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FIRST PERSON First person Daniel Sobrido-Camea ́ n First Person is a series of interviews with the first authors of a selection of papers published in Disease Models & Mechanisms (DMM), helping early-career researchers promote themselves alongside their papers. Daniel Sobrido-Camea ́ n is first author on Serotonin inhibits axonal regeneration of identifiable descending neurons after a complete spinal cord injury in lampreys, published in DMM. Daniel is a PhD student in the lab of Marı ́ a Celina Rodicio and Anto ́ n Barreiro-Iglesias at Universidade de Santiago de Compostela, Santiago de Compostela, Spain, investigating the mechanisms involved in the development and regeneration of the nervous system. How would you explain the main findings of your paper to non-scientific family and friends? Humans suffer an irreversible loss of sensory and locomotor function after a spinal cord injury. In contrast to humans, lampreys recover the ability to swim following a complete spinal cord injury. The spinal cord is formed, among other things, by descending axons coming from the brain. Axons are the wiresused by neurons to send orders to the muscles to perform movements. Spinal cord injuries damage these axons; therefore, the ability to control muscles below the site of injury is lost. Axons of lampreys are able to regenerate after injury, which allows them to recover swimming capacity after a spinal cord injury. We use lampreys to find molecules that control axon regeneration. Serotonin is a molecule used by neurons as a signal to talk to each other. Neurons have special antennasto receive these signals. These antennasare known as receptors. Neurons express serotonin receptors to respond to serotonin. In our study, we show that serotonin, acting through one of its receptors, inhibits axon regeneration after spinal cord injury in lampreys. Moreover, we demonstrated that, if we inhibit the activation of these receptors using drugs, we can improve axon regeneration. I believe that my research will provide a new way to design potential treatments for spinal cord injury. What are the potential implications of these results for your field of research? In this work we demonstrate the role of endogenous serotonin in the regeneration of lamprey axons following spinal cord injury. This work provides a possible new way to promote regeneration after spinal cord injury in non-regenerating animal models. Moreover, there are treatments that modulate the serotonergic system that are used in humans, for example to treat depressive disorders, and their effects in neurological recovery after spinal cord injury are unknown. This work opens the door to study other possible uses of these drugs. What are the main advantages and drawbacks of the model system you have used as it relates to the disease you are investigating? Lampreys recover locomotion spontaneously after a complete spinal cord injury, but, in spite of the amazing regenerative capacity of their central nervous system, not all neurons show the same abilities for axon regeneration. Among the brain descending neurons of lampreys, there are 36 individually identifiable giant descending neurons. These identifiable descending neurons vary greatly in their regenerative abilities following a complete spinal cord injury, even when their axons run in similar paths in a spinal cord that is permissive for axonal regrowth. So, lampreys offer an interesting animal model to study the molecular mechanisms that underlie the ability of neurons to regenerate. The main disadvantage of the lamprey model is related to their life cycle. It takes between 5 and 7 years from birth to sexual maturity; therefore, it is impossible to generate stable mutant or transgenic lines in the laboratory. In any case, we have been able to implement both drug and genetic treatments (morpholinos) to be able to carry out these functional studies. Seeing a lamprey with a complete spinal cord injury that has completely recovered its swimming capacity never ceases to amaze meThe plasticity of the nervous system in these animals is amazing.What has surprised you the most while conducting your research? Seeing a lamprey with a complete spinal cord injury that has completely recovered its swimming capacity never ceases to amaze Daniel Sobrido-Camea ́ n Daniel Sobrido-Cameá ns contact details: Department of Functional Biology, CIBUS, Faculty of Biology, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain. E-mail: [email protected] This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. 1 © 2019. Published by The Company of Biologists Ltd | Disease Models & Mechanisms (2019) 12, dmm039214. doi:10.1242/dmm.039214 Disease Models & Mechanisms

First person – Daniel Sobrido-Cameán...Daniel Sobrido-Cameán ’s contact details: Department of Functional Biology, CIBUS, Faculty of Biology, Universidade de Santiago de Compostela,

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Page 1: First person – Daniel Sobrido-Cameán...Daniel Sobrido-Cameán ’s contact details: Department of Functional Biology, CIBUS, Faculty of Biology, Universidade de Santiago de Compostela,

FIRST PERSON

First person – Daniel Sobrido-CameanFirst Person is a series of interviews with the first authors of a selectionof papers published in DiseaseModels &Mechanisms (DMM), helpingearly-career researchers promote themselves alongside their papers.Daniel Sobrido-Camean is first author on ‘Serotonin inhibits axonalregeneration of identifiable descending neurons after a complete spinalcord injury in lampreys’, published in DMM. Daniel is a PhD student inthe lab of Marıa Celina Rodicio and Anton Barreiro-Iglesias atUniversidade de Santiago de Compostela, Santiago de Compostela,Spain, investigating the mechanisms involved in the development andregeneration of the nervous system.

How would you explain the main findings of your paperto non-scientific family and friends?Humans suffer an irreversible loss of sensory and locomotor functionafter a spinal cord injury. In contrast to humans, lampreys recover theability to swimfollowingacomplete spinal cord injury.The spinal cord isformed, among other things, by descending axons coming from thebrain.Axonsare the ‘wires’usedbyneuronsto sendorders to themusclesto perform movements. Spinal cord injuries damage these axons;therefore, the ability to control muscles below the site of injury is lost.Axons of lampreys are able to regenerate after injury, which allows themto recover swimming capacityafter a spinal cord injury.Weuse lampreysto findmolecules that control axon regeneration. Serotonin is amoleculeused by neurons as a signal to ‘talk to each other’. Neurons have special‘antennas’ to receive these signals. These ‘antennas’ are known asreceptors.Neurons express serotonin receptors to respond to serotonin. Inour study, we show that serotonin, acting through one of its receptors,inhibits axon regeneration after spinal cord injury in lampreys.Moreover,we demonstrated that, if we inhibit the activation of these receptors usingdrugs, we can improve axon regeneration. I believe that my researchwillprovide a new way to design potential treatments for spinal cord injury.

What are the potential implications of these results for yourfield of research?In this work we demonstrate the role of endogenous serotonin in theregeneration of lamprey axons following spinal cord injury. Thiswork provides a possible new way to promote regeneration afterspinal cord injury in non-regenerating animal models. Moreover,there are treatments that modulate the serotonergic system that areused in humans, for example to treat depressive disorders, and theireffects in neurological recovery after spinal cord injury are unknown.This work opens the door to study other possible uses of these drugs.

What are the main advantages and drawbacks of the modelsystem you have used as it relates to the disease you areinvestigating?Lampreys recover locomotion spontaneously after a complete spinalcord injury, but, in spite of the amazing regenerative capacity of theircentral nervous system, not all neurons show the same abilities for

axon regeneration. Among the brain descending neurons of lampreys,there are 36 individually identifiable giant descending neurons. Theseidentifiable descending neurons vary greatly in their regenerativeabilities following a complete spinal cord injury, even when theiraxons run in similar paths in a spinal cord that is permissive for axonalregrowth. So, lampreys offer an interesting animal model to study themolecular mechanisms that underlie the ability of neurons toregenerate. The main disadvantage of the lamprey model is relatedto their life cycle. It takes between 5 and 7 years from birth to sexualmaturity; therefore, it is impossible to generate stable mutant ortransgenic lines in the laboratory. In any case, we have been able toimplement both drug and genetic treatments (morpholinos) to be ableto carry out these functional studies.

“Seeing a lamprey with a complete spinalcord injury that has completely recoveredits swimming capacity never ceases toamaze me… The plasticity of the nervoussystem in these animals is amazing.”

What has surprised you the most while conducting yourresearch?Seeing a lamprey with a complete spinal cord injury that hascompletely recovered its swimming capacity never ceases to amaze

Daniel Sobrido-Camean

Daniel Sobrido-Camean’s contact details: Department of Functional Biology,CIBUS, Faculty of Biology, Universidade de Santiago de Compostela, 15782Santiago de Compostela, Spain.E-mail: [email protected]

This is an Open Access article distributed under the terms of the Creative Commons AttributionLicense (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use,distribution and reproduction in any medium provided that the original work is properly attributed.

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© 2019. Published by The Company of Biologists Ltd | Disease Models & Mechanisms (2019) 12, dmm039214. doi:10.1242/dmm.039214

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Page 2: First person – Daniel Sobrido-Cameán...Daniel Sobrido-Cameán ’s contact details: Department of Functional Biology, CIBUS, Faculty of Biology, Universidade de Santiago de Compostela,

me. Specifically, in this study, I was surprised to see that lampreys inwhich axon regeneration was inhibited with different treatmentswere still able to recover locomotion similarly to control animals.The plasticity of the nervous system in these animals is amazing.

Describe what you think is the most significant challengeimpacting your research at this time and how will this beaddressed over the next 10 years?There is no cure for spinal cord injury. Stem cells, tissueengineering, pharmacological treatments, physiotherapy, etc. havebeen investigated as a potential solution for spinal cordregeneration. However, I believe that there is strength in numbersand that combinatorial approaches are more likely to give the

answer. The challenge is to combine the data provided bypharmacological studies, such as this, with advances in tissueengineering and other strategies. We must promote interdisciplinaryresearch.

What changes do you think could improve the professionallives of early-career scientists?The greatest difficulty in succeeding in a scientific career is theeconomic difficulty. Research is the basis of progress anddevelopment. But, many non-scientists are unaware of the workwe do in the laboratory. I think that making society aware of researchis key in leading countries to support young scientists.

“I think that making society aware ofresearch is key in leading countries tosupport young scientists.”

What’s next for you?My next goal is to finish my PhD thesis in the following months.Then, I will look for an interesting place for a postdoctoral positionthat would allow me to continue studying the nervous system.

Whydid youchooseDiseaseModels&Mechanismsto submityour paper?Lampreys are widely known as a model for evo-devo studies, butthey are not so commonly used as a model for spinal cordregeneration. I like the focus of Disease Models & Mechanismson the use of a wide variety of animal models, including non-conventional models like lampreys, to understand diseasemechanisms and develop new treatments. I think that this journalbrings together a very interesting nichewhere different models bringa variety ways of finding solutions to human diseases.

ReferenceSobrido-Camean, D., Robledo, D., Sanchez, L., Rodicio, M. C. and Barreiro-

Iglesias, A. (2019). Serotonin inhibits axonal regeneration of identifiabledescending neurons after a complete spinal cord injury in lamprey. Dis. Model.Mech. 12, dmm037085.

Lamprey axons regenerated following a complete spinal cord injury.

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FIRST PERSON Disease Models & Mechanisms (2019) 12, dmm039214. doi:10.1242/dmm.039214

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