A searchable image resource of Drosophila GAL4-driver expression patterns with single neuron resolution
- Geoffrey Wilson Meissner
- Aljoscha Nern
- Yoshinori Aso
- Gwyneth M Card
- Barry J Dickson
- Wyatt Korff
- Gerald M Rubin
- Janelia Research Campus, United States
- Max Delbrück Center for Molecular Medicine, United States
- Max Delbrück Center for Molecular Medicine, Germany
Abstract
Precise, repeatable genetic access to specific neurons via GAL4/UAS and related methods is a key advantage of Drosophila neuroscience. Neuronal targeting is typically documented using light microscopy of full GAL4 expression patterns, which generally lack the single-cell resolution required for reliable cell type identification. Here we use stochastic GAL4 labeling with the MultiColor FlpOut approach to generate cellular resolution confocal images at large scale. We are releasing aligned images of 74,000 such adult central nervous systems. An anticipated use of this resource is to bridge the gap between neurons identified by electron or light microscopy. Identifying individual neurons that make up each GAL4 expression pattern improves the prediction of split-GAL4 combinations targeting particular neurons. To this end we have made the images searchable on the NeuronBridge website. We demonstrate the potential of NeuronBridge to rapidly and effectively identify neuron matches based on morphology across imaging modalities and datasets.
Data availability
The footprint of this image resource (~105 TB) exceeds our known current practical limits on standard public data repositories. Thus, we have made all the primary data (and a variety of processed outputs) used in this study freely available under a CC BY 4.0 license at https://doi.org/10.25378/janelia.21266625.v1 and through the publicly accessible website https://gen1mcfo.janelia.org. The images are made searchable with the same permissions on the user-friendly NeuronBridge website https://neuronbridge.janelia.org. All other data generated or analysed during this study are included in the manuscript and supporting files.
Article and author information
Author details
Geoffrey Wilson Meissner
Christopher T Zugates
Dagmar Kainmueller
Gabriella R Sterne
Funding
Howard Hughes Medical Institute
- Geoffrey Wilson Meissner
- Aljoscha Nern
- Zachary Dorman
- Gina M DePasquale
- Kaitlyn Forster
- Theresa Gibney
- Joanna H Hausenfluck
- Yisheng He
- Nirmala A Iyer
- Jennifer Jeter
- Lauren Johnson
- Rebecca M Johnston
- Kelley Lee
- Brian Melton
- Brianna Yarbrough
- Christopher T Zugates
- Jody Clements
- Cristian Goina
- Hideo Otsuna
- Konrad Rokicki
- Robert R Svirskas
- Yoshinori Aso
- Gwyneth M Card
- Barry J Dickson
- Erica Ehrhardt
- Jens Goldammer
- Masayoshi Ito
- Dagmar Kainmueller
- Wyatt Korff
- Lisa Mais
- Ryo Minegishi
- Shigehiro Namiki
- Gerald M Rubin
- Gabriella R Sterne
- Tanya Wolff
- Oz Malkesman
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Ilona C Grunwald Kadow, University of Bonn, Germany
Version history
- Preprint posted: May 30, 2020 (view preprint)
- Received: May 30, 2022
- Accepted: February 21, 2023
- Accepted Manuscript published: February 23, 2023 (version 1)
- Version of Record published: March 21, 2023 (version 2)
Copyright
© 2023, Meissner et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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A searchable image resource of Drosophila GAL4-driver expression patterns with single neuron resolution
eLife 12:e80660.
https://doi.org/10.7554/eLife.80660
Further reading
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- Neuroscience
The presence of global synchronization of vasomotion induced by oscillating visual stimuli was identified in the mouse brain. Endogenous autofluorescence was used and the vessel ‘shadow’ was quantified to evaluate the magnitude of the frequency-locked vasomotion. This method allows vasomotion to be easily quantified in non-transgenic wild-type mice using either the wide-field macro-zoom microscopy or the deep-brain fiber photometry methods. Vertical stripes horizontally oscillating at a low temporal frequency (0.25 Hz) were presented to the awake mouse, and oscillatory vasomotion locked to the temporal frequency of the visual stimulation was induced not only in the primary visual cortex but across a wide surface area of the cortex and the cerebellum. The visually induced vasomotion adapted to a wide range of stimulation parameters. Repeated trials of the visual stimulus presentations resulted in the plastic entrainment of vasomotion. Horizontally oscillating visual stimulus is known to induce horizontal optokinetic response (HOKR). The amplitude of the eye movement is known to increase with repeated training sessions, and the flocculus region of the cerebellum is known to be essential for this learning to occur. Here, we show a strong correlation between the average HOKR performance gain and the vasomotion entrainment magnitude in the cerebellar flocculus. Therefore, the plasticity of vasomotion and neuronal circuits appeared to occur in parallel. Efficient energy delivery by the entrained vasomotion may contribute to meeting the energy demand for increased coordinated neuronal activity and the subsequent neuronal circuit reorganization.
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- Medicine
- Neuroscience
Background:
Ketamine has emerged as one of the most promising therapies for treatment-resistant depression. However, inter-individual variability in response to ketamine is still not well understood and it is unclear how ketamine’s molecular mechanisms connect to its neural and behavioral effects.
Methods:
We conducted a single-blind placebo-controlled study, with participants blinded to their treatment condition. 40 healthy participants received acute ketamine (initial bolus 0.23 mg/kg, continuous infusion 0.58 mg/kg/hr). We quantified resting-state functional connectivity via data-driven global brain connectivity and related it to individual ketamine-induced symptom variation and cortical gene expression targets.
Results:
We found that: (i) both the neural and behavioral effects of acute ketamine are multi-dimensional, reflecting robust inter-individual variability; (ii) ketamine’s data-driven principal neural gradient effect matched somatostatin (SST) and parvalbumin (PVALB) cortical gene expression patterns in humans, while the mean effect did not; and (iii) behavioral data-driven individual symptom variation mapped onto distinct neural gradients of ketamine, which were resolvable at the single-subject level.
Conclusions:
These results highlight the importance of considering individual behavioral and neural variation in response to ketamine. They also have implications for the development of individually precise pharmacological biomarkers for treatment selection in psychiatry.
Funding:
This study was supported by NIH grants DP5OD012109-01 (A.A.), 1U01MH121766 (A.A.), R01MH112746 (J.D.M.), 5R01MH112189 (A.A.), 5R01MH108590 (A.A.), NIAAA grant 2P50AA012870-11 (A.A.); NSF NeuroNex grant 2015276 (J.D.M.); Brain and Behavior Research Foundation Young Investigator Award (A.A.); SFARI Pilot Award (J.D.M., A.A.); Heffter Research Institute (Grant No. 1–190420) (FXV, KHP); Swiss Neuromatrix Foundation (Grant No. 2016–0111) (FXV, KHP); Swiss National Science Foundation under the framework of Neuron Cofund (Grant No. 01EW1908) (KHP); Usona Institute (2015 – 2056) (FXV).
Clinical trial number:
