
Circuit Performance ◽  
Heading Direction ◽  
Neuronal Projection ◽  
Connectivity Patterns ◽  
The Brain

AbstractRecent studies of the Central Complex in the brain of the fruit fly have identified neurons with activity that tracks the animal’s heading direction. These neurons are part of a neuronal circuit with dynamics resembling those of a ring attractor. Other insects have a homologous circuit sharing a generally similar topographic structure but with significant structural and connectivity differences. We model the connectivity patterns in two insect species to investigate the effect of the differences on the dynamics of the circuit. We illustrate that the circuit found in locusts can also operate as a ring attractor and identify differences that enable the fruit fly circuit to respond faster to heading changes while they render the locust circuit more tolerant to noise. Our findings demonstrate that subtle differences in neuronal projection patterns can have a significant effect on the circuit performance and emphasise the need for a comparative approach in neuroscience.

Automated long-term two-photon imaging in head-fixed walking Drosophila

2021 ◽  
Author(s):  
Andres Flores Valle ◽  
Rolf Honnef ◽  
Johannes D. Seelig
Keyword(s):  
Structural Changes ◽  
Long Term Memory ◽  
Head Direction ◽  
Multiple Timescales ◽  
Two Photon ◽  
Photon Imaging ◽  
Two Photon Imaging ◽  
Millisecond Range ◽  
The Brain

The brain of Drosophila shows dynamics at multiple timescales, from the millisecond range of fast voltage or calcium transients to functional and structural changes occurring over multiple days. To relate such dynamics to behavior requires monitoring neural circuits across these multiple timescales in behaving animals. Here, we develop a technique for automated long-term two-photon imaging in fruit flies, during wakefulness and sleep, navigating in virtual reality over up to seven days. The method is enabled by laser surgery, a microrobotic arm for controlling forceps for dissection assistance, an automated feeding robot, as well as volumetric, simultaneous multiplane imaging. The approach is validated in the fly's head direction system. Imaging in behaving flies over multiple timescales will be useful for understanding circadian activity, learning and long-term memory, or sleep.

scholarly journals Synaptic dysfunction caused by truncated tau is associated with hyperpolarization-activated cyclic nucleotide-gated channelopathy

2020 ◽  
Author(s):  
Despoina Goniotaki ◽  
Francesco Tamagnini ◽  
Luca Biasetti ◽  
Svenja-Lotta Rumpf ◽  
Kate Fennell ◽  
...  
Keyword(s):  
Cyclic Nucleotide ◽  
Hippocampal Neurons ◽  
Structural Changes ◽  
Network Connectivity ◽  
Network Activity ◽  
Synaptic Dysfunction ◽  
Synaptic Ultrastructure ◽  
Cluster Density ◽  
Carboxy Terminal ◽  
The Brain

Neurodegenerative tauopathies are characterized by deposition in the brain of highly phosphorylated and truncated forms of tau, but how these impact on cellular processes remains unknown. Here, we show that hyperpolarization-induced membrane voltage ‘sag’, which is dependent on hyperpolarization-activated inward-rectifying (Ih) current and hyperpolarization-activated cyclic nucleotide-gated (HCN) cation channels, is increased in the Tau35 mouse model of human tauopathy. Expression of Tau35, corresponding to a fragment comprising the carboxy-terminal half of tau first identified in human tauopathy brain, reduces dendritic branching in mouse brain and in cultured hippocampal neurons, and decreases synaptic density. Neuronal expression of Tau35 results in increased tau phosphorylation and significant disruption to synaptic ultrastructure, including marked and progressive reductions in synaptic vesicle counts and vesicle cluster density. Ultrastructural analysis reveals that the positioning of synaptic vesicles is perturbed by Tau35, causing vesicles to accumulate at sites adjacent to the active zone and at the lateral edges of the cluster. These structural changes induced by Tau35 correlate with functional abnormalities in network activity, including increased width, reduced frequency and slower rate of rise of spontaneous excitatory postsynaptic currents. Collectively, these changes are consistent with a model in which disease-associated tau species disrupt network connectivity and signaling. Our results suggest that the persistence of truncated tau in the brain may underpin the catastrophic synaptic dysfunction observed during the development and progression of human tauopathy.

