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2022_MolMed_Genetic_HerveraA.pdf (1.92 MB)

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Published version

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2022-08-17

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cc by (c) Mesquida Veny, Francina et al., 2022
Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/189186

Genetic control of neuronal activity enhances axonal growth only on permissive substrates

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https://doi.org/10.1186/s10020-022-00524-2

Abstract

Abstract Background Neural tissue has limited regenerative ability. To cope with that, in recent years a diverse set of novel tools has been used to tailor neurostimulation therapies and promote functional regeneration after axonal injuries. Method In this report, we explore cell-specific methods to modulate neuronal activity, including opto- and chemogenetics to assess the effect of specific neuronal stimulation in the promotion of axonal regeneration after injury. Results Opto- and chemogenetic stimulations of neuronal activity elicited increased in vitro neurite outgrowth in both sensory and cortical neurons, as well as in vivo regeneration in the sciatic nerve, but not after spinal cord injury. Mechanistically, inhibitory substrates such as chondroitin sulfate proteoglycans block the activity induced increase in axonal growth. Conclusions We found that genetic modulations of neuronal activity on both dorsal root ganglia and corticospinal motor neurons increase their axonal growth capacity but only on permissive environments.

Subject

Axons, Lesions medul·lars

Subject (English)

Axons, Spinal cord injuries

Citation

Mesquida-Veny, Francina;Martínez-Torres, Sara;del Rio, Jose Antonio;Hervera, Arnau. Genetic control of neuronal activity enhances axonal growth only on permissive substrates. Molecular Medicine, 2022, 28, 1-97

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Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC))

Citation

MESQUIDA VENY, Francina, et al. Genetic control of neuronal activity enhances axonal growth only on permissive substrates. Molecular Medicine. 2022. Vol.  28, num. 1-97. ISSN 1528-3658. [consulted: 15 of August of 2026]. Available at: https://hdl.handle.net/2445/189186

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