Reverse correlation of rapid calcium signals in the zebrafish optic tectum in vivo

2006 ◽  
Vol 157 (2) ◽  
pp. 230-237 ◽  
Author(s):  
Pavan Ramdya ◽  
Bettina Reiter ◽  
Florian Engert
Keyword(s):  
Optic Tectum ◽  
Reverse Correlation ◽  
Calcium Signals ◽  
Zebrafish Optic Tectum

scholarly journals Targeting the Zebrafish Optic Tectum Using In Vivo Electroporation

2010 ◽  
Vol 2010 (7) ◽  
pp. pdb.prot5463-pdb.prot5463 ◽  
Author(s):  
K. J. Hoegler ◽  
J. H. Horne
Keyword(s):  
Optic Tectum ◽  
In Vivo Electroporation ◽  
Zebrafish Optic Tectum

scholarly journals Protocadherins control the modular assembly of neuronal columns in the zebrafish optic tectum

2015 ◽  
Vol 211 (4) ◽  
pp. 807-814 ◽  
Author(s):  
Sharon R. Cooper ◽  
Michelle R. Emond ◽  
Phan Q. Duy ◽  
Brandon G. Liebau ◽  
Marc A. Wolman ◽  
...  
Keyword(s):  
Optic Tectum ◽  
Neural Circuit ◽  
Artificial Chromosome ◽  
Transgenic Zebrafish ◽  
Visually Guided ◽  
Modular Assembly ◽  
Vertebrate Brain ◽  
Columnar Organization ◽  
Zebrafish Optic Tectum

Cell–cell recognition guides the assembly of the vertebrate brain during development. δ-Protocadherins comprise a family of neural adhesion molecules that are differentially expressed and have been implicated in a range of neurodevelopmental disorders. Here we show that the expression of δ-protocadherins partitions the zebrafish optic tectum into radial columns of neurons. Using in vivo two-photon imaging of bacterial artificial chromosome transgenic zebrafish, we show that pcdh19 is expressed in discrete columns of neurons, and that these columnar modules are derived from proliferative pcdh19+ neuroepithelial precursors. Elimination of pcdh19 results in both a disruption of columnar organization and defects in visually guided behaviors. These results reveal a fundamental mechanism for organizing the developing nervous system: subdivision of the early neuroepithelium into precursors with distinct molecular identities guides the autonomous development of parallel neuronal units, organizing neural circuit formation and behavior.

scholarly journals Fiber photometry does not reflect spiking activity in the striatum

2021 ◽  
Author(s):  
Alex A. Legaria ◽  
Julia A. Licholai ◽  
Alexxai V. Kravitz
Keyword(s):  
Neuronal Activity ◽  
Calcium Imaging ◽  
Brain Activity ◽  
Neural Population ◽  
Fluorescence Signal ◽  
Calcium Signals ◽  
Cellular Events ◽  
Neural Populations ◽  
Spiking Activity

AbstractFiber photometry recordings are commonly used as a proxy for neuronal activity, based on the assumption that increases in bulk calcium fluorescence reflect increases in spiking of the underlying neural population. However, this assumption has not been adequately tested. Here, using endoscopic calcium imaging in the striatum we report that the bulk fluorescence signal correlates weakly with somatic calcium signals, suggesting that this signal does not reflect spiking activity, but may instead reflect subthreshold changes in neuropil calcium. Consistent with this suggestion, the bulk fluorescence photometry signal correlated strongly with neuropil calcium signals extracted from these same endoscopic recordings. We further confirmed that photometry did not reflect striatal spiking activity with simultaneous in vivo extracellular electrophysiology and fiber photometry recordings in awake behaving mice. We conclude that the fiber photometry signal should not be considered a proxy for spiking activity in neural populations in the striatum.Significance statementFiber photometry is a technique for recording brain activity that has gained popularity in recent years due to it being an efficient and robust way to record the activity of genetically defined populations of neurons. However, it remains unclear what cellular events are reflected in the photometry signal. While it is often assumed that the photometry signal reflects changes in spiking of the underlying cell population, this has not been adequately tested. Here, we processed calcium imaging recordings to extract both somatic and non-somatic components of the imaging field, as well as a photometry signal from the whole field. Surprisingly, we found that the photometry signal correlated much more strongly with the non-somatic than the somatic signals. This suggests that the photometry signal most strongly reflects subthreshold changes in calcium, and not spiking. We confirmed this point with simultaneous fiber photometry and extracellular spiking recordings, again finding that photometry signals relate poorly to spiking in the striatum. Our results may change interpretations of studies that use fiber photometry as an index of spiking output of neural populations.