About the Brain, the Face, and Emotion

1984 ◽  
Vol 29 (7) ◽  
pp. 567-568
Author(s):  
Gilles Kirouac
Keyword(s):  
The Face ◽  
The Brain

Native Ubiquitin Structural Changes Resulting from Complexation with β-methylamino-L-alanine (BMAA)

2020 ◽  
Author(s):  
Katie Mae Wilson ◽  
Aurora Burkus-Matesevac ◽  
Samuel Maddox ◽  
Christopher Chouinard
Keyword(s):  
Structural Changes ◽  
Noncovalent Complex ◽  
Unfolded Protein ◽  
Protein Size ◽  
High Concentrations ◽  
The Unfolded Protein Response ◽  
Critical Binding ◽  
Protein Response ◽  
The Brain ◽  
Lateral Sclerosis

β-methylamino-L-alanine (BMAA) has been linked to the development of neurodegenerative (ND) symptoms following chronic environmental exposure through water and dietary sources. The brains of those affected by this condition, often referred to as amyotrophic lateral sclerosis-parkinsonism-dementia complex (ALS-PDC), have exhibited the presence of plaques and neurofibrillary tangles (NFTs) from protein aggregation. Although numerous studies have sought to better understand the correlation between BMAA exposure and onset of ND symptoms, no definitive link has been identified. One prevailing hypothesis is that BMAA acts a small molecule ligand, complexing with critical proteins in the brain and reducing their function. The objective of this research was to investigate the effects of BMAA exposure on the native structure of ubiquitin. We hypothesized that formation of a Ubiquitin+BMAA noncovalent complex would alter the protein’s structure and folding and ultimately affect the ubiquitinproteasome system (UPS) and the unfolded protein response (UPR). Ion mobility-mass spectrometry revealed that at sufficiently high concentrations BMAA did in fact form a noncovalent complex with ubiquitin, however similar complexes were identified for a range of additional amino acids. Collision induced unfolding (CIU) was used to interrogate the unfolding dynamics of native ubiquitin and these Ubq-amino acid complexes and it was determined that complexation with BMAA led to a significant alteration in native protein size and conformation, and this complex required considerably more energy to unfold. This indicates that the complex remains more stable under native conditions and this may indicate that BMAA has attached to a critical binding location.

Native Ubiquitin Structural Changes Resulting from Complexation with β-methylamino-L-alanine (BMAA)

2020 ◽  
Author(s):  
Katie Mae Wilson ◽  
Aurora Burkus-Matesevac ◽  
Samuel Maddox ◽  
Christopher Chouinard
Keyword(s):  
Structural Changes ◽  
Noncovalent Complex ◽  
Unfolded Protein ◽  
Protein Size ◽  
High Concentrations ◽  
The Unfolded Protein Response ◽  
Critical Binding ◽  
Protein Response ◽  
The Brain ◽  
Lateral Sclerosis

β-methylamino-L-alanine (BMAA) has been linked to the development of neurodegenerative (ND) symptoms following chronic environmental exposure through water and dietary sources. The brains of those affected by this condition, often referred to as amyotrophic lateral sclerosis-parkinsonism-dementia complex (ALS-PDC), have exhibited the presence of plaques and neurofibrillary tangles (NFTs) from protein aggregation. Although numerous studies have sought to better understand the correlation between BMAA exposure and onset of ND symptoms, no definitive link has been identified. One prevailing hypothesis is that BMAA acts a small molecule ligand, complexing with critical proteins in the brain and reducing their function. The objective of this research was to investigate the effects of BMAA exposure on the native structure of ubiquitin. We hypothesized that formation of a Ubiquitin+BMAA noncovalent complex would alter the protein’s structure and folding and ultimately affect the ubiquitinproteasome system (UPS) and the unfolded protein response (UPR). Ion mobility-mass spectrometry revealed that at sufficiently high concentrations BMAA did in fact form a noncovalent complex with ubiquitin, however similar complexes were identified for a range of additional amino acids. Collision induced unfolding (CIU) was used to interrogate the unfolding dynamics of native ubiquitin and these Ubq-amino acid complexes and it was determined that complexation with BMAA led to a significant alteration in native protein size and conformation, and this complex required considerably more energy to unfold. This indicates that the complex remains more stable under native conditions and this may indicate that BMAA has attached to a critical binding location.

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