Ring attractor models for angular path integration have received strong experimental support. To function as integrators, head direction circuits require precisely tuned connectivity, but it is currently unknown how such tuning could be achieved. Here, we propose a network model in which a local, biologically plausible learning rule adjusts synaptic efficacies during development, guided by supervisory allothetic cues. Applied to the Drosophila head direction system, the model learns to path-integrate accurately and develops a connectivity strikingly similar to the one reported in experiments. The mature network is a quasi-continuous attractor and reproduces key experiments in which optogenetic stimulation controls the internal representation of heading, and where the network remaps to integrate with different gains in rodents. Our model predicts that path integration requires self-supervised learning during a developmental phase, and proposes a general framework to learn to path-integrate with gain-1 even in architectures that lack the physical topography of a ring.
All code used in this work is available at https://github.com/panvaf/LearnPI. The files required to reproduce the figures can be found at https://gin.g-node.org/pavaf/LearnPI.
A Connectome of the Adult Drosophila Central BrainneuPrint https://neuprint.janelia.org/.
- David Owald
- Richard Kempter
- David Owald
- Richard Kempter
- Pantelis Vafidis
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
- Srdjan Ostojic, Ecole Normale Superieure Paris, France
- Received: April 28, 2021
- Accepted: June 17, 2022
- Accepted Manuscript published: June 20, 2022 (version 1)
© 2022, Vafidis 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.
Efficient neurotransmission is essential for organism survival and is enhanced by myelination. However, the genes that regulate myelin and myelinating glial cell development have not been fully characterized. Data from our lab and others demonstrates that cd59, which encodes for a small GPI-anchored glycoprotein, is highly expressed in developing zebrafish, rodent, and human oligodendrocytes (OLs) and Schwann cells (SCs), and that patients with CD59 dysfunction develop neurological dysfunction during early childhood. Yet, the function of Cd59 in the developing nervous system is currently undefined. In this study, we demonstrate that cd59 is expressed in a subset of developing SCs. Using cd59 mutant zebrafish, we show that developing SCs proliferate excessively and nerves may have reduced myelin volume, altered myelin ultrastructure, and perturbed node of Ranvier assembly. Finally, we demonstrate that complement activity is elevated in cd59 mutants and that inhibiting inflammation restores SC proliferation, myelin volume, and nodes of Ranvier to wildtype levels. Together, this work identifies Cd59 and developmental inflammation as key players in myelinating glial cell development, highlighting the collaboration between glia and the innate immune system to ensure normal neural development.
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