High-speed in vivo calcium imaging reveals neuronal network activity with near-millisecond precision

2010 ◽  
Vol 7 (5) ◽  
pp. 399-405 ◽  
Author(s):  
Benjamin F Grewe ◽  
Dominik Langer ◽  
Hansjörg Kasper ◽  
Björn M Kampa ◽  
Fritjof Helmchen
Keyword(s):  
Neuronal Network ◽  
Calcium Imaging ◽  
High Speed ◽  
Network Activity ◽  
Neuronal Network Activity ◽  
In Vivo Calcium Imaging

scholarly journals Erratum: High-speed in vivo calcium imaging reveals neuronal network activity with near-millisecond precision

2010 ◽  
Vol 7 (6) ◽  
pp. 479-479 ◽  
Author(s):  
Benjamin F Grewe ◽  
Dominik Langer ◽  
Hansjörg Kasper ◽  
Björn M Kampa ◽  
Fritjof Helmchen
Keyword(s):  
Neuronal Network ◽  
Calcium Imaging ◽  
High Speed ◽  
Network Activity ◽  
Neuronal Network Activity ◽  
In Vivo Calcium Imaging

Dementia with Lewy bodies—associated ß-synuclein mutations V70M and P123H cause mutation-specific neuropathological lesions

2021 ◽  
Author(s):  
Maryna Psol ◽  
Sofia Guerin Darvas ◽  
Kristian Leite ◽  
Sameehan U Mahajani ◽  
Mathias Bähr ◽  
...  
Keyword(s):  
Neuronal Network ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies ◽  
Sporadic Case ◽  
Network Activity ◽  
Proteinase K ◽  
Neuronal Network Activity ◽  
Distinct Disease

Abstract ß-Synuclein (ß-Syn) has long been considered to be an attenuator for the neuropathological effects caused by the Parkinson’s disease-related α-Synuclein (α-Syn) protein. However, recent studies demonstrated that overabundant ß-Syn can form aggregates and induce neurodegeneration in CNS neurons in vitro and in vivo, albeit at a slower pace as compared to α-Syn. Here we demonstrate that ß-Syn mutants V70M, detected in a sporadic case of Dementia with Lewy Bodies (DLB), and P123H, detected in a familial case of DLB, robustly aggravate the neurotoxic potential of ß-Syn. Intriguingly, the two mutations trigger mutually exclusive pathways. ß-Syn V70M enhances morphological mitochondrial deterioration and degeneration of dopaminergic and non-dopaminergic neurons, but has no influence on neuronal network activity. Conversely, ß-Syn P123H silences neuronal network activity, but does not aggravate neurodegeneration. ß-Syn WT, V70M and P123H formed proteinase K (PK) resistant intracellular fibrils within neurons, albeit with less stable C-termini as compared to α-Syn. Under cell free conditions, ß-Syn V70M demonstrated a much slower pace of fibril formation as compared to WT ß-Syn, and P123H fibrils present with a unique phenotype characterized by large numbers of short, truncated fibrils. Thus, it is possible that V70M and P123H cause structural alterations in ß-Syn, that are linked to their distinct neuropathological profiles. The extent of the lesions caused by these neuropathological profiles is almost identical to that of overabundant α-Syn, and thus likely to be directly involved into etiology of DLB. Over all, this study provides insights into distinct disease mechanisms caused by mutations of ß-Syn.

In Vivo Calcium Imaging of Neural Network Function

Physiology ◽  
2007 ◽  
Vol 22 (6) ◽  
pp. 358-365 ◽  
Author(s):  
Werner Göbel ◽  
Fritjof Helmchen
Keyword(s):  
Calcium Imaging ◽  
Activity Patterns ◽  
Network Activity ◽  
Network Function ◽  
Two Photon ◽  
Calcium Indicators ◽  
Recent Developments ◽  
In Vivo Calcium Imaging ◽  
Function Network

Spatiotemporal activity patterns in local neural networks are fundamental to brain function. Network activity can now be measured in vivo using two-photon imaging of cell populations that are labeled with fluorescent calcium indicators. In this review, we discuss basic aspects of in vivo calcium imaging and highlight recent developments that will help to uncover operating principles of neural circuits.

scholarly journals Neuronal network activity controls microglial process surveillance in awake mice via norepinephrine signaling

2019 ◽  
Author(s):  
Yong Liu ◽  
Yujiao Li ◽  
Ukpong B. Eyo ◽  
Tingjun Chen ◽  
Anthony D. Umpierre ◽  
...  
Keyword(s):  
Neuronal Network ◽  
Sensory Deprivation ◽  
Brain Parenchyma ◽  
Network Activity ◽  
Process Dynamics ◽  
Two Photon ◽  
Neural Activities ◽  
Neuronal Network Activity ◽  
Health And Disease

AbstractMicroglia are resident immune cells that dynamically survey the brain parenchyma, interacting with neurons in both health and disease. However, it is still unclear how neuronal network activity drives microglial dynamics. Utilizing in vivo two-photon imaging of microglia in awake mice, we found that inhibition of neuronal activity under general anesthesia dramatically increased microglial process surveillance. Accordingly, both sensory deprivation and optogenetic inhibition of local neuronal network activity in awake mice resulted in similar increases in microglial process surveillance. We further determined that reduced norepinephrine signaling is responsible for the observed increase in microglial process surveillance. Our results demonstrate that microglial process dynamics are directly influenced by neural activities through norepinephrine signaling in awake animals and indicate the importance of awake imaging for studying microglia-neuron interactions.

scholarly journals Extracellular matrix supports excitation-inhibition balance in neuronal networks by stabilizing inhibitory synapses

2020 ◽  
Author(s):  
Egor Dzyubenko ◽  
Michael Fleischer ◽  
Daniel Manrique-Castano ◽  
Mina Borbor ◽  
Christoph Kleinschnitz ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Neuronal Network ◽  
Neuronal Plasticity ◽  
Neuronal Networks ◽  
Network Activity ◽  
Inhibitory Synapses ◽  
Neuronal Network Activity ◽  
The Brain

AbstractMaintaining the balance between excitation and inhibition is essential for the appropriate control of neuronal network activity. Sustained excitation-inhibition (E-I) balance relies on the orchestrated adjustment of synaptic strength, neuronal activity and network circuitry. While growing evidence indicates that extracellular matrix (ECM) of the brain is a crucial regulator of neuronal excitability and synaptic plasticity, it remains unclear whether and how ECM contributes to neuronal circuit stability. Here we demonstrate that the integrity of ECM supports the maintenance of E-I balance by retaining inhibitory connectivity. Depletion of ECM in mature neuronal networks preferentially decreases the density of inhibitory synapses and the size of individual inhibitory postsynaptic scaffolds. After ECM depletion, inhibitory synapse strength homeostatically increases via the reduction of presynaptic GABAB receptors. However, the inhibitory connectivity reduces to an extent that inhibitory synapse scaling is no longer efficient in controlling neuronal network activity. Our results indicate that the brain ECM preserves the balanced network state by stabilizing inhibitory synapses.Significance statementThe question how the brain’s extracellular matrix (ECM) controls neuronal plasticity and network activity is key for an appropriate understanding of brain functioning. In this study, we demonstrate that ECM depletion much more strongly affects the integrity of inhibitory than excitatory synapses in vitro and in vivo. We revealed that by retaining inhibitory connectivity, ECM ensures the efficiency of inhibitory control over neuronal network activity. Our work significantly expands our current state of knowledge about the mechanisms of neuronal network activity regulation. Our findings are similarly relevant for researchers working on the physiological regulation of neuronal plasticity in vitro and in vivo and for researchers studying the remodeling of neuronal networks upon brain injury, where prominent ECM alterations occur.

"In vivo" monitoring of neuronal network activity in zebrafish by two-photon Ca2+ imaging

2003 ◽  
Vol 446 (6) ◽  
pp. 766-773 ◽  
Author(s):  
E. Brustein ◽  
N. Marandi ◽  
Y. Kovalchuk ◽  
P. Drapeau ◽  
A. Konnerth
Keyword(s):  
Neuronal Network ◽  
Network Activity ◽  
In Vivo Monitoring ◽  
Two Photon ◽  
Neuronal Network Activity

scholarly journals Essential role for InSyn1 in dystroglycan complex integrity and cognitive behaviors in mice

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Akiyoshi Uezu ◽  
Erin Hisey ◽  
Yoshihiko Kobayashi ◽  
Yudong Gao ◽  
Tyler WA Bradshaw ◽  
...  
Keyword(s):  
Neuronal Network ◽  
Neuronal Firing ◽  
Network Activity ◽  
Inhibitory Synapses ◽  
Molecular Architecture ◽  
Synaptic Organization ◽  
Cognitive Behaviors ◽  
Neuronal Network Activity

Human mutations in the dystroglycan complex (DGC) result in not only muscular dystrophy but also cognitive impairments. However, the molecular architecture critical for the synaptic organization of the DGC in neurons remains elusive. Here, we report Inhibitory Synaptic protein 1 (InSyn1) is a critical component of the DGC whose loss alters the composition of the GABAergic synapses, excitatory/inhibitory balance in vitro and in vivo, and cognitive behavior. Association of InSyn1 with DGC subunits is required for InSyn1 synaptic localization. InSyn1 null neurons also show a significant reduction in DGC and GABA receptor distribution as well as abnormal neuronal network activity. Moreover, InSyn1 null mice exhibit elevated neuronal firing patterns in the hippocampus and deficits in fear conditioning memory. Our results support the dysregulation of the DGC at inhibitory synapses and altered neuronal network activity and specific cognitive tasks via loss of a novel component, InSyn1.

Desynchronisation of neuronal network activity in traumatic brain injury

2008 ◽  
Vol 39 (01) ◽  
Author(s):  
F Otto ◽  
J Opatz ◽  
R Hartmann ◽  
D Willbold ◽  
E Donauer ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Network ◽  
Network Activity ◽  
Neuronal Network Activity
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