scholarly journals Interactions between calmodulin and neurogranin govern the dynamics of CaMKII as a leaky integrator

2019 ◽  
Author(s):  
Mariam Ordyan ◽  
Tom Bartol ◽  
Mary Kennedy ◽  
Padmini Rangamani ◽  
Terrence Sejnowski
Keyword(s):  
Long Term Potentiation ◽  
Time Averaging ◽  
Calcium Signals ◽  
Term Potentiation ◽  
High Calcium ◽  
Leaky Integrator ◽  
Voltage Dependent ◽  
High Calcium Concentration ◽  
Voltage Dependent Calcium Channels

AbstractCalmodulin-dependent kinase II (CaMKII) has long been known to play an important role in learning and memory as well as long term potentiation (LTP). More recently it has been suggested that it might be involved in the time averaging of synaptic signals, which can then lead to the high precision of information stored at a single synapse. However, the role of the scaffolding molecule, neurogranin (Ng), in governing the dynamics of CaMKII is not yet fully understood. In this work, we adopt a rule-based modeling approach through the Monte Carlo method to study the effect of Ca2+ signals on the dynamics of CaMKII phosphorylation in the postsynaptic density (PSD). Calcium surges are observed in synaptic spines during an EPSP and back-propagating action potential due to the opening of NMDA receptors and voltage dependent calcium channels. We study the differences between the dynamics of phosphorylation of CaMKII monomers and dodecameric holoenzymes. The scaffolding molecule Ng, when present in significant concentration, limits the availability of free calmodulin (CaM), the protein which activates CaMKII in the presence of calcium. We show that it plays an important modulatory role in CaMKII phosphorylation following a surge of high calcium concentration. We find a non-intuitive dependence of this effect on CaM concentration that results from the different affinities of CaM for CaMKII depending on the number of calcium ions bound to the former. It has been shown previously that in the absence of phosphatase CaMKII monomers integrate over Ca2+ signals of certain frequencies through autophosphorylation (Pepke et al, Plos Comp. Bio., 2010). We also study the effect of multiple calcium spikes on CaMKII holoenzyme autophosphorylation, and show that in the presence of phosphatase CaMKII behaves as a leaky integrator of calcium signals, a result that has been recently observed in vivo. Our models predict that the parameters of this leaky integrator are finely tuned through the interactions of Ng, CaM, CaMKII, and PP1. This is a possible mechanism to precisely control the sensitivity of synapses to calcium signals.

Light-Induced Calcium Influx Into Retinal Axons Is Regulated by Presynaptic Nicotinic Acetylcholine Receptor Activity In Vivo

1999 ◽  
Vol 81 (2) ◽  
pp. 895-907 ◽  
Author(s):  
James A. Edwards ◽  
Hollis T. Cline
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Visual Stimulus ◽  
Optic Tectum ◽  
Visual Stimulation ◽  
Calcium Influx ◽  
Nicotinic Acetylcholine ◽  
Retinal Axons ◽  
Retinotectal System

Light-induced calcium influx into retinal axons is regulated by presynaptic nicotinic acetylcholine receptor activity in vivo. Visual activity is thought to be a critical factor in controlling the development of central retinal projections. Neuronal activity increases cytosolic calcium, which was hypothesized to regulate process outgrowth in neurons. We performed an in vivo imaging study in the retinotectal system of albino Xenopus laevis tadpoles with the fluorescent calcium indicator calcium green 1 dextran (CaGD) to test the role of calcium in regulating axon arbor development. We find that visual stimulus to the retina increased CaGD fluorescence intensity in retinal ganglion cell (RGC) axon arbors within the optic tectum and that branch additions to retinotectal axon arbors correlated with a local rise in calcium in the parent branch. We find three types of responses to visual stimulus, which roughly correlate with theon, off, and sustained response types of RGC reported by physiological criteria. Imaging in bandscan mode indicated that patterns of calcium transients were nonuniform throughout the axons. We tested whether the increase in calcium in the retinotectal axons required synaptic activity in the retina; intraocular application of tetrodotoxin (10 μM) or nifedipine (1 and 10 μM) blocked the stimulus-induced increase in RGC axonal fluorescence. A second series of pharmacological investigations was designed to determine the mechanism of the calcium elevation in the axon terminals within the optic tectum. Injection of bis-( o-aminophenoxy)- N, N, N′, N′-tetraacetic acid-AM (BAPTA-AM) (20 mM) into the tectal ventricle reduced axonal calcium levels, supporting the idea that visual stimulation increases axonal calcium. Injection of BAPTA (20 mM) into the tectal ventricle to chelate extracellular calcium also attenuated the calcium response to visual stimulation, indicating that calcium enters the axon from the extracellular medium. Caffeine (10 mM) caused a large increase in axonal calcium, indicating that intracellular stores contribute to the calcium signal. Presynaptic nicotinic acetylcholine receptors (nAChRs) may play a role in axon arbor development and the formation of the topographic retinotectal projection. Injection of nicotine (10 μM) into the tectal ventricle significantly elevated RGC axonal calcium levels, whereas application of the nAChR antagonist αBTX (100 nM) reduced the stimulus-evoked rise in RGC calcium fluorescence. These data suggest that light stimulus to the retina increases calcium in the axon terminal arbors through a mechanism that includes influx through nAChRs and amplification by calcium-induced calcium release from intracellular calcium stores. Such a mechanism may contribute to developmental plasticity of the retinotectal system by influencing both axon arbor elaboration and the strength of synaptic transmission.

scholarly journals Optogenetic manipulation of calcium signals in single T cells in vivo

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Armelle Bohineust ◽  
Zacarias Garcia ◽  
Béatrice Corre ◽  
Fabrice Lemaître ◽  
Philippe Bousso
Keyword(s):  
T Cells ◽  
Calcium Signals

Spreading depression in vivo potentiates electrically-driven responses in frog optic tectum

2005 ◽  
Vol 1036 (1-2) ◽  
pp. 109-114 ◽  
Author(s):  
Rubem Carlos Araújo Guedes ◽  
Kazuya Tsurudome ◽  
Nobuyoshi Matsumoto
Keyword(s):  
Optic Tectum ◽  
Spreading Depression

scholarly journals Valproic acid, a histone deacetylase inhibitor, regulates cell proliferation in the adult zebrafish optic tectum

2014 ◽  
Vol 243 (11) ◽  
pp. 1401-1415 ◽  
Author(s):  
Miki Dozawa ◽  
Hiromitsu Kono ◽  
Yuki Sato ◽  
Yoko Ito ◽  
Hideomi Tanaka ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Cell Proliferation ◽  
Histone Deacetylase ◽  
Optic Tectum ◽  
Histone Deacetylase Inhibitor ◽  
Adult Zebrafish ◽  
Deacetylase Inhibitor ◽  
Zebrafish Optic Tectum

scholarly journals Distinct signatures of calcium activity in brain mural cells

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Chaim Glück ◽  
Kim David Ferrari ◽  
Noemi Binini ◽  
Annika Keller ◽  
Aiman S Saab ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Brain Slices ◽  
Extracellular Potassium ◽  
Calcium Dynamics ◽  
Calcium Signals ◽  
Calcium Activity ◽  
Mural Cells ◽  
Vascular Smcs

Pericytes have been implicated in various neuropathologies, yet, little is known about their function and signaling pathways in health. Here, we characterized calcium dynamics of cortical mural cells in anesthetized or awake Pdgfrb-CreERT2;Rosa26 mice and in acute brain slices. Smooth muscle cells (SMCs) and ensheathing pericytes (EPs), also named as terminal vascular SMCs, revealed similar calcium dynamics in vivo. In contrast, calcium signals in capillary pericytes (CPs) were irregular, higher in frequency and occurred in cellular microdomains. In the absence of the vessel constricting agent U46619 in acute slices, SMCs and EPs revealed only sparse calcium signals whereas CPs retained their spontaneous calcium activity. Interestingly, chemogenetic activation of neurons in vivo and acute elevations of extracellular potassium in brain slices strongly decreased calcium activity in CPs. We propose that neuronal activation and an extracellular increase in potassium suppress calcium activity in CPs, likely mediated by Kir2.2 and KATP channels.

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