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Rey, U.

Publications and source records attributed to Rey, U..

2 recordsLinked to original sources

An intrinsic neuronal manifold underlies brain-wide hierarchical organization of behavior in C. elegans

Large-scale neuronal recordings in various species have revealed behavior-related activity patterns. Surprisingly, these activities are distributed across brain regions, including sensory areas. However, their origins and functions are incompletely understood. Using whole-brain imaging in freely behaving C. elegans, we discover that such distributed brain activity is dominated by a low dimensional manifold, corresponding to the major action sequence of C. elegans. The manifold originates largely from intrinsic dynamics, with minor contributions from movement-induced sensations. We discover a new function of the manifold: to gate the activity of a large number of neuron classes. This gating constrains them to selectively encode faster time-scale motor patterns during specific brain states. We therefore propose that one principle function of brain-wide dynamics is to enable hierarchical organization of behavior: information about major actions is broadcast via a distributed manifold, to enable nesting of granular motor patterns within those major actions.

neuroscience↗

Rapid active zone remodeling consolidates presynaptic potentiation

Synaptic transmission is mediated by neurotransmitter release at presynaptic active zones (AZs) followed by postsynaptic neurotransmitter detection. Plastic changes in transmission maintain functionality during perturbations and enable memory formation. Postsynaptic plasticity targets neurotransmitter receptors, but presynaptic plasticity mechanisms directly regulating the neurotransmitter release apparatus remain largely enigmatic. Here we describe that AZs consist of nano-modular release site units and identify a molecular sequence adding more modules within minutes of plasticity induction. This requires cognate transport machinery and a discrete subset of AZ scaffold proteins. Structural remodeling is not required for the immediate potentiation of neurotransmitter release, but rather necessary to sustain this potentiation over longer timescales. Finally, mutations in Unc13 that disrupt homeostatic plasticity at the neuromuscular junction also impair shot-term memory when central neurons are targeted, suggesting that both forms of plasticity operate via Unc13. Together, while immediate synaptic potentiation capitalizes on available material, it triggers the coincident incorporation of modular release sites to consolidate stable synapse function.

neuroscience↗