Arnau Llobet Rosell

Abstract After injury, the severed axon separated from the soma activates programmed axon degeneration, an evolutionarily conserved pathway to initiate its degeneration within a day. Conversely, severed projections deficient in programmed axon degeneration remain morphologically preserved with functional synapses for weeks to months after injury. How this synaptic function is sustained remains currently unknown.

Abstract After injury, the axon separated from the soma activates programmed axon degeneration, an evolutionarily conserved pathway to initiate its degeneration within a day. However, in various species, severed axonal and synaptic (anucleate) projections remain preserved for weeks to months after injury. How they preserve themselves remains currently unknown. Here, we demonstrate that dNmnat-mediated over- expression attenuates programmed axon degeneration in distinct neuronal populations.

Abstract After injury, the axon separated from the soma activates an evolutionarily conserved pathway to initiate its degeneration within a day. Attenuation of this pathway results in morphologically preserved severed axons and synapses for weeks after injury. When evoked, these projections remain able to elicit a postsynaptic behavior, a phenomenon that we define as preserved circuit integrity. The mechanism enabling the preservation of circuit integrity is currently unknown.